scientificamerican--2020-12-09--Artificial Intelligence Is Now Shockingly Good at Sounding Human

Synthetic voices have become ubiquitous .
They feed us directions in the morning , shepherd us through phone calls by day and broadcast the news on smart speakers at night .
And as the technology used to make them improves , these voices are becoming more and more human-sounding .
This is the final frontier in synthetic speech : replicating not just what we say but how we say it .
Rupal Patel heads a research group at Northeastern University that studies speech prosody—the changes in pitch , loudness and duration that we use to convey intent and emotion through @ @ @ @ @ @ @ it as the icing on the cake , ” she explains .
“ You have the message , and now it ’ s how you modulate that message , but I really think it ’ s the scaffolding that gives meaning to the message itself.
” Patel says she grew interested in prosody after finding it was the only element of vocal communication that seemed to be available to people with some kinds of severe speech disorders .
These patients were able to make expressive sounds even if they could not speak clearly @ @ @ @ @ @ @ to build custom synthetic voices for nonspeaking individuals .
VocaliD has since expanded to commercial brands and influencers .
Synthetic speech has come a long way over the years .
At age nine , Siri is the oldest virtual assistant—but in the world of speaking machines , she ’ s a baby .
People have been trying to synthesize speech since at least the 18th century , when an Austro-Hungarian inventor built a crude replica of the human vocal tract that could articulate entire phrases ( albeit in a monotone ) .
Current @ @ @ @ @ @ @ complete with awkward pauses and lip smacks .
Still , training on thousands of samples per second is prohibitively expensive for most real-world systems .
Researchers , including those at VocaliD , are continually implementing newer and more efficient methods .
But even as the remaining gaps between human and synthetic speech are steadily closing , truly lifelike prosody continues to elude even the most sophisticated systems .
Maybe what ’ s still missing requires machines not only to mimic humans but also to feel like us .

Synthetic voices have become ubiquitous. They feed us directions in the morning, shepherd us through phone calls by day and broadcast the news on smart speakers at night. And as the technology used to make them improves, these voices are becoming more and more human-sounding. This is the final frontier in synthetic speech: replicating not just what we say but how we say it.
Rupal Patel heads a research group at Northeastern University that studies speech prosody—the changes in pitch, loudness and duration that we use to convey intent and emotion through voice. “Sometimes people think of it as the icing on the cake,” she explains. “You have the message, and now it’s how you modulate that message, but I really think it’s the scaffolding that gives meaning to the message itself.”
Patel says she grew interested in prosody after finding it was the only element of vocal communication that seemed to be available to people with some kinds of severe speech disorders. These patients were able to make expressive sounds even if they could not speak clearly. In 2014 Patel founded a company to build custom synthetic voices for nonspeaking individuals. VocaliD has since expanded to commercial brands and influencers.
Synthetic speech has come a long way over the years. At age nine, Siri is the oldest virtual assistant—but in the world of speaking machines, she’s a baby. People have been trying to synthesize speech since at least the 18th century, when an Austro-Hungarian inventor built a crude replica of the human vocal tract that could articulate entire phrases (albeit in a monotone).
Current machine-learning techniques can model human speech, complete with awkward pauses and lip smacks. Still, training on thousands of samples per second is prohibitively expensive for most real-world systems. Researchers, including those at VocaliD, are continually implementing newer and more efficient methods.
But even as the remaining gaps between human and synthetic speech are steadily closing, truly lifelike prosody continues to elude even the most sophisticated systems. Maybe what’s still missing requires machines not only to mimic humans but also to feel like us.


scientificamerican--2020-12-11--These Nine Women Should Have Key Roles in the New Administration

President-elect Joe Biden is starting to announce nominees to prominent science positions in his administration .
As the U.S. grapples with the consequences of the last four years of the Trump administration undermining science and harming already marginalized groups at every turn , it is crucial that the Biden team choose highly qualified leaders who bring strong scientific expertise and who reflect the values and diversity of the nation .
During the campaign , Biden said that his administration would “ choose science over fiction ” ; now is the time to fulfill that campaign promise .
We need leaders @ @ @ @ @ @ @ scientific infrastructure , repair the damage to our credibility , ensure science is guiding agency actions , and help address long-standing inequities in access to science and government support .
Given the long history of science advisors and cabinet positions held by white men , we are heartened that the incoming administration has made an explicit commitment to build a diverse administration that is intersectional , with women , nonbinary individuals and people of color elevated to senior positions .
500 Women Scientists strongly supports the appointment of outstanding women for leadership positions @ @ @ @ @ @ @ these women will be incredible assets to the administration , will value science , and will serve the nation with honor and dignity .
This list is by no means exhaustive , as there are many enormously talented and qualified people to choose from , but we are especially enthusiastic to support the following people for a Biden-Harris Science Squad ( and if the goes to someone else for any of these positions , the women on our list would still be excellent candidates for other roles in the administration ) .
On @ @ @ @ @ @ @ no one more qualified for this position than Lubchenco .
She has the science chops as a marine ecologist with expertise in oceans and climate change and has worked in the government as the U.S. undersecretary of commerce for oceans and atmosphere and as administrator of the National Oceanic and Atmospheric Administration ( NOAA ) under President Obama .
She also served on the inaugural Obama science team during 2009–2013 and 2014–2016 was the first U.S. State Department science envoy for the oceans .
Lubchenco has also collaborated with industry , communities , @ @ @ @ @ @ @ to address a variety of environmental challenges .
Note : The OSTP Director should be elevated to a Cabinet level position , as President-elect Biden has previously suggested .
Given the need for bold and progressive climate action , we recommend someone with a strong background in climate change science and a record of leadership in environmental justice—areas the administration has named as top priorities .
Current position : Co-founder and Executive Director of the Center for Earth , Energy and Democracy ( CEED ) On the science squad because : The organization @ @ @ @ @ @ @ and analytic support to environmental justice groups and coalitions .
They helped shape and launch the Equitable and Just Climate Platform in 2018 , which centers the needs and concerns of those most affected by pollution .
Martinez was part of Biden 's Climate Engagement Advisory Council helping to mobilize voters around climate , was an advisor on developing his policy plan to combat climate change and is now leading the CEQ agency review team for the Biden transition team .
She was recently named in Time ’ s 100 Most Influential People @ @ @ @ @ @ @ because : Toney , an attorney and former local elected official , has worked with the EPA in two separate roles between 2009 and 2017 .
She was the chairwoman of the EPA 's Local Government Advisory Committee , and then in 2014 , she was appointed by President Obama to serve as the regional administrator for the EPA Southeast Region .
She has a strong record of using science to guide EPA policy and she will be a great advocate for science agenda at the agency .
Since 2017 , Toney has @ @ @ @ @ @ @ focused on environmental justice and air pollution and has argued that combating climate change and protecting the environment are racial justice issues .
Current position : Senior fellow at Harvard Kennedy School of Government 's Belfer Center for Science and International Affairs ; advises national laboratories , energy investment funds and start-ups On the science squad because : She is a nuclear scientist well-versed in the priorities for the Department of Energy ( DOE ) , including managing the U.S. ’ s nuclear resources , supporting an innovation research agenda and overseeing large-scale @ @ @ @ @ @ @ the DOE undersecretary during the Obama administration , Sherwood-Randall could hit the ground running in an agency that is in need of a leader who will support DOE employees and protect their scientific integrity .
On the science squad because : She has a deep and stellar scientific background in oceanography and geography and has both academic and private sector chops directly applicable to NOAA ’ s work on oceans , satellites , weather and atmospheric science .
Wright has provided guidance to federal science programs and has served on NOAA ’ s @ @ @ @ @ @ @ of Sciences Ocean Studies Board .
She is also committed to equity and inclusion and will help foster a diverse and vibrant culture at NOAA .
Secretary of the Interior : U.S. Representative Deb Haaland , J.D .
Current position : U.S. Representative for New Mexico ’ s 1st district On the science squad because : As an attorney , politician , and one of the first Native American women elected to Congress , Haaland has demonstrated leadership both nationally and for communities in New Mexico .
She sits on the House Committee @ @ @ @ @ @ @ .
in Indian Law and has worked with the private sector to successfully advocate for environmentally friendly practices .
She has a strong record of supporting science and making evidence-based decisions .
The U.S. Department of the Interior needs the experience and perspective of Rep. Haaland at the helm .
Science and Technology Advisor to the Secretary of State : Frances Colón , Ph.D. On the science squad because : Colón is a climate and international environmental policy expert who has diligently worked to keep science front and center in foreign policy dialogues @ @ @ @ @ @ @ for global engagement .
She was the deputy science and technology adviser to the secretary of state from 2012 to 2017 , was also the highest-ranking Hispanic scientist at the State Department at that time , and led the Energy and Climate Partnership for the Americas ( ECPA ) , an initiative to accelerate sustainable energy in the Americas .
Colón is also a loud and proud advocate for the advancement of women and girls in STEM as evidenced by several bold initiatives she has led and created throughout her career .
Current @ @ @ @ @ @ @ CEO of Ocean Collectiv and founder of Urban Ocean Lab , a think tank for coastal cities .
On the science squad because : Johnson is a climate policy expert who advised the Warren campaign on the development of the Blue New Deal , the co-editor of a book of essays called All We Can Save that features the writings of women climate leaders and the co-host of a climate podcast called “ How to Save a Planet ” focused on everyday climate solutions .
She is committed to working for climate justice @ @ @ @ @ @ @ .
Current Position : Stokes is an assistant professor in the Department of Political Science at the University of California , Santa Barbara .
On the science squad because : Stokes is an expert in public policy , with a focus on energy , environment and climate change .
She has written a book Short Circuiting Policy that examines the roles interest groups play in weakening U.S. clean energy laws , and she launched a climate podcast called “ A Matter of Degrees ” focused on climate .
She is a leader in @ @ @ @ @ @ @ to ensuring climate action is inclusive , equitable and just .
The U.S. federal government is in dire need of new talent , and many important science positions have been empty or underutilized under the Trump administration .
There is an opportunity to build back better by leveraging the full diversity of scientists and people who can bring their lived experiences to these critical government positions .
There is a squad of exceptionally qualified women and nonbinary scientists who are ready to support the Biden administration , many on the 500 Women Scientists @ @ @ @ @ @ @ confirmed to the many open science positions within the federal government , we expect Biden appointees to embody the change we want to see .
We expect them to use science to inform policy .
We expect them to lift the voices that have been overlooked and marginalized .
We expect them to use science to protect people and communities , not corporations .
We expect them to work tirelessly to create a safer and more equitable world .

President-elect Joe Biden is starting to announce nominees to prominent science positions in his administration. As the U.S. grapples with the consequences of the last four years of the Trump administration undermining science and harming already marginalized groups at every turn, it is crucial that the Biden team choose highly qualified leaders who bring strong scientific expertise and who reflect the values and diversity of the nation. During the campaign, Biden said that his administration would “choose science over fiction”; now is the time to fulfill that campaign promise. We need leaders who can rebuild our nation’s scientific infrastructure, repair the damage to our credibility, ensure science is guiding agency actions, and help address long-standing inequities in access to science and government support.
Given the long history of science advisors and cabinet positions held by white men, we are heartened that the incoming administration has made an explicit commitment to build a diverse administration that is intersectional, with women, nonbinary individuals and people of color elevated to senior positions. 500 Women Scientists strongly supports the appointment of outstanding women for leadership positions within the Biden-Harris administration; we know these women will be incredible assets to the administration, will value science, and will serve the nation with honor and dignity.
This list is by no means exhaustive, as there are many enormously talented and qualified people to choose from, but we are especially enthusiastic to support the following people for a Biden-Harris Science Squad (and if the goes to someone else for any of these positions, the women on our list would still be excellent candidates for other roles in the administration).
White House Science Advisor: Jane Lubchenco, Ph.D.
Current position: University Distinguished Professor at Oregon State University
On the science squad because: There is no one more qualified for this position than Lubchenco. She has the science chops as a marine ecologist with expertise in oceans and climate change and has worked in the government as the U.S. undersecretary of commerce for oceans and atmosphere and as administrator of the National Oceanic and Atmospheric Administration (NOAA) under President Obama. She also served on the inaugural Obama science team during 2009–2013 and 2014–2016 was the first U.S. State Department science envoy for the oceans. Lubchenco has also collaborated with industry, communities, civil society, academia and faith-based organizations to address a variety of environmental challenges.
Note: The OSTP Director should be elevated to a Cabinet level position, as President-elect Biden has previously suggested. Given the need for bold and progressive climate action, we recommend someone with a strong background in climate change science and a record of leadership in environmental justice—areas the administration has named as top priorities.
White House Council on Environmental Quality: Cecilia Martinez, Ph.D.
Current position: Co-founder and Executive Director of the Center for Earth, Energy and Democracy (CEED)
On the science squad because: The organization Martinez leads, CEED, provides research and analytic support to environmental justice groups and coalitions. They helped shape and launch the Equitable and Just Climate Platform in 2018, which centers the needs and concerns of those most affected by pollution. Martinez was part of Biden's Climate Engagement Advisory Council helping to mobilize voters around climate, was an advisor on developing his policy plan to combat climate change and is now leading the CEQ agency review team for the Biden transition team. She was recently named in Time’s 100 Most Influential People of 2020.
Environmental Protection Agency: Heather McTeer Toney, J.D.
Current position: Senior Director for Moms Clean Air Force
On the science squad because: Toney, an attorney and former local elected official, has worked with the EPA in two separate roles between 2009 and 2017. She was the chairwoman of the EPA's Local Government Advisory Committee, and then in 2014, she was appointed by President Obama to serve as the regional administrator for the EPA Southeast Region. She has a strong record of using science to guide EPA policy and she will be a great advocate for science agenda at the agency. Since 2017, Toney has led field operations and grassroots organizing efforts focused on environmental justice and air pollution and has argued that combating climate change and protecting the environment are racial justice issues.
Secretary of Energy: Elizabeth Sherwood-Randall, Ph.D.
Current position: Senior fellow at Harvard Kennedy School of Government's Belfer Center for Science and International Affairs; advises national laboratories, energy investment funds and start-ups
On the science squad because: She is a nuclear scientist well-versed in the priorities for the Department of Energy (DOE), including managing the U.S.’s nuclear resources, supporting an innovation research agenda and overseeing large-scale scientific programs. With her experience as the DOE undersecretary during the Obama administration, Sherwood-Randall could hit the ground running in an agency that is in need of a leader who will support DOE employees and protect their scientific integrity.
National Oceanic and Atmospheric Administration Administrator: Dawn Wright, Ph.D.
Current position: Chief Scientist, Esri
On the science squad because: She has a deep and stellar scientific background in oceanography and geography and has both academic and private sector chops directly applicable to NOAA’s work on oceans, satellites, weather and atmospheric science. Wright has provided guidance to federal science programs and has served on NOAA’s Science Advisory Board and the National Academy of Sciences Ocean Studies Board. She is also committed to equity and inclusion and will help foster a diverse and vibrant culture at NOAA.
Secretary of the Interior: U.S. Representative Deb Haaland, J.D.
Current position: U.S. Representative for New Mexico’s 1st district
On the science squad because: As an attorney, politician, and one of the first Native American women elected to Congress, Haaland has demonstrated leadership both nationally and for communities in New Mexico. She sits on the House Committee on Natural Resources, earned a J.D. in Indian Law and has worked with the private sector to successfully advocate for environmentally friendly practices. She has a strong record of supporting science and making evidence-based decisions. The U.S. Department of the Interior needs the experience and perspective of Rep. Haaland at the helm.
Science and Technology Advisor to the Secretary of State: Frances Colón, Ph.D.
Current position: President and CEO, Jasperi Consulting
On the science squad because: Colón is a climate and international environmental policy expert who has diligently worked to keep science front and center in foreign policy dialogues and has used science as a tool for global engagement. She was the deputy science and technology adviser to the secretary of state from 2012 to 2017, was also the highest-ranking Hispanic scientist at the State Department at that time, and led the Energy and Climate Partnership for the Americas (ECPA), an initiative to accelerate sustainable energy in the Americas. Colón is also a loud and proud advocate for the advancement of women and girls in STEM as evidenced by several bold initiatives she has led and created throughout her career.
Domestic White House Climate Change Advisor: Ayana Elizabeth Johnson, Ph.D.
Current Position: Johnson is the founder and CEO of Ocean Collectiv and founder of Urban Ocean Lab, a think tank for coastal cities.
On the science squad because: Johnson is a climate policy expert who advised the Warren campaign on the development of the Blue New Deal, the co-editor of a book of essays called All We Can Save that features the writings of women climate leaders and the co-host of a climate podcast called “How to Save a Planet” focused on everyday climate solutions. She is committed to working for climate justice and broader inclusion in the climate movement.
Domestic White House Climate Change Advisor: Leah Stokes, Ph.D.
Current Position: Stokes is an assistant professor in the Department of Political Science at the University of California, Santa Barbara.
On the science squad because: Stokes is an expert in public policy, with a focus on energy, environment and climate change. She has written a book Short Circuiting Policy that examines the roles interest groups play in weakening U.S. clean energy laws, and she launched a climate podcast called “A Matter of Degrees” focused on climate. She is a leader in her field and has demonstrated a commitment to ensuring climate action is inclusive, equitable and just.
The U.S. federal government is in dire need of new talent, and many important science positions have been empty or underutilized under the Trump administration. There is an opportunity to build back better by leveraging the full diversity of scientists and people who can bring their lived experiences to these critical government positions. There is a squad of exceptionally qualified women and nonbinary scientists who are ready to support the Biden administration, many on the 500 Women Scientists team.
No matter who is ultimately confirmed to the many open science positions within the federal government, we expect Biden appointees to embody the change we want to see. We expect them to use science to inform policy. We expect them to lift the voices that have been overlooked and marginalized. We expect them to use science to protect people and communities, not corporations. We expect them to work tirelessly to create a safer and more equitable world.


scientificamerican--2020-12-11--What Science Has Learned About the Coronavirus One Year On

Jeffery DelViscio : [ 00:00:00 ] This is a Science Talk podcast from Scientific American I 'm Jeff DelViscio .
Today 's guest is Britt Glaunsinger , a virologist at the university of California , Berkeley , and the Howard Hughes Medical Institute .
She 's a specialist in infectious viruses , and she 's been studying them with a focus on the herpes virus in particular for the last 25 years .
Welcome to science talk , Brit .
Great to have you .
[ 00:00:26 ] Britt Glaunsinger : [ 00:00:26 ] Thank you , Jeff .
It @ @ @ @ @ @ @ 00:00:29 ] Jeffery DelViscio : [ 00:00:29 ] It 's a really important moment to look back at our very different reality just 12 months ago .
In December 2019 , the first infections were just emerging inside of China .
SARS-CoV-2 , did n't have a name yet , and no one could imagine the global effects that the virus would have on us all .
But it was also clear that this novel coronavirus lit a fire underneath the seat of science .
So my question is how far has our @ @ @ @ @ @ @ behavior of the virus come since then ?
[ 00:00:58 ] Britt Glaunsinger : [ 00:00:58 ] Yeah , we have learned some really critical things about how the virus works and also importantly about how our immune system responds to it and how this virus SARS-CoV-2 , essentially causes our immune system to misfire in cases of severe COVID-19 and misfiring really centers on the very early immune responses that our body mounts , these are called innate immune responses .
This innate immunity is a part of our body that really @ @ @ @ @ @ @ , like the CoV-2 virus that are not from our own body .
And once these factors or sensors detect these viral bids they sound out an immediate alarm system that operates through molecules called cytokines and interferons .
And these are important for activating those later immune responses like T-cells and antibodies that we hear about .
And what we think is that it 's likely that people who sound this innate immune alarm early upon exposure to the virus and induce early and high levels of that interferon alarm system go @ @ @ @ @ @ @ the virus .
So these might be the individuals with asymptomatic or moderate or mild disease .
[ 00:02:25 ] However , what scientists have learned is that people who go on to develop severe COVID do so probably because in them , the virus causes a misfiring of that immune response .
So like the wrong sets of immune cells may be brought in and they might not induce that early interferon alarm system quickly or strongly .
And then they ca n't control the viral load .
The virus amplifies to @ @ @ @ @ @ @ So their body responds to this continued presence of the virus , basically by increasing production of factors that are involved in inflammation .
[ 00:03:02 ] This is an overexuberant inflammation or inflammatory response .
And that 's what leads to the lung tissue damage , which is really a hallmark of COVID pathology .
So what we 've discovered scientists over the past year is that there are biomarkers that can give clues about who ultimately goes on to get severe disease .
[ 00:03:24 ] Scientists have also discovered genetic @ @ @ @ @ @ @ in those innate immune genes that can contribute to poor initial control of the virus .
I think that this understanding that there are essentially two phases of COVID-19 disease , that initial phase that 's dominated by viral amplification .
And a second phase that in severe cases is dominated by a misfiring of the immune response is really important .
It 's important because it illustrates that there are two types of therapies that are probably needed depending on the phase of the disease .
So drugs that target the virus @ @ @ @ @ @ @ 00:04:07 ] These would be things like Remdesivir that we 've heard a lot about in the news , or maybe treating with things like recombinant interferon .
This is something that is used to treat other chronic viral infections .
Those types of therapies are probably only going to be effective at stopping that first phase of the disease , um , but are not going to be very effective if they 're given during that second phase , because , uh , it 's then it 's not the virus , @ @ @ @ @ @ @ illness .
And so conversely drugs that dampen that overexuberant inflammatory response , and dexamethazone is one of those these , might be dangerous of given during that first phase , when you really want a rapid and robust immune response , but could be helpful at dampening the damage that 's caused by the immune system at later stages .
[ 00:04:59 ] Jeffery DelViscio : [ 00:04:59 ] One of the key parts of understanding the virus itself and how we fight it is scientifically really about timing , right ?
@ @ @ @ @ @ @ 00:05:05 ] Exactly , timing is really key .
A timing of figure out how your body responds very early and later .
And you know , the timing and the dose of the virus that you might receive , understanding how sort of , you know , that timing or the kinetics of infection and response are essential .
And we 've made a lot of progress on that over the last year .
[ 00:05:27 ] Jeffery DelViscio : [ 00:05:27 ] So let 's talk about some of that specific @ @ @ @ @ @ @ UC Berkeley .
What kind of work have you been doing over the last year ?
And what kind of work is being done across the university itself ?
[ 00:05:39 ] Britt Glaunsinger : [ 00:05:39 ] Yeah .
So what my lab has been working on , uh , during this past year related to Coronavirus is understanding the viral side of things .
So we know that this virus has a lot of strategies to try and dampen those early innate immune sensors .
It is evolved to try and @ @ @ @ @ @ @ response because that part of the immune response is so essential in essentially dampening down the ability of the virus to replicate very early on .
[ 00:06:12 ] And so what my lab and others at UC Berkeley have been doing is trying to figure out the strategies that the virus is using to fight that innate immune response -- how it is lowering the levels of these innate immune sensor , proteins and genes that could be used by your body to counteract the virus .
And so we study this @ @ @ @ @ @ @ level of the individual RNAs that the virus is targeting and blocking from being expressed .
[ 00:06:45 ] But there 's a wide variety of other research that 's going on across campus .
That sort of spans the scales of , uh , trying to solve the atomic structures of various viral components .
Because with these , you can use that information to design specific inhibitors against viral enzymes , and also at the scale of designing diagnostic tests and setting up testing centers to , to do community-based surveillance @ @ @ @ @ @ @ .
So really , uh , you know , Spanning the understanding the fine molecular details of how the virus works and interacts with its host cell up through community-based surveillance work .
[ 00:07:27 ] Jeffery DelViscio : [ 00:07:27 ] So , can we step back a little bit , and just talk about the innate immune response .
Maybe we can go from when the body first encounters it to post-infection .
And could you talk a little bit about what we know about immunity post-infection and how long that @ @ @ @ @ @ @ the innate immune response ?
How can it be useful and effective or not , and helping them body to , to fight the virus ?
[ 00:07:48 ] Britt Glaunsinger : [ 00:07:48 ] Yeah , well , it is known of course that the innate immune response plays really important roles in activating the adaptive immune response , those T cells and B cells that will either produce antibody in the case of B cells or T cells are components of the adaptive immune response that will come in and kill @ @ @ @ @ @ @ recognize them .
[ 00:08:11 ] So there , these are two arms of the immunity the immune system , the innate and the adaptive , but there are clear links and crosstalk between them .
We know that .
A very important question , which you bring up is to what extent does our body have the capacity to remember this particular virus ?
If you encounter the virus naturally through an infection and mount long lasting .
adaptive immunity to the virus .
And this is a really important question , @ @ @ @ @ @ @ , for example , if you 've already been infected with SARS-CoV-2 , are you protected against reinfection ?
And it 's possible that you are , but it 's also possible that you 're not .
We know from work that 's been done with the cold causing Corona viruses .
[ 00:09:02 ] There are circulating Corona viruses .
Of course , that caused about 30 % of the common cold .
Um , we know that individuals who are infected with these cold causing Corona viruses .
Can get reinfected @ @ @ @ @ @ @ year later , uh , with that same virus , which suggests that they do n't have what we would call sterilizing immunity , meaning that your immunity is so good that your immune system blocks the virus from setting up any kind of infection .
[ 00:09:30 ] But the good news is is that these individuals , even if they get reinfected are generally protected against disease .
And so that says that there is , uh , an immune response that can protect at least against disease and that 's @ @ @ @ @ @ @ know yet what the situation is going to look like for SARS-CoV-2 , because we 're still barely a year into this pandemic .
Um , although there are rare cases that have been reported already of reinfection with CoV-2 in individuals , um , from various parts of the world , including Hong Kong and the US and in Europe , et cetera , these are pretty rare examples , but they could be emblematic of the fact that natural infection with this virus , um , may not completely protect against @ @ @ @ @ @ @ , relatively short period of time .
Although it 's possible that natural re-infection could protect against , um , severe disease .
So the idea is that what we want to do is generate vaccines that could , um , in fact , improve that level of protection .
[ 00:10:36 ] So you could get a better , more long lasting immune response from a vaccine than you could from the virus in part , because we know that the virus itself has a lot of mechanisms built into dampen that @ @ @ @ @ @ @ hide itself in ways that makes it difficult for our bodies to generate a robust , adaptive immune response .
[ 00:11:00 ] And by delivering pieces of virus , uh , through vaccines , we may actually get a better response .
And I think that 's the hope , but it is still too early for us to know whether that is going to bear out because you simply just have to wait the length of time and see , you know , one year out how many people are protected @ @ @ @ @ @ @ from disease two years out , five years out , uh , what happens there that unfortunately is just a long waiting game .
There 's no way to speed up getting an answer to that question .
[ 00:11:34 ] Jeffery DelViscio : [ 00:11:34 ] I 'm glad you bring up vaccines because obviously there 's a lot of focus on that right now .
And that 's because there are a few vaccine candidates who 've done phase three trials by now , which is the last step before some @ @ @ @ @ @ @ Drug Administration .
And that emergency approval may even come in the time between when we 're recording this and when it goes live , that 's how fast this process is moving .
[ 00:11:55 ] So two companies are reporting better than 90 % efficacy .
Those are Pfizer and Moderna .
It should also somebody noted that there 's another vaccine candidate from the University of Oxford and the drug company , AstraZeneca that 's showing promise .
[ 00:12:08 ] But to go back to the Pfizer and maternal @ @ @ @ @ @ @ .
Could you talk a little bit about what an mRNA vaccine actually is and how it works ?
[ 00:12:18 ] Britt Glaunsinger : [ 00:12:18 ] Certainly , yeah , these two vaccines are ... the data , first of all , are incredibly exciting to , to most , all of us in that the efficacy appears from these initial results that have been released to be very high .
And , um , that 's exceptionally great news .
There are many unanswered questions , uh , related to @ @ @ @ @ @ @ on .
So it 's not that that we have all of the information yet , but I think that 's great news in part , because these messenger RNA vaccines .
We do n't have any track record with them .
[ 00:12:52 ] This is the first rollout or testing phase three testing of any mRNA vaccine .
So we did n't know if this was going to work at all .
Um , and the fact that they appear to be working so well is extremely exciting .
So what @ @ @ @ @ @ @ a traditional vaccine ?
Uh , to understand this , I need to just take a second to explain the concept of what an antigen is .
[ 00:13:15 ] An antigen is a bit of virus that you are , or a pathogen in general , but for our purposes , we 're , we 're talking about Cove too .
So it 's , it 's a bit of virus that you 're going to show to the immune system and tell the immune system essentially make .
Antibodies against this @ @ @ @ @ @ @ this and , you know , vaccine context , you are showing it an exact bit of virus that we know that if an antibody is made to that bit , that antibody can block or neutralize the virus .
[ 00:13:48 ] This is important because in the context of a natural infection , your immune system , does n't a priori know which bit of the virus , if it makes an antibody to it is going to stop that virus .
So it makes lots of antibodies to everything it @ @ @ @ @ @ @ those may bind the virus , but not bind it in a way that 's actually gon na block it .
[ 00:14:10 ] And so the benefit of a vaccine for , um , developing immunity is that you 're basically telling your immune system exactly what are the right kind of antibodies , hopefully for it to make .
And so that 's the benefit of that over a natural infection for acquiring immunity .
And there are a couple of ways to give that antigen or that bit of the @ @ @ @ @ @ @ traditional way would be to , uh , inject a person with a vaccine that , that has that protein already made .
[ 00:14:40 ] And so that the antigen of course , that all of the vaccines are targeting is the spike protein of the virus .
That 's that surface protein that is essential for allowing the viruses to bind cells and enter cells .
And so if you can block spike protein binding , and the function , you essentially have stopped the virus in its tracks because it @ @ @ @ @ @ @ [ 00:15:03 ] And a virus that ca n't get into a cell is for all practical purposes inert , and non-pathogenic .
So traditional vaccines would deliver that protein directly .
Either you grow up the protein , uh , you know , in a , in a big bio-reactor and injected itself , these are called subunit vaccines , or the protein is already present on the surface of an inactivated virus in some way .
[ 00:15:30 ] The thing that 's different about the messenger RNA vaccines , and @ @ @ @ @ @ @ similar for the , um , the , the adenovirus , the vector based vaccines , which is the weakened non-infectious , uh , vectors , all of the basic , you know , the front runners that we 're going to hear about early on for the phase three trials is that they do n't deliver the protein directly .
They deliver the sequence , the gene coding sequence for that spike protein , uh , into your cells and use your own cells to then , uh , make the protein @ @ @ @ @ @ @ spikes .
So the messenger RNA is basically delivering the gene sequence for the spike protein , or maybe just the RNA , the receptor binding domain of the spike protein , uh , which is then , uh , used by your cells to produce protein in your own cells to then show the immune system .
[ 00:16:28 ] Do you think Mr. And a vaccines would have come so far so fast without the virus around ?
Is it a chicken , egg virus , vaccine situation ?
[ 00:16:39 @ @ @ @ @ @ @ as quickly .
And in fact , you know what we have here as a platform , unlike we 've ever had before , where all of the possible types of vaccines are basically being generated and tested simultaneously .
Both the sort of more classic tried and true , uh , strategies for vaccine making that have been used for other FDA approved vaccines and these newer platforms like the DNA based vaccines and the MRNs vaccines that have shown promise , but have never , um , been tested in these @ @ @ @ @ @ @ .
So we 'll be able to cross compare them .
Uh , and of course the speed with which we 're getting data for these is accelerated dramatically .
We 've never had a phase three trial results within less than .
a year after a virus has emerged .
The fastest and of course , with a four to five years , which was lightning fast compared to how long it takes to develop most vaccines .
[ 00:17:42 ] Jeffery DelViscio : [ 00:17:42 ] So it seems that SARS @ @ @ @ @ @ @ science works .
[ 00:17:47 ] Britt Glaunsinger : [ 00:17:47 ] It is definitely remodeled the way that science works .
Uh , I ca n't think of a time , um , in recent history or even maybe an older history where the entire scientific community and medical community has turned their expertise with laser-like focus onto one thing , in particular .
We have a lot of big diseases , right ?
We 've got cancer , we 've got TB , we 've got AIDS , we 've got @ @ @ @ @ @ @ a lot of effort dedicated towards them .
But this virus has really brought the world to its knees in such a dramatic way that , um , that everybody is working , uh , together , uh , to use their expertise , whatever it may be to try and find ways to learn about and combat this virus and other viruses .
And so the hope of course , is that , um , the , what comes out of , of this , uh , parallel approaches from many , @ @ @ @ @ @ @ and expertise can be extrapolated to other diseases as well , other viral diseases , other pathogens .
[ 00:18:54 ] So for example , the mRNA platform or the DNA platform for a vaccines , the benefit there is that you can do this plug and play of inserting the gene sequence , very easily , they can be very rapidly designed .
And if they worked here that provides , uh , you know , a proof of principle , well , the next emerging pathogen that comes .
We can @ @ @ @ @ @ @ have a good sense that , that , uh , they 're going to be effective .
[ 00:19:23 ] Jeffery DelViscio : [ 00:19:23 ] As much damage as this virus has done to people 's lives to the economy in a strange way , it sort of seems like a bit of a catalyst .
[ 00:19:30 ] Britt Glaunsinger : [ 00:19:30 ] Yeah , you could see it as a catalyst , a catalyst based on need .
[ 00:19:37 ] Jeffery DelViscio : [ 00:19:37 ] That 's @ @ @ @ @ @ @ [ 00:19:39 ] Britt Glaunsinger : [ 00:19:39 ] That 's right .
That 's right .
[ 00:19:41 ] Jeffery DelViscio : [ 00:19:41 ] Let 's talk about the future .
Let 's not try to project a year ahead .
That seems unknowable .
Given how much changed in the last year .
So let 's talk about the next few months .
And maybe we can start in the White House .
There 's a change in the administration coming .
How do you think the federal response to @ @ @ @ @ @ @ month ?
[ 00:19:59 ] Britt Glaunsinger : [ 00:19:59 ] I would say I do n't have any insider information , but I can give you what is just my opinion from what I 've read in the news and whatnot .
Uh , and that 's what , what I 'm coming to expect is that there 's going to be more of a coordinated federal response instead of , um , relying on sort of state to state .
Uh , uh , responses , uh , you know , @ @ @ @ @ @ @ own and , and doing their own thing .
My , my expectation is that there 's going to be more coordination and more of a unified response that is led by the federal government , which I think will be very important , particularly for issues related to vaccine distribution and prioritization of course , of who gets the vaccine first and which factors do they get et cetera .
And also in thinking about , you know , policy of should the federal government be the one , uh , eliciting @ @ @ @ @ @ @ or mask wearing or shut downs instead of relying on States .
And we may be seeing a more heavy hand there is , is my guess .
[ 00:21:06 ] Jeffery DelViscio : [ 00:21:06 ] And in terms of what happens with the virus , it 's not waiting for anything , obviously .
Can you talk to me about mutation ?
How important is it for the future of the virus ?
How might that change our approach to fighting it ?
[ 00:21:17 ] Britt Glaunsinger : [ 00:21:17 @ @ @ @ @ @ @ we always think about in the context of pathogens and viruses in particular , because they randomly incorporate errors into their sequence every time they make a copy of themselves .
Uh , and that 's because for , for most viruses , they do n't have the capacity of copying their genome sequence in a way that is error free .
Our own cells have lots of ways of copying our own genome , um , and , and proofreading and checking and double checking it to make sure that errors are @ @ @ @ @ @ @ know , our own genome and ourselves as cells , divide viruses by and larger many viruses , particularly viruses with them RNA genomes do not have that capacity .
[ 00:22:04 ] And this leads usually to , uh , for RNA viruses , very rapid mutation .
And that mutation , uh , is something that can be really challenging in the context of developing antiviral drugs and in developing vaccines , because the concern is always that a very interim mutant version , a changed version of the virus will @ @ @ @ @ @ @ , an antibody or to a , um , an antiviral drug .
[ 00:22:38 ] Now there 's good news on that front for the coronavirus , which is that yes , it mutates all viruses mutate , but that it is not mutating at the hyper speed rate that some other RNA viruses , mutate like influenza and HIV .
Those are really tricky problems because of the rates that they , they , um , are undergoing mutation .
[ 00:23:04 ] Coronavirus has a special sort of feature that @ @ @ @ @ @ @ um , in which it can actually correct errors that occur as it is copying its genome .
It can proofread its own genome copying mechanism .
And what that means is that the virus accumulates fewer errors than many other RNA viruses .
Does n't mean no errors .
So of course people are constantly looking at how this virus is changing and they are identifying mutants that can arise .
And in some cases , mutants that may help the virus bind to cells better or enter cells better .
So @ @ @ @ @ @ @ an infectability .
[ 00:23:55 ] And so those mutations , um , do exist and , but they are not arising at a super rapid clip .
It 's not like we 're , we 're seeing tons of escape mutations , particularly in the spike protein for where the receptor binding domain might be .
It 's relatively speaking stable , which I think is good news for the vaccine front , but it 's definitely something that people are continuing to actively monitor .
There are hundreds of thousands of @ @ @ @ @ @ @ the database that , um , evolutionary biologists and genomic scientists are looking at exactly how these mutants are arising and what they mean for antibody escape and things like that .
[ 00:24:40 ] Jeffery DelViscio : [ 00:24:40 ] Well , in a seemingly unrelentingly bad year , that seems like a hint of at least a little good news .
Am I being too hasty ?
[ 00:24:48 ] Britt Glaunsinger : [ 00:24:48 ] I mean , that 's it .
What one might consider good news in this @ @ @ @ @ @ @ it 's important to keep in mind that as you mentioned , the virus is raging right now .
Um , we 're undergoing the third wave of infection here in the United States , the first being in April or may , and then we had a second wave in the summer and we 're now encountering the third wave .
We 're seeing exponential growth of the virus pretty much across the nation .
Um , and so there 's a lot of concern that our darkest days may be ahead @ @ @ @ @ @ @ news on the vaccine front potentially , but that 's not going to materialize even in a best case scenario for several more months to come .
And those several months , I think we 're going to see a large number of deaths and severe infections and transmissions .
And it 's partly because we 're entering the traditional respiratory illness season , right ?
This cold and flu season and coronavirus is one of those viruses that is a respiratory virus and tends to have seasonality to it .
[ 00:26:04 @ @ @ @ @ @ @ know , there 's a real concern that , you know , part of it is exponential growth that is linked to people being indoors more and much of our lives are spent in doors and that 's a , of course , much more so during the cold winter months .
[ 00:26:18 ] The problem with indoors and coldness is this tends to be environments where there 's decreased humidity , uh , so low relative humidity , maybe , uh , 20 to 40 % , uh , cold dry @ @ @ @ @ @ @ tend to be more stable and easier to transmit through the airborne route .
Um , dry air can also , uh , clear out some of the antiviral sort of mucus based clearing mechanisms that are in our airways that can impair that early innate immune response .
[ 00:26:53 ] And so , um , there are reasons to think that the , you know , the cold fall and winter air can exacerbate this problem , uh , of infection and that , uh , you know , so we @ @ @ @ @ @ @ , even though we 've got these great pieces of news from the vaccine that does not mean we can let down our guard , people need to be extremely careful during the wintertime about distancing and mask wearing and hand-washing and things like that .
It 's going to be up to all of us to , to prevent the spread as much as we can , as we wait for the vaccine distribution to happen and , you know , antiviral drugs to be discovered , et cetera .
We all @ @ @ @ @ @ @ , it 's you get a time when boy , if we let our guard down , it 's going to be a disaster over the next couple months .
[ 00:27:40 ] Jeffery DelViscio : [ 00:27:40 ] Well , it seems that science is not going to stop pushing on this .
Finally , could you talk just a little bit about what it means to be you right now ?
Someone who 's really been engaged with this kind of research for 25 years .
What is it like to @ @ @ @ @ @ @ closely given how important it is to really the whole world ?
[ 00:27:59 ] Britt Glaunsinger : [ 00:27:59 ] It 's a humbling experience on the one hand , because I , my perspective having worked on viruses so long helps me realize the magnitude of the problem and the magnitude of the challenge that , that faces us in a pandemic like this .
And , and so , um , that 's a very humbling , uh , experience , but also it 's one that , that makes @ @ @ @ @ @ @ and scientists in general , feel a sense of , of duty that we have something to contribute .
We have a knowledge base .
We have a skillset that can help us learn how this virus works and fight it .
And , and that 's a really motivating and invigorating feeling to , to know that that we have something to contribute and that my knowledge , you know , hopefully is useful in this context and as we go on in the future as well .
And so , um @ @ @ @ @ @ @ to fuel my passion for virology , which has always been strong .
[ 00:29:00 ] Britt Glaunsinger is a virologist at the University of California , Berkeley , and the Howard Hughes Medical Institute .
Thank you so much for joining us on Science Talk , Britt .
[ 00:29:08 ] Thank you so much for having me , Jeff .

Full Transcript
Jeffery DelViscio: [00:00:00] This is a Science Talk podcast from Scientific American I'm Jeff DelViscio. Today's guest is Britt Glaunsinger, a virologist at the university of California, Berkeley, and the Howard Hughes Medical Institute. She's a specialist in infectious viruses, and she's been studying them with a focus on the herpesvirus in particular for the last 25 years. Welcome to science talk, Brit. Great to have you.
[00:00:26] Britt Glaunsinger: [00:00:26] Thank you, Jeff. It's great to be here.
[00:00:29] Jeffery DelViscio: [00:00:29] It's a really important moment to look back at our very different reality just 12 months ago. In December 2019, the first infections were just emerging inside of China. SARS-CoV-2, didn't have a name yet, and no one could imagine the global effects that the virus would have on us all. But it was also clear that this novel coronavirus lit a fire underneath the seat of science. So my question is how far has our scientific understanding about the biology and the behavior of the virus come since then?
[00:00:58] Britt Glaunsinger: [00:00:58] Yeah, we have learned some really critical things about how the virus works and also importantly about how our immune system responds to it and how this virus SARS-CoV-2, essentially causes our immune system to misfire in cases of severe COVID-19 and misfiring really centers on the very early immune responses that our body mounts, these are called innate immune responses. This innate immunity is a part of our body that really uses sensors that detect pieces of pathogens, like the CoV-2 virus that are not from our own body. And once these factors or sensors detect these viral bids they sound out an immediate alarm system that operates through molecules called cytokines and interferons. And these are important for activating those later immune responses like T-cells and antibodies that we hear about. And what we think is that it's likely that people who sound this innate immune alarm early upon exposure to the virus and induce early and high levels of that interferon alarm system go on to pretty rapidly and effectively clear the virus. So these might be the individuals with asymptomatic or moderate or mild disease.
[00:02:25] However, what scientists have learned is that people who go on to develop severe COVID do so probably because in them, the virus causes a misfiring of that immune response. So like the wrong sets of immune cells may be brought in and they might not induce that early interferon alarm system quickly or strongly. And then they can't control the viral load. The virus amplifies to really high levels in their body. So their body responds to this continued presence of the virus, basically by increasing production of factors that are involved in inflammation.
[00:03:02] This is an overexuberant inflammation or inflammatory response. And that's what leads to the lung tissue damage, which is really a hallmark of COVID pathology. So what we've discovered scientists over the past year is that there are biomarkers that can give clues about who ultimately goes on to get severe disease.
[00:03:24] Scientists have also discovered genetic differences or mutations that some people have in those innate immune genes that can contribute to poor initial control of the virus. I think that this understanding that there are essentially two phases of COVID-19 disease, that initial phase that's dominated by viral amplification. And a second phase that in severe cases is dominated by a misfiring of the immune response is really important. It's important because it illustrates that there are two types of therapies that are probably needed depending on the phase of the disease. So drugs that target the virus directly to stop its replication.
[00:04:07] These would be things like Remdesivir that we've heard a lot about in the news, or maybe treating with things like recombinant interferon. This is something that is used to treat other chronic viral infections. Those types of therapies are probably only going to be effective at stopping that first phase of the disease, um, but are not going to be very effective if they're given during that second phase, because, uh, it's then it's not the virus, but the immune system that's driving illness. And so conversely drugs that dampen that overexuberant inflammatory response, and dexamethazone is one of those these, might be dangerous of given during that first phase, when you really want a rapid and robust immune response, but could be helpful at dampening the damage that's caused by the immune system at later stages.
[00:04:59] Jeffery DelViscio: [00:04:59] One of the key parts of understanding the virus itself and how we fight it is scientifically really about timing, right?
[00:05:05] Britt Glaunsinger: [00:05:05] Exactly, timing is really key. A timing of figure out how your body responds very early and later. And you know, the timing and the dose of the virus that you might receive, understanding how sort of, you know, that timing or the kinetics of infection and response are essential. And we've made a lot of progress on that over the last year.
[00:05:27] Jeffery DelViscio: [00:05:27] So let's talk about some of that specific progress inside your own lab and within UC Berkeley. What kind of work have you been doing over the last year? And what kind of work is being done across the university itself?
[00:05:39] Britt Glaunsinger: [00:05:39] Yeah. So what my lab has been working on, uh, during this past year related to Coronavirus is understanding the viral side of things. So we know that this virus has a lot of strategies to try and dampen those early innate immune sensors. It is evolved to try and shut down that component of the immune response because that part of the immune response is so essential in essentially dampening down the ability of the virus to replicate very early on.
[00:06:12] And so what my lab and others at UC Berkeley have been doing is trying to figure out the strategies that the virus is using to fight that innate immune response--how it is lowering the levels of these innate immune sensor, proteins and genes that could be used by your body to counteract the virus. And so we study this at the molecular level, at the level of the individual RNAs that the virus is targeting and blocking from being expressed.
[00:06:45] But there's a wide variety of other research that's going on across campus. That sort of spans the scales of, uh, trying to solve the atomic structures of various viral components. Because with these, you can use that information to design specific inhibitors against viral enzymes, and also at the scale of designing diagnostic tests and setting up testing centers to, to do community-based surveillance and campus testing and things like that. So really, uh, you know, Spanning the understanding the fine molecular details of how the virus works and interacts with its host cell up through community-based surveillance work.
[00:07:27] Jeffery DelViscio: [00:07:27] So, can we step back a little bit, and just talk about the innate immune response. Maybe we can go from when the body first encounters it to post-infection. And could you talk a little bit about what we know about immunity post-infection and how long that might last given what you understand about the innate immune response? How can it be useful and effective or not, and helping them body to, to fight the virus?
[00:07:48] Britt Glaunsinger: [00:07:48] Yeah, well, it is known of course that the innate immune response plays really important roles in activating the adaptive immune response, those T cells and B cells that will either produce antibody in the case of B cells or T cells are components of the adaptive immune response that will come in and kill already infected cells and be able to recognize them.
[00:08:11] So there, these are two arms of the immunity the immune system, the innate and the adaptive, but there are clear links and crosstalk between them. We know that. A very important question, which you bring up is to what extent does our body have the capacity to remember this particular virus? If you encounter the virus naturally through an infection and mount long lasting. adaptive immunity to the virus. And this is a really important question, right? Because it will tell us, for example, if you've already been infected with SARS-CoV-2, are you protected against reinfection? And it's possible that you are, but it's also possible that you're not. We know from work that's been done with the cold causing Corona viruses.
[00:09:02] There are circulating Corona viruses. Of course, that caused about 30% of the common cold. Um, we know that individuals who are infected with these cold causing Corona viruses. Can get reinfected, um, as early as a year later, uh, with that same virus, which suggests that they don't have what we would call sterilizing immunity, meaning that your immunity is so good that your immune system blocks the virus from setting up any kind of infection.
[00:09:30] But the good news is is that these individuals, even if they get reinfected are generally protected against disease. And so that says that there is, uh, an immune response that can protect at least against disease and that's hopeful. And so we don't know yet what the situation is going to look like for SARS-CoV-2, because we're still barely a year into this pandemic. Um, although there are rare cases that have been reported already of reinfection with CoV-2 in individuals, um, from various parts of the world, including Hong Kong and the US and in Europe, et cetera, these are pretty rare examples, but they could be emblematic of the fact that natural infection with this virus, um, may not completely protect against re-infection, uh, within a short, relatively short period of time. Although it's possible that natural re-infection could protect against, um, severe disease. So the idea is that what we want to do is generate vaccines that could, um, in fact, improve that level of protection.
[00:10:36] So you could get a better, more long lasting immune response from a vaccine than you could from the virus in part, because we know that the virus itself has a lot of mechanisms built into dampen that innate immune response, and it may hide itself in ways that makes it difficult for our bodies to generate a robust, adaptive immune response.
[00:11:00] And by delivering pieces of virus, uh, through vaccines, we may actually get a better response. And I think that's the hope, but it is still too early for us to know whether that is going to bear out because you simply just have to wait the length of time and see, you know, one year out how many people are protected or from infection at all versus protected from disease two years out, five years out, uh, what happens there that unfortunately is just a long waiting game. There's no way to speed up getting an answer to that question.
[00:11:34] Jeffery DelViscio: [00:11:34] I'm glad you bring up vaccines because obviously there's a lot of focus on that right now. And that's because there are a few vaccine candidates who've done phase three trials by now, which is the last step before some kind of approval by the Food and Drug Administration. And that emergency approval may even come in the time between when we're recording this and when it goes live, that's how fast this process is moving.
[00:11:55] So two companies are reporting better than 90% efficacy. Those are Pfizer and Moderna. It should also somebody noted that there's another vaccine candidate from the University of Oxford and the drug company, AstraZeneca that's showing promise.
[00:12:08] But to go back to the Pfizer and maternal vaccines, they're both mRNA vaccines. Could you talk a little bit about what an mRNA vaccine actually is and how it works?
[00:12:18] Britt Glaunsinger: [00:12:18] Certainly, yeah, these two vaccines are... the data, first of all, are incredibly exciting to, to most, all of us in that the efficacy appears from these initial results that have been released to be very high. And, um, that's exceptionally great news. There are many unanswered questions, uh, related to these vaccines that we can certainly touch on. So it's not that that we have all of the information yet, but I think that's great news in part, because these messenger RNA vaccines. We don't have any track record with them.
[00:12:52] This is the first rollout or testing phase three testing of any mRNA vaccine. So we didn't know if this was going to work at all. Um, and the fact that they appear to be working so well is extremely exciting. So what is a messenger RNA vaccine compared to a traditional vaccine? Uh, to understand this, I need to just take a second to explain the concept of what an antigen is.
[00:13:15] An antigen is a bit of virus that you are, or a pathogen in general, but for our purposes, we're, we're talking about Cove too. So it's, it's a bit of virus that you're going to show to the immune system and tell the immune system essentially make. Antibodies against this, make an adaptive immune response against this and, you know, vaccine context, you are showing it an exact bit of virus that we know that if an antibody is made to that bit, that antibody can block or neutralize the virus.
[00:13:48] This is important because in the context of a natural infection, your immune system, doesn't a priori know which bit of the virus, if it makes an antibody to it is going to stop that virus. So it makes lots of antibodies to everything it sees and can. And many of those may bind the virus, but not bind it in a way that's actually gonna block it.
[00:14:10] And so the benefit of a vaccine for, um, developing immunity is that you're basically telling your immune system exactly what are the right kind of antibodies, hopefully for it to make. And so that's the benefit of that over a natural infection for acquiring immunity. And there are a couple of ways to give that antigen or that bit of the virus to an individual. The more traditional way would be to, uh, inject a person with a vaccine that, that has that protein already made.
[00:14:40] And so that the antigen of course, that all of the vaccines are targeting is the spike protein of the virus. That's that surface protein that is essential for allowing the viruses to bind cells and enter cells. And so if you can block spike protein binding, and the function, you essentially have stopped the virus in its tracks because it can't get into the cell.
[00:15:03] And a virus that can't get into a cell is for all practical purposes inert, and non-pathogenic. So traditional vaccines would deliver that protein directly. Either you grow up the protein, uh, you know, in a, in a big bio-reactor and injected itself, these are called subunit vaccines, or the protein is already present on the surface of an inactivated virus in some way.
[00:15:30] The thing that's different about the messenger RNA vaccines, and this is similar for DNA vaccines, similar for the, um, the, the adenovirus, the vector based vaccines, which is the weakened non-infectious, uh, vectors, all of the basic, you know, the front runners that we're going to hear about early on for the phase three trials is that they don't deliver the protein directly. They deliver the sequence, the gene coding sequence for that spike protein, uh, into your cells and use your own cells to then, uh, make the protein from that set of genetic instructions for spikes. So the messenger RNA is basically delivering the gene sequence for the spike protein, or maybe just the RNA, the receptor binding domain of the spike protein, uh, which is then, uh, used by your cells to produce protein in your own cells to then show the immune system.
[00:16:28] Do you think Mr. And a vaccines would have come so far so fast without the virus around? Is it a chicken, egg virus, vaccine situation?
[00:16:39] It certainly wouldn't have happened as quickly. And in fact, you know what we have here as a platform, unlike we've ever had before, where all of the possible types of vaccines are basically being generated and tested simultaneously. Both the sort of more classic tried and true, uh, strategies for vaccine making that have been used for other FDA approved vaccines and these newer platforms like the DNA based vaccines and the MRNs vaccines that have shown promise, but have never, um, been tested in these large scale clinical trials for vaccines before. So we'll be able to cross compare them. Uh, and of course the speed with which we're getting data for these is accelerated dramatically. We've never had a phase three trial results within less than. a year after a virus has emerged. The fastest and of course, with a four to five years, which was lightning fast compared to how long it takes to develop most vaccines.
[00:17:42] Jeffery DelViscio: [00:17:42] So it seems that SARS, cov two has remodeled the way science works.
[00:17:47] Britt Glaunsinger: [00:17:47] It is definitely remodeled the way that science works. Uh, I can't think of a time, um, in recent history or even maybe an older history where the entire scientific community and medical community has turned their expertise with laser-like focus onto one thing, in particular. We have a lot of big diseases, right? We've got cancer, we've got TB, we've got AIDS, we've got heart disease, all of which have a lot of effort dedicated towards them. But this virus has really brought the world to its knees in such a dramatic way that, um, that everybody is working, uh, together, uh, to use their expertise, whatever it may be to try and find ways to learn about and combat this virus and other viruses. And so the hope of course, is that, um, the, what comes out of, of this, uh, parallel approaches from many, many, many different angles and scientists and expertise can be extrapolated to other diseases as well, other viral diseases, other pathogens.
[00:18:54] So for example, the mRNA platform or the DNA platform for a vaccines, the benefit there is that you can do this plug and play of inserting the gene sequence, very easily, they can be very rapidly designed. And if they worked here that provides, uh, you know, a proof of principle, well, the next emerging pathogen that comes. We can use these as a starting point and have a good sense that, that, uh, they're going to be effective.
[00:19:23] Jeffery DelViscio: [00:19:23] As much damage as this virus has done to people's lives to the economy in a strange way, it sort of seems like a bit of a catalyst.
[00:19:30] Britt Glaunsinger: [00:19:30] Yeah, you could see it as a catalyst, a catalyst based on need.
[00:19:37] Jeffery DelViscio: [00:19:37] That's desperation in some ways, right?
[00:19:39] Britt Glaunsinger: [00:19:39] That's right. That's right.
[00:19:41] Jeffery DelViscio: [00:19:41] Let's talk about the future. Let's not try to project a year ahead. That seems unknowable. Given how much changed in the last year. So let's talk about the next few months. And maybe we can start in the White House. There's a change in the administration coming. How do you think the federal response to the virus might change in the coming month?
[00:19:59] Britt Glaunsinger: [00:19:59] I would say I don't have any insider information, but I can give you what is just my opinion from what I've read in the news and whatnot. Uh, and that's what, what I'm coming to expect is that there's going to be more of a coordinated federal response instead of, um, relying on sort of state to state. Uh, uh, responses, uh, you know, sort of figuring it out on their own and, and doing their own thing. My, my expectation is that there's going to be more coordination and more of a unified response that is led by the federal government, which I think will be very important, particularly for issues related to vaccine distribution and prioritization of course, of who gets the vaccine first and which factors do they get et cetera. And also in thinking about, you know, policy of should the federal government be the one, uh, eliciting perhaps mandates about, uh, distancing or mask wearing or shut downs instead of relying on States. And we may be seeing a more heavy hand there is, is my guess.
[00:21:06] Jeffery DelViscio: [00:21:06] And in terms of what happens with the virus, it's not waiting for anything, obviously. Can you talk to me about mutation? How important is it for the future of the virus? How might that change our approach to fighting it?
[00:21:17] Britt Glaunsinger: [00:21:17] Yeah. Mutation is something that we always think about in the context of pathogens and viruses in particular, because they randomly incorporate errors into their sequence every time they make a copy of themselves. Uh, and that's because for, for most viruses, they don't have the capacity of copying their genome sequence in a way that is error free. Our own cells have lots of ways of copying our own genome, um, and, and proofreading and checking and double checking it to make sure that errors are not made when we amplify, you know, our own genome and ourselves as cells, divide viruses by and larger many viruses, particularly viruses with them RNA genomes do not have that capacity.
[00:22:04] And this leads usually to, uh, for RNA viruses, very rapid mutation. And that mutation, uh, is something that can be really challenging in the context of developing antiviral drugs and in developing vaccines, because the concern is always that a very interim mutant version, a changed version of the virus will emerge that is resistant to, uh, an antibody or to a, um, an antiviral drug.
[00:22:38] Now there's good news on that front for the coronavirus, which is that yes, it mutates all viruses mutate, but that it is not mutating at the hyper speed rate that some other RNA viruses, mutate like influenza and HIV. Those are really tricky problems because of the rates that they, they, um, are undergoing mutation.
[00:23:04] Coronavirus has a special sort of feature that is very unusual for RNA viruses, um, in which it can actually correct errors that occur as it is copying its genome. It can proofread its own genome copying mechanism. And what that means is that the virus accumulates fewer errors than many other RNA viruses. Doesn't mean no errors. So of course people are constantly looking at how this virus is changing and they are identifying mutants that can arise. And in some cases, mutants that may help the virus bind to cells better or enter cells better. So called increase its uh, transmissibility or an infectability.
[00:23:55] And so those mutations, um, do exist and, but they are not arising at a super rapid clip. It's not like we're, we're seeing tons of escape mutations, particularly in the spike protein for where the receptor binding domain might be. It's relatively speaking stable, which I think is good news for the vaccine front, but it's definitely something that people are continuing to actively monitor. There are hundreds of thousands of coronavirus sequences that have been deposited into the database that, um, evolutionary biologists and genomic scientists are looking at exactly how these mutants are arising and what they mean for antibody escape and things like that.
[00:24:40] Jeffery DelViscio: [00:24:40] Well, in a seemingly unrelentingly bad year, that seems like a hint of at least a little good news. Am I being too hasty?
[00:24:48] Britt Glaunsinger: [00:24:48] I mean, that's it. What one might consider good news in this things. But I also think that it's important to keep in mind that as you mentioned, the virus is raging right now. Um, we're undergoing the third wave of infection here in the United States, the first being in April or may, and then we had a second wave in the summer and we're now encountering the third wave. We're seeing exponential growth of the virus pretty much across the nation. Um, and so there's a lot of concern that our darkest days may be ahead of us. We've got great news on the vaccine front potentially, but that's not going to materialize even in a best case scenario for several more months to come. And those several months, I think we're going to see a large number of deaths and severe infections and transmissions. And it's partly because we're entering the traditional respiratory illness season, right? This cold and flu season and coronavirus is one of those viruses that is a respiratory virus and tends to have seasonality to it.
[00:26:04] So I think that, you know, there's a real concern that, you know, part of it is exponential growth that is linked to people being indoors more and much of our lives are spent in doors and that's a, of course, much more so during the cold winter months.
[00:26:18] The problem with indoors and coldness is this tends to be environments where there's decreased humidity, uh, so low relative humidity, maybe, uh, 20 to 40%, uh, cold dry air. These are conditions where viruses tend to be more stable and easier to transmit through the airborne route. Um, dry air can also, uh, clear out some of the antiviral sort of mucus based clearing mechanisms that are in our airways that can impair that early innate immune response.
[00:26:53] And so, um, there are reasons to think that the, you know, the cold fall and winter air can exacerbate this problem, uh, of infection and that, uh, you know, so we've just got to be extra vigilant, even though we've got these great pieces of news from the vaccine that does not mean we can let down our guard, people need to be extremely careful during the wintertime about distancing and mask wearing and hand-washing and things like that. It's going to be up to all of us to, to prevent the spread as much as we can, as we wait for the vaccine distribution to happen and, you know, antiviral drugs to be discovered, et cetera. We all have pandemic fatigue, but you know, it's you get a time when boy, if we let our guard down, it's going to be a disaster over the next couple months.
[00:27:40] Jeffery DelViscio: [00:27:40] Well, it seems that science is not going to stop pushing on this. Finally, could you talk just a little bit about what it means to be you right now? Someone who's really been engaged with this kind of research for 25 years. What is it like to be working on this particular subject so closely given how important it is to really the whole world?
[00:27:59] Britt Glaunsinger: [00:27:59] It's a humbling experience on the one hand, because I, my perspective having worked on viruses so long helps me realize the magnitude of the problem and the magnitude of the challenge that, that faces us in a pandemic like this. And, and so, um, that's a very humbling, uh, experience, but also it's one that, that makes all of us who work on viruses and scientists in general, feel a sense of, of duty that we have something to contribute. We have a knowledge base. We have a skillset that can help us learn how this virus works and fight it. And, and that's a really motivating and invigorating feeling to, to know that that we have something to contribute and that my knowledge, you know, hopefully is useful in this context and as we go on in the future as well. And so, um, you know, if it continues to fuel my passion for virology, which has always been strong.
[00:29:00] Britt Glaunsinger is a virologist at the University of California, Berkeley, and the Howard Hughes Medical Institute. Thank you so much for joining us on Science Talk, Britt.
[00:29:08] Thank you so much for having me, Jeff.


scientificamerican--2020-12-11--Abortion and Contraception in the Middle Ages

Today , conversations around abortion in modern Christianity tend to take as a given the longstanding moral , religious and legal prohibition of the practice .
Stereotypes of medical knowledge in the ancient and medieval worlds sustain the misguided notion that abortive and contraceptive pharmaceuticals and surgeries could not have existed in the premodern past .
This could not be further from the truth .
While official legal and religious opinions condemned the practice , often citing the health of women , a wealth of medical treatises produced by and for wealthy Christian women across the Middle Ages betray a @ @ @ @ @ @ @ a host of pharmaceutical contraceptives , various practices for inducing miscarriages , and surgical procedures for the termination of pregnancies .
When it came to saving a woman ’ s life , Christian physicians unhesitatingly recommended these procedures .
Since antiquity , the termination of pregnancies has long been associated with women at the margins of society , such as sex workers , and highlighted not only for the termination of the fetus ’ s life , but for the great danger it posed to women .
For instance , in the Hippocratic @ @ @ @ @ @ @ or recommend euthanasia and additionally refuses to give women abortifacients given the danger to which they put the life of the mother .
Religiously , the Church Council of Ancyra in 314 A.D. stated that women found to have committed or attempted an abortion on themselves or others were to be exiled from the Church for 10 years , revising earlier suggestions that they be exiled for life .
Yet , in the mid-fourth century , the Church Father Basil the Great revises these decrees , suggesting that time should not be proscriptive @ @ @ @ @ @ @ person .
There , however , he focuses not just on the fetus , but again on the danger of these procedures for women , who “ usually die from such attempts.
” The laws of the early Christian world generally reflected these prohibitions , outlining exile as the punishment for whomever has undertaken an abortion or aided in one—or , death if the person dies in the process .
Many of these laws were codified in the sixth-century Digest of Justinian , a legal compendium culled from ancient legislative opinions .
Nevertheless @ @ @ @ @ @ @ complexity that abortions had in the ancient and medieval worlds .
For example , the Digest cites the opinion of the jurist Tryphonius , where a woman was sentenced to death for undertaking an abortion , precisely because she did so with the malicious intent of denying her husband an heir by aborting the unborn inheritor .
Legally , we see abortions being intimately associated with a patriarchal control of lineage and reproduction .
The Digest clarifies that if a woman undertakes an abortion after a divorce , “ so as to avoid @ @ @ @ @ @ @ is now hateful , ” however , she should only be temporarily exiled .
The fourth-century Church Father John Chrysostom even turned these stereotypes on their head .
Though criticizing abortions , in one sermon he offers the example of a sex worker forced to have an abortion so as to not lose her livelihood .
While damning the act as a murderous practice , he places blame not on the woman , but on her client , chastising the man by saying that the sex worker can not be criticized for seeking @ @ @ @ @ @ @ while “ the shameless act is hers , the cause of it is yours.
” Thus , it is the sex worker ’ s client who is the cause of the murder , not she who requires her attractive body to survive .
Despite the prohibition in the Hippocratic Oath , gynecological texts were replete with recipes for contraceptive and abortive suppositories .
The second-century gynecology of Soranus of Ephesus details these recipes and advocates their use for women who have a medical reason to prevent pregnancy , strongly opposing their use simply @ @ @ @ @ @ @ a consideration for youthful beauty , ” given the health risks involved .
Thus , adultery and a conceited desire to preserve one ’ s good looks were often lodged against women known to practice abortions .
The recipes of Soranus were transmitted across the centuries in various texts , each demonstrating an active history of use and commentary .
For example , in Aëtius of Amida ’ s sixth-century medical treatise , the author details the use of contraceptive vaginal suppositories , elaborating on the improvements to the recipe from Soranus ’ @ @ @ @ @ @ @ that once the contraceptive has been used , “ if she wishes , [ the woman ] may have intercourse with a man .
It is infallible because of its many trials.
” Aëtius ’ s gynecological treatise has often been associated with the patronage of the elite imperial circle of Empress Theodora in Constantinople , an empress whom the court historian Procopius once described as often conceiving , “ but by using almost all known techniques she could induce immediate miscarriage.
” The use and efficacy of contraceptives and abortifacients extend throughout @ @ @ @ @ @ @ 12th-century text from Salerno , the author offers the example of sex workers , who frequently have intercourse yet only rarely conceive .
Therefore , the medical historical evidence proposes a very different story from that told by official religious or legal texts .
The fact of the matter is that good Christian women were indeed undertaking abortions and using contraceptives .
Yet , wealthy and elite Christian women had not only recourse to the best medical knowledge of their era but also the privacy to undertake these practices without shame .
Most @ @ @ @ @ @ @ were not only relegated to herbal , pharmaceutical contraceptives and abortifacient drugs , but also the various surgical interventions , what today we would refer to as a late-term abortion .
In the early 10th-century Life of Patriarch Ignatios , by Nicetas David Paphlagon , a narrative of a religious figure , the author recounts the story of a woman in labor with a breeched birth .
There , she is in immense pain and the author writes that “ in order to prevent the woman too from perishing with her child , @ @ @ @ @ @ @ on the baby and draw it out by cutting it limb by limb.
” While the procedure ultimately does not need to happen thanks to the miraculous workings of a relic , the author , without any moralization or shame , details here the contemporaneous procedures for an embryotomy , as described in medieval surgical manuals .
Further corroborating the continued use of this surgery , we can note that the sixth-century text by Aëtius of Amida ( citing a certain Philumenos and Soranus ) , details the operation for an embryotomy similarly @ @ @ @ @ @ @ perfectly in Paul of Aegina ’ s own seventh-century compendium on surgical practices .
These late-term abortions echo their modern counterpart , demonstrating that this was a known and established practice in the Middle Ages .
This medical knowledge flourished in particular in the Greek-speaking , eastern Roman Empire , most commonly known to us today as the Byzantine Empire .
Glimmers of the medical prowess of the Byzantine Empire and its long-thriving history are scattered across medieval sources .
In fact , one of the first recorded uses of a Caesarian section @ @ @ @ @ @ @ us from Visigothic Spain , but the text tells us the deed was performed by a skilled “ Greek ” ( aka Byzantine ) doctor , who is called to save the life of a living mother whose child has died in the womb .
While Caesarians were used in antiquity , they were deployed then only to rescue a child from a dead mother .
In the Lives of the Fathers of Mérida , composed in the 630s , the author chronicles the life of Paul , bishop of Mérida around 540/550 @ @ @ @ @ @ @ trained as a doctor in his youth .
In order to save the life of a wealthy woman , he must put his clerical garments aside and sully his hands with an embryotomy .
The text describes how “ with wonderous skill he made a most skillful incision by his cunning use of a knife and extracted the already decaying body of the infant , limb by limb , piece by piece , ” in order to save the woman ’ s life .
The only difference between the figure of the sex @ @ @ @ @ @ @ persons for whom these gynecological and surgical books were commissioned is that the latter were courtly elites .
Therefore , they had better recourses to medical knowledge , treatment and privacy .
But , the fact that stories of late-term abortions even find their way into saints ’ lives without judgment belie a more important fact : that abortions undertaken for the preservation of a woman ’ s life or health were rarely , if ever , under attack by medieval Christian authors .
Not even the moralizing religious texts touch upon such @ @ @ @ @ @ @ modern Christian pundits have not merely forgotten , but just never learned .

Today, conversations around abortion in modern Christianity tend to take as a given the longstanding moral, religious and legal prohibition of the practice. Stereotypes of medical knowledge in the ancient and medieval worlds sustain the misguided notion that abortive and contraceptive pharmaceuticals and surgeries could not have existed in the premodern past.
This could not be further from the truth.
While official legal and religious opinions condemned the practice, often citing the health of women, a wealth of medical treatises produced by and for wealthy Christian women across the Middle Ages betray a radically different history—one in which women had a host of pharmaceutical contraceptives, various practices for inducing miscarriages, and surgical procedures for the termination of pregnancies. When it came to saving a woman’s life, Christian physicians unhesitatingly recommended these procedures.
Since antiquity, the termination of pregnancies has long been associated with women at the margins of society, such as sex workers, and highlighted not only for the termination of the fetus’s life, but for the great danger it posed to women. For instance, in the Hippocratic Oath, Hippocrates refuses to assist in or recommend euthanasia and additionally refuses to give women abortifacients given the danger to which they put the life of the mother.
Religiously, the Church Council of Ancyra in 314 A.D. stated that women found to have committed or attempted an abortion on themselves or others were to be exiled from the Church for 10 years, revising earlier suggestions that they be exiled for life. Yet, in the mid-fourth century, the Church Father Basil the Great revises these decrees, suggesting that time should not be proscriptive but dependent on the repentance of the person. There, however, he focuses not just on the fetus, but again on the danger of these procedures for women, who “usually die from such attempts.”
The laws of the early Christian world generally reflected these prohibitions, outlining exile as the punishment for whomever has undertaken an abortion or aided in one—or, death if the person dies in the process. Many of these laws were codified in the sixth-century Digest of Justinian, a legal compendium culled from ancient legislative opinions.
Nevertheless, these legal opinions betray the real complexity that abortions had in the ancient and medieval worlds. For example, the Digest cites the opinion of the jurist Tryphonius, where a woman was sentenced to death for undertaking an abortion, precisely because she did so with the malicious intent of denying her husband an heir by aborting the unborn inheritor. Legally, we see abortions being intimately associated with a patriarchal control of lineage and reproduction. The Digest clarifies that if a woman undertakes an abortion after a divorce, “so as to avoid giving a son to her husband who is now hateful,” however, she should only be temporarily exiled.
The fourth-century Church Father John Chrysostom even turned these stereotypes on their head. Though criticizing abortions, in one sermon he offers the example of a sex worker forced to have an abortion so as to not lose her livelihood. While damning the act as a murderous practice, he places blame not on the woman, but on her client, chastising the man by saying that the sex worker cannot be criticized for seeking out an abortion, writing, that while “the shameless act is hers, the cause of it is yours.” Thus, it is the sex worker’s client who is the cause of the murder, not she who requires her attractive body to survive.
Despite the prohibition in the Hippocratic Oath, gynecological texts were replete with recipes for contraceptive and abortive suppositories. The second-century gynecology of Soranus of Ephesus details these recipes and advocates their use for women who have a medical reason to prevent pregnancy, strongly opposing their use simply “because of adultery or out of a consideration for youthful beauty,” given the health risks involved. Thus, adultery and a conceited desire to preserve one’s good looks were often lodged against women known to practice abortions.
The recipes of Soranus were transmitted across the centuries in various texts, each demonstrating an active history of use and commentary. For example, in Aëtius of Amida’s sixth-century medical treatise, the author details the use of contraceptive vaginal suppositories, elaborating on the improvements to the recipe from Soranus’s time. There, Aëtius writes that once the contraceptive has been used, “if she wishes, [the woman] may have intercourse with a man. It is infallible because of its many trials.”
Aëtius’s gynecological treatise has often been associated with the patronage of the elite imperial circle of Empress Theodora in Constantinople, an empress whom the court historian Procopius once described as often conceiving, “but by using almost all known techniques she could induce immediate miscarriage.” The use and efficacy of contraceptives and abortifacients extend throughout the Christian Middle Ages. In one 12th-century text from Salerno, the author offers the example of sex workers, who frequently have intercourse yet only rarely conceive.
Therefore, the medical historical evidence proposes a very different story from that told by official religious or legal texts. The fact of the matter is that good Christian women were indeed undertaking abortions and using contraceptives. Yet, wealthy and elite Christian women had not only recourse to the best medical knowledge of their era but also the privacy to undertake these practices without shame.
Most surprisingly, however, these medical practices were not only relegated to herbal, pharmaceutical contraceptives and abortifacient drugs, but also the various surgical interventions, what today we would refer to as a late-term abortion.
In the early 10th-century Life of Patriarch Ignatios, by Nicetas David Paphlagon, a narrative of a religious figure, the author recounts the story of a woman in labor with a breeched birth. There, she is in immense pain and the author writes that “in order to prevent the woman too from perishing with her child, the doctors [attended] to operate on the baby and draw it out by cutting it limb by limb.” While the procedure ultimately does not need to happen thanks to the miraculous workings of a relic, the author, without any moralization or shame, details here the contemporaneous procedures for an embryotomy, as described in medieval surgical manuals.
Further corroborating the continued use of this surgery, we can note that the sixth-century text by Aëtius of Amida (citing a certain Philumenos and Soranus), details the operation for an embryotomy similarly. The same operation is also recounted perfectly in Paul of Aegina’s own seventh-century compendium on surgical practices.
These late-term abortions echo their modern counterpart, demonstrating that this was a known and established practice in the Middle Ages. This medical knowledge flourished in particular in the Greek-speaking, eastern Roman Empire, most commonly known to us today as the Byzantine Empire. Glimmers of the medical prowess of the Byzantine Empire and its long-thriving history are scattered across medieval sources.
In fact, one of the first recorded uses of a Caesarian section on a living woman comes down to us from Visigothic Spain, but the text tells us the deed was performed by a skilled “Greek” (aka Byzantine) doctor, who is called to save the life of a living mother whose child has died in the womb.
While Caesarians were used in antiquity, they were deployed then only to rescue a child from a dead mother. In the Lives of the Fathers of Mérida, composed in the 630s, the author chronicles the life of Paul, bishop of Mérida around 540/550. Paul is a Greek who had trained as a doctor in his youth. In order to save the life of a wealthy woman, he must put his clerical garments aside and sully his hands with an embryotomy. The text describes how “with wonderous skill he made a most skillful incision by his cunning use of a knife and extracted the already decaying body of the infant, limb by limb, piece by piece,” in order to save the woman’s life.
The only difference between the figure of the sex worker shamed for her abortions and the persons for whom these gynecological and surgical books were commissioned is that the latter were courtly elites. Therefore, they had better recourses to medical knowledge, treatment and privacy.
But, the fact that stories of late-term abortions even find their way into saints’ lives without judgment belie a more important fact: that abortions undertaken for the preservation of a woman’s life or health were rarely, if ever, under attack by medieval Christian authors. Not even the moralizing religious texts touch upon such cases. This is a fact that modern Christian pundits have not merely forgotten, but just never learned.