Coronavirus (CoV) infections are commonly associated with respiratory and 
enteric disease in humans and animals. In 2012, a new human disease called 
Middle East respiratory syndrome (MERS) emerged in the Middle East. MERS was 
caused by a virus that was originally called human coronavirus-Erasmus Medical 
Center/2012 but was later renamed as Middle East respiratory syndrome 
coronavirus (MERS-CoV). MERS-CoV causes high fever, cough, acute respiratory 
tract infection, and multiorgan dysfunction that may eventually lead to the 
death of the infected individuals. The exact origin of MERS-CoV remains unknown, 
but the transmission pattern and evidence from virological studies suggest that 
dromedary camels are the major reservoir host, from which human infections may 
sporadically occur through the zoonotic transmission. Human to human 
transmission also occurs in healthcare facilities and communities. Recent 
studies on Middle Eastern respiratory continue to highlight the need for further 
understanding the virus-host interactions that govern disease severity and 
infection outcome. In this review, we have highlighted the major mechanisms of 
immune evasion strategies of MERS-CoV. We have demonstrated that M, 4a, 4b 
proteins and Plppro of MERS-CoV inhibit the type I interferon (IFN) and nuclear 
factor-κB signaling pathways and therefore facilitate innate immune evasion. In 
addition, nonstructural protein 4a (NSP4a), NSP4b, and NSP15 inhibit 
double-stranded RNA sensors. Therefore, the mentioned proteins limit early 
induction of IFN and cause rapid apoptosis of macrophages. MERS-CoV strongly 
inhibits the activation of T cells with downregulation of antigen presentation. 
In addition, uncontrolled secretion of interferon ɣ-induced protein 10 and 
monocyte chemoattractant protein-1 can suppress proliferation of human myeloid 
progenitor cells.