Human coronaviruses (hCoVs) can be divided into low pathogenic and highly 
pathogenic coronaviruses. The low pathogenic CoVs infect the upper respiratory 
tract and cause mild, cold-like respiratory illness. In contrast, highly 
pathogenic hCoVs such as severe acute respiratory syndrome CoV (SARS-CoV) and 
Middle East respiratory syndrome CoV (MERS-CoV) predominantly infect lower 
airways and cause fatal pneumonia. Severe pneumonia caused by pathogenic hCoVs 
is often associated with rapid virus replication, massive inflammatory cell 
infiltration and elevated pro-inflammatory cytokine/chemokine responses 
resulting in acute lung injury (ALI), and acute respiratory distress syndrome 
(ARDS). Recent studies in experimentally infected animal strongly suggest a 
crucial role for virus-induced immunopathological events in causing fatal 
pneumonia after hCoV infections. Here we review the current understanding of how 
a dysregulated immune response may cause lung immunopathology leading to 
deleterious clinical manifestations after pathogenic hCoV infections.