Figure 2.

Plausible host immune responses during COVID-19 infection. The SARS-CoV-2 virus infects through the naso-oral route, followed by infection in cells expressing ACE2 receptor in the lung, such as type 2 alveolar cells. These viruses dampen anti-viral IFN responses by evading the innate immune cells as a consequence of unrestrained virus replication. The infiltration of monocytes/macrophages, neutrophils, and several other adaptive immune cells leads to increased pro-inflammatory cytokines. In the helper T cell subset, stimulation of Th1/Th17 cells with viral epitopes may lead to aggravated inflammatory responses. This inflammatory response results in “cytokine storms” that lead to immunopathologies like pulmonary edema and pneumonia. Cytotoxic T cells recruited to the site of infection try to kill virus-infected cells in the lungs. B cells/plasma cells also recognize viral proteins and are activated to produce antibodies specific to SARS-CoV-2, which may help in deactivating viruses and provide systemic immunity in different organs.