SARS-CoV-2 and Immunological Response

Abstract

Viruses require host cellular machinery for protein translation and replication. Upon proliferation, virions damage the cells and are released from the infected cells prior to infecting other cells. Acute inflammation is observed when host cells are damaged by infection. Receptors for SARS-CoV-2 on cells are distributed more widely than those specific for other viruses, resulting in a wide range of symptoms such as rhinitis, pneumonia, and enteritis. Typically, RNA viruses, including SARS-CoV-2, demonstrate high frequencies of gene mutations. Antigenic modulation due to genetic mutations in the spike protein causes cytokine storms due to strong activation of the innate immune system. This is similar to the phenomenon previously observed in highly pathogenic avian influenza. The proportion of severely ill patients due to COVID-19 varies from country to country. Factors that are responsible for the severity of the disease include antibody-dependent enhancement (ADE), BCG (Bacille de Calmette et Guérin) vaccination, and HLA (Human leukocyte antigen) type. ADE and HLA types may also contribute to the protective effect during an immune reaction including vaccine response against SARS-CoV-2.