Figure 1.

Virulence factors and immune mechanisms during severe acute respiratory syndrome coronavirus 2 infection. After the recognition of the virus by angiotensin-converting enzyme 2 and/or TMPRSS2 receptors, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) internalizes in the host cell. Via several secondary messengers, the respiratory mucosal cell is stimulated to secrete cytokines and present viral antigens via major histocompatibility complex (human leukocyte antigen) class II molecules to cytotoxic CD8+ T cells, which further secrete cytokines, such as interferon gamma. Additionally, natural killer cells (not shown) also contribute to the killing of infected host cells along with T cytotoxic cells as a part of cellular immunity against every viral infection. Antigen-presenting cells, such as macrophages and dendritic cells, can present viral particles via human leukocyte antigen class II molecules and prime CD4+ T helper cells, which further differentiate to different Th cells, such as Th17 cells (showed), which secrete a vast majority of cytokines, leading to cytokines storms and acute respiratory distress syndrome. Th cells stimulate B cells to produce antibodies against some SARS-CoV-2 antigens, part of the humoral immunity against the virus. Viral replication and shedding are not shown. ARDS: Acute respiratory distress syndrome; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; ACE2: Angiotensin-converting enzyme 2.