Enteroviruses Activate Cellular Innate Immune Responses Prior to Adaptive Immunity and Tropism Contributes to Severe Viral Pathogenesis

Abstract

Numerous innate immune mechanisms have been shown to be activated during viral infections, including pattern recognition receptors (PRRs) functioning outside and inside the cell along with other sensors promoting the production of interferon and other cytokines. Innate cells, including NK cells, NKT cells, γδ T cells, dendritic cells, macrophages, and even neutrophils, have been shown to respond to viral infections. Several innate humoral responses to viral infections have also been identified. Adaptive immunity includes common cell-mediated immunity (CMI) and humoral responses. Th1, Th2, and Tfh CD4+ T cell responses have been shown to help activate cytotoxic T lymphocytes (CTLs) and to help promote the class switching of antiviral antibodies. Enteroviruses were shown to induce innate immune responses and the tropism of the virus that was mediated through viral attachment proteins (VAPs) and cellular receptors was directly related to the risk of severe disease in a primary infection. Adaptive immune responses include cellular and humoral immunity, and its delay in primary infections underscores the importance of vaccination in ameliorating or preventing severe viral pathogenesis.

Keywords: Toll-like receptors; adaptive immunity; antibodies; cell-mediated immunity; complement; cytokines; innate immunity; interferon; tropism; viral sensors; viruses.