How SARS-CoV-2 dodges immune surveillance and facilitates infection: an analytical review

Effective treatments for the ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic are limited. The virus has evolved strategies to evade the immune system or hijack immune responses to facilitate infection and escape immune surveillance. Mechanistically, SARS-CoV-2 takes advantage of TLR4 and cytokine-induced integrins to promote its entrance into the cell. Furthermore, the activation of pattern recognition receptors (PRR)-mediated signaling pathways is compromised by SARS-CoV-2 non-structural proteins (NSPs), accessory protein open reading frames (ORFs), and structural proteins upon infection, contributing to viral infection and replication. Host factors necessary for cellular protein synthesis, metabolism, and viral replication can also be inhibited by the SARS-CoV-2 proteins. Exploring specific mechanisms would optimize the therapy methods and benefit drug research and development.

We describe pathways and mechanisms by which SARS-CoV-2 evades immune system; these include the mechanisms that operate during virus entry, signaling pathways involved, and processes at RNA and protein levels.

Increased understanding of how viruses interfere with immune responses would provide more evidence for drug development. Drugs targeting conserved viral proteins to inhibit their replication or host factors to enhance immune responses would minimize the impact of virus mutations and prepare for future coronavirus outbreaks.