A snapshot of protein trafficking in SARS‐CoV‐2 infection

Abstract

SARS‐CoV‐2 is a human pathogenic virus responsible for the COVID‐19 (coronavirus disease 2019) pandemic. The infection cycle of SARS‐CoV‐2 involves several related steps, including virus entry, gene expression, RNA replication, assembly of infectious virions and their egress. For all of these steps, the virus relies on and exploits host cell factors, cellular organelles, and processes such as endocytosis, nuclear transport, protein secretion, metabolite transport at membrane contact sites (MSC) and exocytotic pathways. To do this, SARS‐CoV‐2 has evolved multifunctional viral proteins that hijack cellular factors and modulate their function by unique strategies. In this Review, we highlight cellular trafficking factors, processes, and organelles of relevance to the SARS‐CoV‐2 infection cycle and how viral proteins make use of and perturb cellular transport during the viral infection cycle.

Abstract

The replication of SARS‐CoV‐2 in host cells is influenced by cellular proteins, organelles and processes. Viral proteins efficiently modulate host factors and principles that govern endocytosis, nuclear transport, cytoplasmic trafficking of proteins and metabolites, membrane contact sites (MSC) and exocytotic pathways. This review discusses the examples of viral and host factor interactions affecting these processes.