The Autophagic Pathway and Enterovirus Infection
William T. Jackson
from: Enteroviruses: Omics, Molecular Biology, and Control (Edited by: William T. Jackson and Carolyn B. Coyne). Caister Academic Press, U.K. (2018) Pages: 113-128.
Abstract
A common feature of enteroviruses is the rapid rearrangement of the cytoplasm of infected cells. In general, cellular organelles are altered or disrupted and virus-specific vesicles, which take up a large perinuclear region of the cytoplasm, proliferate. One role of the newly generated vesicles is to act as substrates for RNA-dependent RNA replication complexes. One subset of these vesicles, observed later in infection, is a double-membraned population which strongly resemble autophagosomes, the organelles of the autophagy pathway. Autophagy, a degradative mechanism which maintains cellular homeostasis, is markedly increased during times of cellular stress, including starvation and infection. Autophagy is an important part of the innate immune response, degrading cytosolic pathogens and providing peptides for MHC presentation. However, for a subset of pathogens, including many enteroviruses, the autophagic pathway is subverted to promote replication of the invader. In this chapter we discuss the ways in which enteroviruses are known to interact with the autophagy pathway, often to promote viral replication read more ...
