Viruses Binding to Host Receptors Interacts with Autophagy

Abstract

Viruses must cross the plasma membrane to infect cells, making them eager to overcome this barrier in order to replicate in hosts. They bind to cell surface receptors as the first step of initiating entry. Viruses can use several surface molecules that allow them to evade defense mechanisms. Various mechanisms are stimulated to defend against viruses upon their entry into cells. Autophagy, one of the defense systems, degrades cellular components to maintain homeostasis. The presence of viruses in the cytosol regulates autophagy; however, the mechanisms by which viral binding to receptors regulates autophagy have not yet been fully established. This review discusses recent findings on autophagy induced by interactions between viruses and receptors. It provides novel perspectives on the mechanism of autophagy as regulated by viruses.

Autophagy in Cell Survival and Death

“…Yang discussed autophagic regulation during the viral binding to cell surface receptors [16]. A virus binds to its specific receptors to infect cells.…”

Extracellular vesicles promote autophagy in human microglia through lipid raft-dependent mechanisms

“…It has been shown that autophagy regulates integrin-mediated cell adhesion and may promote cell migration affecting the turnover of focal adhesions [48,49]. Interestingly, integrins may also play an important role in the autophagosome formation by direct interactions with LC3 proteins [50,51]. We speculate that EVs can affect bidirectional interplay between integrin recycling and autophagy thereby promoting remodeling of focal adhesions and microglial motility.…”

Host Subcellular Organelles: Targets of Viral Manipulation

“…Viral infections affect the membrane components of cells in various ways, depending on the specific virus and the host cell type [17,63]. Viruses interact with cell surface receptors, membrane proteins, and lipids to facilitate entry into the host cell and promote viral replication [28,[64][65][66]. For example, the spike protein of SARS-CoV-2 facilitates virus entry into host cells by interacting with the ACE2 receptor on the cell membrane [67].…”

“…Furthermore, the impact of viral infection in host cells extends to other cellular structures and processes, such as autophagosomes and lysosomes [27,28]. These organelles play crucial roles in cellular homeostasis, protein synthesis, and degradation [29,30].…”

“…These organelles undergo significant structural and functional changes during viral infections, with viruses often repurposing them to create an environment conducive to their lifecycle [24][25][26]. Furthermore, the impact of viral infection in host cells extends to other cellular structures and processes, such as autophagosomes and lysosomes [27,28]. These organelles play crucial roles in cellular homeostasis, protein synthesis, and degradation [29,30].…”