Suppression of the host antiviral response by non-infectious varicella zoster virus extracellular vesicles.

ABSTRACT: Varicella zoster virus (VZV) reactivates from ganglionic sensory neurons to produce herpes zoster (shingles) in a unilateral dermatomal distribution, typically in the thoracic region. Reactivation not only heightens the risk of stroke and other neurological complications but also increases susceptibility to co-infections with various viral and bacterial pathogens at sites distant from the original infection. The mechanism by which VZV results in complications remote from the initial foci remains unclear. Small extracellular vesicles (sEVs) are membranous signaling structures that can deliver proteins and nucleic acids to modify the function of distal cells and tissues during normal physiological conditions. Although viruses have been documented to exploit the sEV machinery to propagate inf

SUBMITTER: Niemeyer CS 

PROVIDER: S-EPMC11334484 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature