Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration.

ABSTRACT: Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that V

SUBMITTER: Gonzalez-Motos V 

PROVIDER: S-EPMC5444840 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature