Immunobiology of Varicella-Zoster Virus Infection. (22nd September 2018)

• Record Type: Journal Article
• Authors: Laing, Kerry J; Ouwendijk, Werner J D; Koelle, David M; Verjans, Georges M G M
• Is Part Of: Journal of infectious diseases. Volume 218(2018)Supplement 2
• Page Start: S68
• Page End: S74
• Publication Date: 2018-09-22
• Subjects: adaptive immunity -- chickenpox -- innate immunity -- shingles -- varicella-zoster virus; Communicable diseases -- Periodicals; Diseases -- Causes and theories of causation -- Periodicals; Medicine -- Periodicals; Communicable Diseases -- Periodicals; Electronic journals; 616.9
• DOI: 10.1093/infdis/jiy403
• Languages: English
• ISSNs: 0022-1899

Abstract

Abstract: Varicella-zoster virus (VZV) causes clinically significant illness during acute and recurrent infection accompanied by robust innate and acquired immune responses. Innate immune cells in skin and ganglion secrete type I interferon (IFN-I) and proinflammatory cytokines to control VZV. Varicella-zoster virus subverts pattern recognition receptor sensing to modulate antigen presentation and IFN-I production. During primary infection, VZV hijacks T cells to disseminate to the skin and establishes latency in ganglia. Durable T- and B-cell memory formed within a few weeks of infection is boosted by reactivation or re-exposure. Antigen-specific T cells are recruited and potentially retained in VZV-infected skin to counteract reactivation. In latently VZV-infected ganglia, however, virus-specific T cells have not been recovered, suggesting that local innate immune responses control VZV latency. Antibodies prevent primary VZV infection, whereas T cells are fundamental to resolving disease, limiting severity, and preventing reactivation. In this study, we review current knowledge on the interactions between VZV and the human immune system.