Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus.

Abstract

Varicella zoster virus (VZV) is a medically important human herpesvirus that has co-evolved with the human host to become a highly successful and ubiquitous pathogen. Whilst it is clear the innate and adaptive arms of the immune response play key roles in controlling this virus during both primary and reactivated infections, it is also apparent that VZV "fights back" by encoding multiple functions that impair a wide range of immune molecules. This capacity to manipulate the immune response is likely to be important in underpinning the success of VZV as a human pathogen. In this review, we will focus on the plethora of mechanisms that VZV has evolved to prevent and/or delay immune functions via regulating the expression of major histocompatibility complex (MHC) class I and MHC class II molecules, as well as several MHC-like molecules. In doing so, we will highlight both established and newly emerged VZV-encoded immunomodulatory capabilities and provide context to new avenues of research that seek to build the most comprehensive understanding of how this virus interfaces with these aspects of host immunity.