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.
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Acknowledgements
The authors wish to thank the many colleagues in the field whose pioneering studies have contributed to understanding the complexity of VZV and its interactions with the host immune response and apologize to those whose work has not been included due to the scope of this review and/or page limits. The authors also wish to acknowledge past and present members of our laboratories, particularly Renee Traves, Gavin Morrow, Tessa Campbell, Jennifer Huch, Jarrod Kennedy, Shivam Purohit, Carolyn Samer for their work in this area and insightful contributions.
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Abendroth, A., Slobedman, B. (2022). Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus. In: Arvin, A.M., Moffat, J.F., Abendroth, A., Oliver, S.L. (eds) Varicella-zoster Virus. Current Topics in Microbiology and Immunology, vol 438. Springer, Cham. https://doi.org/10.1007/82_2022_254
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