Immunological evasion of immediate-early varicella zoster virus proteins
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The varicella zoster virus (VZV) causes the childhood disease commonly known as chickenpox and can later in life reactivate as herpes zoster. The adaptive immune system is known to play an important role in suppressing VZV reactivation. A central aspect of this system is the presentation of VZV-derived peptides by the major histocompatibility complex (MHC) proteins. Here, we investigate if key VZV proteins have evolved their amino acid sequence to avoid presentation by MHC based on predictive models of MHC-peptide affinity. This study shows that the immediate-early proteins of all characterized VZV strains are profoundly depleted for high-affinity MHC-I-restricted epitopes. The same depletion can be found in its closest animal analog, the simian varicella virus. Further orthology analysis towards other herpes viruses suggests that the protein amino acid frequency is one of the primary drivers of targeted epitope depletion.
KeywordsVaricella zoster virus HLA association MHC affinity prediction Viral immune evasion
This work was supported by the Fund for Scientific Research—Flanders (FWO-Vlaanderen; personal grant to B.O., and project grants G.0409.12N and G.0903.13N) and the University of Antwerp Concerted Research Action 30730 and Small Project 31034.
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