MHC class I up‐regulation by flaviviruses: Immune interaction with unknown advantage to host or pathogen

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Abstract
In contrast to many other viruses that escape from cytotoxic T cell recognition by down‐regulating major histocompatibility complex class I‐restricted antigen presentation, flavivirus infection of mammalian cells up‐regulates cell surface expression of major histocompatibility complex class I molecules. Two putative mechanisms for flavivirus‐induced major histocompatibility complex class I up‐regulation, one via activation of the transcription factor NF‐κB, the second by augmentation of peptide import into the lumen of the endoplasmic reticulum, are reviewed, and the biological effect of the flavivirus‐mediated phenomenon on target cell recognition by natural killer and cytotoxic T cells is addressed. Finally, we speculate on the physiological role of flavivirus‐mediated modulation of major histocompatibility complex class I antigen presentation in the context of the biology of flavivirus transmission between the vertebrate host and arthropod vector and suggest that it may represent a strategy for immune evasion from the natural killer cell response or, alternatively, that up‐regulation of major histocompatibility complex class I is a by‐product of flavivirus replication without significance for virus growth.