Cytokine determinants of viral tropism

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Abstract
Viral tropism is the ability of a given virus to productively infect a particular cell (cellular tropism), tissue (tissue tropism) or host species (host tropism). Various host innate immune antiviral cytokines, in particular the interferons (IFNs) and tumour necrosis factor (TNF), have a role in mediating viral tropism at these different levels. Type I IFNs have a key role in determining the tropism of various viruses. These IFNs probably mediate their effects through the induction of interferon-stimulated genes; however, the exact genes that determine tropism for each virus have not been fully characterized. Type II IFN has a more limited role in determining viral tropism, contributing mainly in the central nervous system. The ability of type III IFNs to dictate viral tropism is largely determined by the tissue-specific expression of the type III IFN receptor. Type III IFNs probably have a major role in determining viral tropism in tissues and cells of epithelial origin. TNF influences viral tropism through altering the expression of cell surface receptors required for viral infection. TNF can alter viral tropism in both a positive and negative manner. Pro-inflammatory cytokines, particularly the IFNs, might be good therapeutic agents against various viruses that are capable of causing zoonotic infections. However, a better understanding of the mechanisms involved in these treatments is needed. Defects in the IFN and TNF responsiveness of cancer cells can be exploited to create tumour-specific viral infections in an approach known as viral oncolysis. The synergistic responses of multiple cytokines might have a key role in this phenomenon.