Journal
CURRENT OPINION IN VIROLOGY
Volume 3, Issue 6, Pages 670-675Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coviro.2013.08.003
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Funding
- Biotechnology and Biological Sciences Research Council (BBSRC)
- Wellcome Trust
- Biotechnology and Biological Sciences Research Council [BB/D008425/1] Funding Source: researchfish
- Medical Research Council [G0300387] Funding Source: researchfish
- BBSRC [BB/D008425/1] Funding Source: UKRI
- MRC [G0300387] Funding Source: UKRI
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The feline and human immunodeficiency viruses (FIV and HIV) target helper T cells selectively, and in doing so they induce a profound immune dysfunction. The primary determinant of HIV cell tropism is the expression pattern of the primary viral receptor CD4 and co-receptor(s), such as CXCR4 and CCR5. FIV employs a distinct strategy to target helper T cells; a high affinity interaction with CD134 (OX40) is followed by binding of the virus to its sole co-receptor, CXCR4. Recent studies have demonstrated that the way in which FIV interacts with its primary receptor, CD134, alters as infection progresses, changing the cell tropism of the virus. This review examines the contribution of the virus-receptor interaction to replication in vivo as well as the significance of these findings to the' development of vaccines and therapeutics.
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