A dual-tropic primary HIV-1 isolate that uses Fusin and the beta-chemokine receptors CKR-5, CKR-3, and CKR-2b as fusion cofactors

Article Abstract:

HIV-1 isolate 89.6 uses Fusin and CKR-5 as entry cofactors indicating that the evolution from a M-tropic to T-tropic phenotype probably occurs due to changes in HIV-1 env that allow the use of dual cofactors. The beta-chemokine receptors CKR-3 and CHR-2b allow the formation of syncytia mediated by HIV-1 89.6 env proteins but fail to allow fusion by T-tropic and M-tropic strains. Expression of CKR-5 with CD4 allows nonpermissive cells to form syncytia with cells expressing M-tropic proteins. However, CKR-5 fails to allow entry of cells expressing T-tropic and HIV-1 env proteins.

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CD4-independent infection by HIV-2 is mediated by fusin/CXCR4

Article Abstract:

Fusin, a member of the chemokine receptor family, can serve as an alternative receptor for some isolates of HIV-2 in the absence of CD4. This was gleaned from findings that CD4-independent infection by these viruses is inhibited by an anti-Fusin monoclonal antibody, that Fusin expression makes human and nonhuman CD4-negative cell lines sensitive to HIV-2-induced syncytium induction and/or infection and that Fusin is selectively downregulated from the cell surface following HIV-2 infection. These indicate that the HIV envelope glycoprotein has a binding site for these proteins.

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Regions in beta-chemokine receptors CCR5 and CCR2b that determine HIV-1 cofactor specificity

Article Abstract:

The beta-chemokine receptors CCR5 and CCR2b are the cofactors for entry of M-tropic viruses into cells. Previous studies have reported that M-tropic trains are more sensitive to substitutions in the regions of CCR5 than CCR2b. To understand the molecular basis of CCR5 usage in viral tropism, chimeric molecules of both CCR5 and CCR2b were constructed and regions involved in cofactor utilization by HIV-1 strains were mapped. The chimeras showed that the amino terminus and the first extracellular loop of CCR5 contribute to enhancing the entry of HIV-1 cofactors into the cell.

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