Tropic Strains of HIV

Inhibition of R5 strain replication in blood lymph nodes by P-chemokines may also contribute to the emergence and predominance of X4 strains in late disease.  

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Kinter A, Catanzaro A, Monaco J, et al. CC-chemokines enhance the replication of T-tropic strains of HIV-1 in CD4(-I-) T cells role of signal transduction. Proc Natl Acad Sci USA 1998 95 11880-11885. 

Collman R, Hassan NF, Walker R et al. Infection of monocyte-derived macrophages with human immunodeficiency virus type 1 (HIV-1). Monocyte-tropic and lymphocyte-tropic strains of HIV-1 show distinctive patterns of replication in a panel of cell types. J Exp Med 1989 170 1149-1163. 

In addition to the above, laboratory strains of HIV-1 exhibited a cellular tropism distinct from that of many primary HIV-1 isolates. All isolates of HIV-1 are able to infect primary T lymphocytes. However, as viral stocks were cultured and expanded in the laboratory, they gained a greater ability to infect T cell lines and lost the ability to infect macrophages. At least three distinct phenotypes were observed primary isolates that infected primary T cells and macrophages (M-tropic), primary isolates that infected primary T cells and macrophages as well as T cell lines (dual-tropic), and laboratory-adapted isolates able to infect primary T cells and T cell lines (T-tropic). Cellular tropism was then found to be conferred by the V3 loop of gpl20 (23,24). 

The chemokine receptors are a family of seven transmembrane G-protein-coupled receptors that have been most closely studied in connection with leukocyte homing and recruitment. Two members of this family are known to mediate infection by all primary HIV strains. The first to be identified, CXCR4 or fusin, is the receptor for the T-cell-Iine adapted (TCLA) strains of HIV whereas the second coreceptor CCR5 was originally identified as the coreceptor for macrophage tropic strains. 

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