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Genotypic Inference of HIV-1 Tropism Using Population-based Sequencing of V3
Published on: December 27, 2010
Redefinition of tropism of common macrophage-tropic human immunodeficiency virus type 1
I H Chowdhury1, M J Potash, D J Volsky
1Molecular Virology Laboratory, Columbia University, New York, New York 10019, USA.
Previous studies have suggested that the abilities of human immunodeficiency virus type 1 (HIV-1) to infect primary macrophages and transformed T cell lines are mutually exclusive and define an important biological distinction among HIV-1 strains. In a survey of eight macrophage-tropic HIV-1 strains and nine T cell lines, all frequently used in studies of tropism, we have found that six virus strains replicate in one or more T cell lines and that four T cell lines are highly susceptible to macrophage-tropic HIV-1. Passage through T cell lines did not affect the tropism or the env V3 sequence of monocytotropic HIV-1 strains. We conclude that HIV-1 replication in transformed T cells and primary macrophages are not mutually exclusive, and that as such, these definitions of tropism per se are not generally useful markers for other biological properties of HIV-1.
Previous studies have suggested that the abilities of human immunodeficiency virus type 1 (HIV-1) to infect primary macrophages and transformed T cell lines are mutually exclusive and define an important biological distinction among HIV-1 strains. In a survey of eight macrophage-tropic HIV-1 strains and nine T cell lines, all frequently used in studies of tropism, we have found that six virus strains replicate in one or more T cell lines and that four T cell lines are highly susceptible to macrophage-tropic HIV-1. Passage through T cell lines did not affect the tropism or the env V3 sequence of monocytotropic HIV-1 strains. We conclude that HIV-1 replication in transformed T cells and primary macrophages are not mutually exclusive, and that as such, these definitions of tropism per se are not generally useful markers for other biological properties of HIV-1.

