Evolution of CXCR4-using human immunodeficiency virus type 1 SF162 is associated with two unique envelope mutations.
CCR5-using human immunodeficiency virus type 1 (HIV-1) isolates typically gain CXCR4 use via multiple mutations in V3 and often V1/V2 regions of envelope, and patterns of mutations are distinct for each isolate. Here, we report that multiple CXCR4-using variants of a parental CCR5-using HIV-1 isolate, SF162, obtained by either target cell selection or CCR5 inhibition have a common mutation pattern characterized by the same two V3 mutations and that these mutations preexisted in some of the SF162 stocks. These results imply that SF162 has a single pathway for acquiring CXCR4 use and that prolonged culture is sufficient to select for R5X4 variants.
Kiselyeva
Yana
Y
Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development/NIH, 10 Center Drive, Bethesda, MD 20892, USA.
Nedellec
Rebecca
R
Ramos
Alejandra
A
Pastore
Cristina
C
Margolis
Leonid B
LB
Mosier
Donald E
DE
D002478:Cells, Cultured; D019143:Evolution, Molecular; D015497:HIV-1 / Q000235:genetics* / Q000302:isolation & purification / Q000378:metabolism; D006801:Humans; D009154:Mutation / Q000235:genetics; D019718:Receptors, CXCR4 / Q000235:genetics*; D012680:Sensitivity and Specificity; D014759:Viral Envelope Proteins / Q000235:genetics*; D014779:Virus Replication
D019718:Receptors, CXCR4; D014759:Viral Envelope Proteins