Abstract
Background It has been hypothesized that the RV144 immune correlate, V1V2 antibodies, block binding to gut homing receptor, alpha4 beta7, which may limit virus access to gut associated lymphoid tissue. We hypothesized that if alpha4 beta7 binding is important during HIV-1 acquisition, viruses with envelopes isolated from newly infected subjects should have enhanced ability to bind the alpha4 beta7 integrin and/or infect cells with high levels of alpha4 beta7 receptor compared to variants present in the chronically infected transmitting partner.
Highlights
It has been hypothesized that the RV144 immune correlate, V1V2 antibodies, block binding to gut homing receptor, alpha4 beta7, which may limit virus access to gut associated lymphoid tissue
We hypothesized that if alpha4 beta7 binding is important during HIV-1 acquisition, viruses with envelopes isolated from newly infected subjects should have enhanced ability to bind the alpha4 beta7 integrin and/or infect cells with high levels of alpha4 beta7 receptor compared to variants present in the chronically infected transmitting partner
Samples from 9 newly infected subjects were collected a median of 93 days after estimated HIV-1 seroconversion, and all the transmitting partners had chronic persistent infection of more than two years duration at the time of estimated transmission
Summary
It has been hypothesized that the RV144 immune correlate, V1V2 antibodies, block binding to gut homing receptor, alpha beta, which may limit virus access to gut associated lymphoid tissue. We hypothesized that if alpha beta binding is important during HIV-1 acquisition, viruses with envelopes isolated from newly infected subjects should have enhanced ability to bind the alpha beta integrin and/or infect cells with high levels of alpha beta receptor compared to variants present in the chronically infected transmitting partner
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