Abstract

The immunodeficiency-defining AIDS results from a progressive decline of CD4 cell count. We previously showed that 3S, a unique motif of the HIV-1 gp41 envelop protein, is highly conserved in HIV-1 strains and induces expression of NKp44L, rendering CD4 cells sensitive to NK killing. Here we found from a well-characterized cohort of 244 untreated HIV-1 seroconverters that high levels of anti-3S antibodies significantly delay spontaneous disease progression in the first years after seroconversion; this effect was not mediated through baseline viral load or CD4. These results could have important implications both for clinical care and better understanding of pathogenicity.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call