HIV superinfection associated with accelerated viral load increase but has no impact on clinical disease progression

HIV superinfection has no impact on clinical disease progression, investigators report in the online edition of AIDS. Superinfection was associated with accelerated viral load increase and had a modest impact on CD4 cell loss. However, this did not translate into faster clinical disease progression – a decline in CD4 count to below 200 cells/mm³, initiation of antiretroviral therapy (ART) or death.

“We did not detect a significant effect of superinfection on time to clinical events,” comment the authors. “We found that super-infected individuals showed significantly accelerated viral load increase over time and a trend for accelerated CD4 cell count decline.”

HIV super-infection involves acquisition of a different viral variant at a later time. It had been thought to be rare, but research involving women at high risk in Mombasa, Kenya, showed an annual superinfection incidence of approximately 3%.

The impact of superinfection on HIV disease progression is controversial. The team of investigators who demonstrated the high superinfection incidence in Mombasa therefore compared changes in viral load and CD4 count between women with HIV superinfection and women with HIV infection with a single viral variant, and also rates of clinical disease progression between the two groups.

Between 1993 and 2008 a total of 144 women were recruited and 21 became superinfected.

Comparison of the superinfected women and those who remained singly infected showed that individuals with superinfection had a significantly faster increase in viral load (0.009 log₁₀ copies/ml per month; p = 0.0008). There was also trend of borderline significance suggesting superinfection caused accelerated CD4 count loss (p = 0.06).

These findings were unaffected when the investigators took into account factors associated with disease progression, including genital ulcer disease at HIV acquisition, initial viral subtype and host genetic factors.

Pre-infection viral load was significantly lower among the women who became superinfected compared to the singly infected women (p = 0.05). The investigators therefore suggest, “there may be host or viral determinants of susceptibility to super-infection. Elucidation of these factors may shed light on early events in HIV-1 acquisition and potential avenues for its prevention.”

Despite its impact on viral load and CD4 count, there was no evidence that superinfection affected the risk of clinical disease progression.

“Our findings suggest that superinfection is associated with a modest increase in viral load, but no large difference in clinical outcomes,” conclude the authors.