27LB
Protective Effect of Vaginal Lactobacillus on Genital HIV-1 RNA Concentrations: Longitudinal Data from a US Cohort Study
Jane Hitti*1, K Paul1, K Agnew1, R Gausman1, D Lockhart1, S Cohn2, A Luque2, and R Coombs1
1Univ of Washington, Seattle, US and 2Univ of Rochester, NY, US
Background: Hydrogen peroxide-producing (H202+)
Lactobacillus is a key regulator of the vaginal ecosystem and may
decrease HIV-1 replication through direct effects as well as by suppression of
pathogenic bacteria. We evaluated the effects of H202+
Lactobacillus on cervicovaginal lavage (CVL) HIV-1 RNA concentrations
over time, with the hypothesis that acquisition of H202+
Lactobacillus would result in a decrease in CVL HIV RNA.
Methods: For this prospective, observational cohort
study, 57 HIV-1-infected women from Seattle, Washington (n = 38) and Rochester, N ew York (n = 19) contributed 390 visits (median 6, range 1 to 15). Data
collection was completed on November 30, 2007. Study visits occurred every 3 to
4 months and included collection of plasma (lower limit of quantitation (LLQ)
30 copies/mL) and CVL (LLQ 1500 copies/mL) samples for HIV RNA quantitation by
an independently validated real-time polymerase chain reaction (PCR) assay, and
vaginal cultures to identify H202+ Lactobacillus.
Longitudinal analyses used linear regression with generalized estimating
equations to examine the change in log-transformed CVL HIV RNA between 2 consecutive
visits for the same subject, as a function of change in H202+
Lactobacillus colonization, with adjustment for plasma HIV RNA log10
copies/mL and ART.
Results: Of 57 participants, 31 (54%) were on ART
and 22 (39%) had undetectable plasma HIV RNA <30 copies/mL at study entry.
The 390 study visits yielded 270 visit pairs with complete data for this
longitudinal analysis. HIV RNA was detectable in CVL at 47 (17%) of visits, and
was highly associated with plasma HIV RNA (P< .001) but not ART (p <0.78).
H202+ Lactobacillus colonization appeared
to be dynamic: 121 (47%) of visit pairs had stable colonization between visits,
39 (15%) acquired and 36 (14%) lost H202+ Lactobacillus,
and 62 (24%) showed no evidence of H202+ Lactobacillus
at either visit. Acquisition of H202+ Lactobacillus
resulted in a 0.7 log10 decrease in CVL HIV RNA (p = 0.015),
while loss of H202+ Lactobacillus
resulted in a 0.5 log10 increase in CVL HIV RNA (p = 0.029)
compared to stable colonization after adjustment for change in plasma HIV RNA
and ART status.
Conclusions: These prospective, longitudinal data
demonstrate that acquisition of H202+ Lactobacillus
is associated with a significant reduction in vaginal HIV load, while loss of H202+
Lactobacillus results in an increase in vaginal HIV load. These findings
may have relevance for secondary prevention strategies.
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