Background:  Among persons using combination antiretroviral therapy (cART), the impact of rectal sexually transmitted infection (STI) on rectal HIV-1 shedding is not well understood. We examined the association of rectal HIV-1 RNA levels with blood viral loads in the presence and absence of rectal STI among mostly cART-using men who have sex with men (MSM).

Methods:  We used a convenience sample of 93 rectal swabs collected from 81 HIV-1-infected MSM enrolled in the CDC-sponsored SUN Study. The swabs were collected for Neisseria gonorrhea (GC) and Chlamydia trachomatis (CT) screening by nucleic acid testing and were stored in Gen-Probe APTIMA^® media, aliquots of which were centrifuged (400 x g) and filtered (0.45 µm pore size) before ultra-centrifugation (10⁵ x g). Nucleic acids in the pelleted material were extracted and HIV-1 was quantified using an FDA-approved virus load kit. Preliminary virus spiking studies established that our protocol’s sensitivity for quantification was 150 HIV-1 RNA copies/rectal swab. HSV antibody status and yearly anal cytology are collected on study participants. We determined the correlation between ordinal categories of rectal and plasma viral load with Kendall’s tau. We used multinomial regression models with robust variances to examine factors associated with rectal viral load.

Results:  Sixty-five (70%) swabs were from MSM on cART with a median plasma viral load of 2.18 log₁₀ copies/mL (IQR <1.7 to 4.34) and CD4 count 457 cells/mm³ (IQR 312 to 554). Fifty-five (68%) men were HSV-2 seropositive at baseline and 40 (49%) had abnormal rectal cytology. Thirty-two (34%) swabs were positive for rectal GC or CT. Rectal and plasma HIV-1 RNA levels were highly correlated (Kendall’s tau 0.68 P <0.0001). The presence of rectal GC or CT did not enhance detection of rectal HIV-1 shedding when plasma viral loads were <2.0 log₁₀ copies/mL (P =0.94). Only plasma viral load, but not rectal GC or CT infection, CD4 cell count, abnormal anal cytology, or HSV-2 serostatus, was significantly associated with rectal HIV RNA levels in multinomial regression.

Conclusions:  In this small sample of HIV-infected MSM with a high prevalence of STI and access to cART, plasma HIV-1 viral load was the only independent correlate of rectal HIV-1 shedding. Rectal GC or CT infection did not appreciably alter this relationship. Suppressing plasma HIV-1 viral load with cART is a priority in order to reduce HIV transmission related to exposure to rectal secretions.