We enrolled 302 HIV-positive Indian MSM and of these, 7 (2%) had beta-globin-negative samples and were excluded from further analysis. Of the 295 remaining participants, the median age was 34 years, the median monthly income was 3,000 rupees (approximately $50), and most (65%) had 1-10 years of education. Participants from our two clinical sites were different demographically. Men from Humsafar Trust were younger (38 vs. 32 years), a greater proportion had completed more than 10 years of school (27% vs 9%), they had a higher median income (6000 INR vs. 2000 INR), and more reported their religion as being “Muslim” (24% vs. 3%) (all comparisons p≤0.05).
Almost half of our participants reported being married to a woman (47%). Only 30% of men reported that they have ever smoked 100 or more cigarettes, and only 31% reporting chewing tobacco ‘regularly’. More than half of our participants reported consuming alcoholic beverages in their lifetime, but 46% drank less than one day per week.
The median CD4+ level of the study population was 424 cells/uL (interquartile range [IQR]: 273-581 cells/uL) and the median HIV VL was 8,307 IU/mL (IQR: ≤400-79,400 IU/mL) 36% had undetectable levels. Forty-eight percent of participants were taking antiretroviral therapy (ART) and of those 69% of participants had been taking ART for more than a year. Men from the two different sites did not differ significantly in their lifestyle behaviors or HIV disease status.
Prevalence of oral HPV infection
The prevalence of oral HPV infection among our participants was 23.7% (95% CI: 19-29%) (Table 2). Three percent of participants had oral infection with oncogenic HPV types. Of the 70 men with positive consensus probes for oral HPV infection, only 17 had positive results on HPV type-specific tests included in our testing. Of the 17 who had HPV type-specific results, 14 (82%) had more than one type of HPV detectable. Oral HPV 16 infection was not detected in any of our participants. The prevalence of oral HPV infection did not differ by study location.
Unadjusted associations between demographic factors, lifestyle factors, HIV-related factors and oral HPV infection
There was no significant association between any of the demographic factors examined and oral HPV infection (Table 2). Of the lifestyle factors investigated, two factors commonly associated with OSCC, cigarette smoking and alcohol consumption, were not associated with oral HPV infection in this population. However, chewing tobacco ‘regularly’ was associated with lower prevalence of oral HPV infection among HIV-positive MSM (14%) compared with men who did not chew tobacco (28%) (p=0.01, OR 0.4 [95% CI 0.2-0.8]). However, among the 93 men who did chew tobacco regularly, when we examined the frequency that they chewed tobacco by week, the prevalence of oral HPV infection increased with increasing frequency of weekly chewing tobacco use.
Men with lower CD4+ levels had a higher prevalence of oral HPV infection when compared with men with higher CD4+ levels (500+ cells/uL). Men with <200 cells/uL had a prevalence of 43% and men with 500+ cells/uL had a prevalence of 20% (p=0.01). HIV VL and ART use were not associated with oral HPV infection.
Sexual behavior and oral HPV infection
Several oral sexual behaviors were associated with a reduction in prevalence of oral HPV infection among our participants (Table 3). Men who reported having performed oral sex on a woman in their lifetime had a lower prevalence of oral HPV compared with men who reported never performing oral sex on a woman (17% vs. 32%, p=0.02). However, among those reporting that they had performed oral sex on a woman, the prevalence of oral HPV increased with increasing number of partners on whom the participant had performed oral sex. Engaging in oral-anal contact (rimming), showed a similar association with a lower prevalence among those who engaged in this behavior. Ever performing genital oral sex on a male partner was not associated with oral HPV infection. Behaviors that measured non-oral sexual contact with other partners were not associated with oral HPV infection including vaginal sex, total number of male partners, insertive anal intercourse with men, or receptive anal intercourse with men.
Evaluation of confounding of select risk factors
We evaluated potential confounding between three risk factors and oral HPV infection (Table 4). We found no evidence of confounding with any of the variables examined in the association between performing oral sex on a woman and engaging in oral-anal contact and oral HPV infection. The addition of vaginal sex to the model with chewing tobacco regularly strengthened the association. None of the potential confounding factors examined in this analysis nullified the associations between the chewing tobacco and oral HPV infection or performing oral sex on a woman and oral HPV infection, and all of the 95% CIs continued to exclude the null value of 1.0.
Multivariable adjusted associations with oral HPV infection
We included each variable that was significant in bivariable analyses in a multivariable model along with the variables that were diagnosed as potential confounders (Table 5). In this model, CD4+ level continued to show an association with oral HPV when <200 cells/uL compared with 500+ (OR: 2.9 [95% CI 1.0-9.1]). Reporting chewing tobacco ‘regularly’ also continued to show a protective effect (OR: 0.2 [95% CI 0.1-0.6]) in adjusted analyses as did performing oral sex on a woman (OR: 0.4 [95% CI 0.2-0.9]). When adjusted for the other factors, engaging in oral-anal contact was no longer significantly associated with oral HPV infection. While not significant in bivariable analyses, when the number of vaginal sex partners was included in the multivariable model, having 1-4 vaginal sex partners increased the odds of having oral HPV infection (OR: 2.7 [95% CI 1.1-6.5]), although the comparisons between having no partners, having 5-39 partners, and having 40+ partners were not significantly associated with oral HPV infection.