Human Papillomavirus Viral Load and Transmission in Young, Recently Formed Heterosexual Couples

Abstract

Background: We studied the association between human papillomavirus (HPV) viral load (VL) and HPV concordance.

Methods: The HITCH cohort study included young, heterosexual, recently formed, sexually active couples. Questionnaires and genital samples were collected at 0 and 4 months. Samples were tested for HPV DNA by polymerase chain reaction (PCR; Linear Array). VLs of HPV6/11/16/18/31/42/51 were quantified using type-specific real-time PCR. Correlations between VL and type-specific HPV prevalence and incidence were evaluated using multilevel, mixed-effects linear/logistic regression models.

Results: We included 492 couples. VLs were higher in penile than vaginal samples. VL at subsequent visits correlated significantly within men (r, 0.373), within women (r, 0.193), and within couples (r range: 0.303-0.328). Men with high VL had more type-specific persistent HPV infections (odds ratio [OR], 4.6 [95% confidence interval {CI}, 2.0-10.5]). High VL in men was associated with prevalent (OR, 5.3 [95% CI, 2.5-11.2]) and incident (OR, 6.7 [95% CI, 1.5-30.7]) type-specific HPV infections in their partner. Women's VL was associated with type-specific HPV prevalence in their partner at the same (OR, 5.9) and subsequent (OR, 4.7) visit.

Conclusions: Persistent HPV infections have limited VL fluctuations. VL between sex partners are correlated and seem predictive of transmission episodes.

Keywords: HPV; HPV11; HPV16; HPV18; HPV6; human papillomavirus; infection transmission; sexually transmitted infections; viral load.

Figure 1.

Study flowchart of patients from the HPV Infection and Transmission Among Couples Through Heterosexual Activity (HITCH) cohort study. Intraindividual analyses consisted of all analyses within men or within women only (ie, no data from the heterosexual partner was needed), which included evaluation of the viral load distribution in men or women, the correlation of human papillomavirus (HPV) viral loads within individuals at visit 1 and 2, and the association between viral loads and HPV prevalence or clearance at the next visit within individuals. Interindividual analyses included all analyses that involved data from both partners of a heterosexual couple.

Figure 2.

Log₁₀ distribution of viral loads by sex, human papillomavirus (HPV) type, and visit number. Boxes represent the 25th to 75th percentiles, the black horizontal line inside the boxes represents the median, and whiskers represent the full range of values up to 1.5 times the interquartile range. For values outside this range, the full range is marked by dots. Average viral loads between HPV types differed significantly, both in men and in women (P < .001, Kruskal–Wallis test).

Figure 3.

Correlation of human papillomavirus (HPV) viral loads within individuals (scatter plots, A and B) or between sexually active partners (scatter plots, C–J). To calculate correlation coefficients (r), multilevel mixed-effects linear regression was used, allowing for adjustment of repeated measures (ie, multiple HPV types were evaluated per individual/couple). A, HPV viral loads were strongly correlated between visit 1 and 2 in men with a persistent HPV infection (n = 152 in 114 men, r = 0.373, P < .001). B, HPV viral loads were significantly correlated between visit 1 and 2 in women with a persistent HPV infection (n = 145 in 117 women, r = 0.193, P = .018). C, HPV viral loads were strongly correlated between sexually active partners who were both positive for an identical HPV type at the baseline visit (n = 141 in 107 dyads, r = 0.318, P < .001). D, HPV viral loads were significantly correlated between sexually active partners who were both positive for an identical HPV type at the follow-up visit (n = 88 in 69 dyads, r = 0.303, P = .040). E, Mean HPV viral loads were strongly correlated in sexually active partners who were positive for an identical HPV type during at least one visit (n = 125 in 87 dyads, r = 0.310, P = .003). F, Mean HPV viral loads were significantly correlated in sexually active partners who both had a persistent infection of an identical HPV type (n = 59 in 49 dyads, r = 0.324, P = .028). G and H, Repeating the analysis in E and F, but using the maximum instead of mean viral load, provided similar results (all infections: r = 0.316, P = .003; persistent infections: r = 0.328, P = .027). I, HPV viral loads in male genital samples at visit 1 were not significantly correlated to type-specific viral loads in their female partner’s genital samples at visit 2 (n = 92 in 79 dyads, r = 0.088, P = .498). J, HPV viral loads in female genital samples at visit 1 were not significantly correlated to type-specific viral loads in their male partner’s genital samples at visit 2 (n = 98 in 76 dyads, r = 0.064, P = .605). *P < .05; **P < .01; ***P < .001.