A quadrivalent HPV vaccine held up for up to nine years in women with HIV
In a Canadian cohort of 228 women with HIV, antibody titres matched those of women without HIV and cervical precancer was not recorded — but protection tracked with viral suppression.
Women living with HIV carry more human papillomavirus infection, and more of the cervical disease it causes, than women without it. That makes them one of the groups in which HPV vaccination matters most — and one in which its durability is least well documented, because immune responses to any vaccine can be blunted when HIV is not controlled. A longitudinal cohort study published in The Lancet HIV on 5 October reports how the quadrivalent HPV vaccine performed in this group over the better part of a decade [s1].
The cohort
The study recruited girls and women with HIV aged nine years and older from 14 clinics providing HIV and gynaecological care across Canada [s1]. Participants received three doses of the quadrivalent vaccine at months 0, 2 and 6, and were followed from 1 July 2008 to 27 June 2019 [s1]. At baseline and every six to twelve months they underwent anti-HPV serology, liquid-based cervical cytology and HPV DNA genotyping [s1].
The per-protocol population was 228 women, with a median age at baseline of 38.5 years (IQR 32.0–45.4) and a median CD4 count of 499.5 cells per µL (IQR 380.8–700.0) [s1]. At entry, 160 of them (70.2%) had suppressed HIV viral loads below 50 copies per mL [s1]. Median follow-up was 5.9 years (IQR 2.3–7.7) [s1].
What the antibodies did
After the very high seroconversion rates recorded at month seven, the question was how long those antibodies lasted. Over follow-up, seroreversion — losing detectable antibody — occurred in 18 of 132 women for HPV6 (13.6%), 22 of 186 for HPV11 (11.8%), 12 of 141 for HPV16 (8.5%) and 60 of 165 for HPV18 (36.4%) [s1]. The pattern is familiar from HPV vaccine studies generally: antibody against HPV18 wanes fastest, while the response to HPV16 — the type behind most cervical cancer — is the most durable.
Crucially, the authors report that anti-HPV geometric mean titres were similar between women with HIV and a historical comparator group of women without HIV for up to nine years [s1]. On the measure the study was built to test, HIV status did not appear to erode the vaccine's antibody response over that window.
What predicted waning was not HIV status in the abstract but how well the virus was controlled. Peak antibody titres and serial HIV viral load were both significant predictors of time to seroreversion [s1]. The implication the authors draw is practical: continual viral load suppression after vaccination matters for keeping protection intact [s1].
What happened clinically
Antibody is a surrogate; disease is the endpoint that counts. In the per-protocol population the incidence of persistent quadrivalent-type HPV infection was 0.52 per 100 person-years (95% CI 0.22–1.10), and genital warts occurred at 0.37 per 100 person-years (0.12–0.87) [s1]. Cervical intraepithelial neoplasia of grade two or higher — the precancerous lesion cervical screening is designed to catch — was recorded at an incidence of 0.00 per 100 person-years (0.00–0.24) [s1].
A zero count is not proof of zero risk; the confidence interval still reaches up to 0.24 events per 100 person-years, and 228 women followed for a median under six years is a modest denominator for a rare outcome. But in a group expected to have elevated rates of exactly this lesion, none was observed over the study. The authors' reading is that infection and disease rates were low in this vaccinated cohort [s1].
How much this settles
The design is a cohort, not a randomised trial, so it cannot by itself attribute the low disease rates to the vaccine rather than to screening, behaviour or the characteristics of women who complete three doses and stay in follow-up. What it adds is long-term immunogenicity data in a population where those data were thin, and a reasonably clean signal that the antibody response holds up when HIV is suppressed.
Two limits are worth stating plainly. The comparison of titres with women without HIV used a published historical cohort rather than a group enrolled alongside these participants [s1]. And the cohort was recruited and dosed before the nonavalent vaccine, which covers five additional cancer-causing types, became standard — so the durability described here is for the quadrivalent product specifically [s1]. The study was funded by the Canadian Institutes of Health Research and its HIV trials network, with in-kind support from Merck Canada [s1].
What to watch
The open questions are whether the same durability holds for the nine-valent vaccine now in use, whether a cohort recruited with contemporaneous HIV-negative controls would show the same titre parity, and whether the near-absence of high-grade cervical lesions persists as this group ages. For now, the result supports a straightforward message already built into most guidelines: vaccinate, and keep HIV suppressed.
This article describes research findings and is not medical advice.
Sources
- [s1] Long-term immunogenicity and efficacy of the quadrivalent human papillomavirus vaccine in women with HIV: a longitudinal cohort study. The Lancet HIV, 5 October 2026. https://doi.org/10.1016/S2352-3018(26)00204-3
Sources
- Long-term immunogenicity and efficacy of the quadrivalent human papillomavirus vaccine in women with HIV: a longitudinal cohort study — The Lancet HIV , October 5, 2026
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