High-risk HPV was common in women with HIV attending a Freetown clinic
Among women living with HIV who attended Connaught Teaching Hospital in Freetown, high-risk human papillomavirus infection was frequent enough to raise immediate concerns for cervical cancer prevention in routine HIV care. The cross-sectional study enrolled 191 women aged 25 to 65 years between September and December 2024 and found high-risk HPV DNA in 60 participants, a prevalence of 31.4% with a 95% confidence interval of 25.3% to 38.3%.
That burden is clinically important because persistent high-risk HPV infection is the biological engine behind most cervical cancers. In women with HIV, impaired immune control can make clearance of oncogenic HPV less reliable, allowing infection to persist, accumulate additional genetic instability, and progress toward precancerous cervical disease more easily than in immunocompetent women.
The cohort itself was relatively young. Mean age was 36.8 years, 44.5% were single, and 67% were employed. Those demographics matter because cervical cancer prevention programs often miss women in their most productive years, especially in health systems where screening is not automatically embedded in HIV services. In Sierra Leone, screening for cervical cancer is not yet integrated into HIV care, leaving a preventable gap between diagnosis of HIV and prevention of an HPV-driven malignancy.
Non-16/18 genotypes dominated the virologic profile
Genotyping patterns carried their own warning. Half of the HPV-positive women, 30 of 60, had multiple serotypes, a pattern that usually signals more complex mucosal exposure and a greater likelihood of persistent infection. The most common genotype was HPV 52, followed by HPV 16 and HPV 51.
Only 30% of HPV-positive women carried genotypes 16 or 18, the two types targeted by the bivalent vaccine. This is a critical point for vaccine policy in settings with high HIV prevalence. When the genotype mix shifts beyond 16 and 18, vaccine programs that focus too narrowly on those two strains may leave substantial residual risk in the population most vulnerable to chronic infection and cervical neoplasia.
The genotype distribution also suggests a broader epidemiologic pattern. HPV 16 remains one of the best-known carcinogenic strains worldwide, yet the prominence of HPV 52 and HPV 51 in this cohort implies that local surveillance cannot assume the genotype hierarchy seen in every region. Cervical cancer prevention in West Africa will depend on knowing which strains are actually circulating in women with HIV, not simply which strains dominate global vaccine conversations.
Former contraceptive use was the only independent predictor identified
On multivariable analysis, former contraceptive use stood out as an independent predictor of HPV positivity, with an adjusted odds ratio of 4.86, a 95% confidence interval of 1.65 to 17.37, and a p value of 0.0032. No other independent risk factor is provided in the abstract, so this association should be interpreted cautiously and within the limits of a cross-sectional design.
The biological explanation is not settled, but several plausible pathways exist. Hormonal or barrier contraceptive histories can correlate with sexual behavior, duration of cervical exposure, health-seeking patterns, or reproductive history, any of which may influence HPV acquisition and persistence. In a population already carrying HIV, even modest shifts in cervical mucosal immunity or exposure timing can tilt the balance toward persistent infection rather than transient colonization.
One caution is unavoidable: an association in a cross-sectional study does not establish causation. Former contraceptive use may be a marker for other unmeasured factors rather than an independent biological cause of HPV infection. Even so, the signal is strong enough to justify more careful screening attention in women with contraceptive histories, especially when other known immunologic vulnerabilities are already present.
What the numbers mean for cervical screening in HIV services
The practical implication is straightforward. Screening for cervical cancer and high-risk HPV cannot remain separate from HIV care in Sierra Leone if the goal is to find disease before symptoms appear. Women living with HIV already carry elevated risk for persistent oncogenic HPV, and this study shows that the prevalence is high enough to make opportunistic screening in routine clinic visits clinically defensible.
Integration would do more than add a test. It would create a pathway from HIV follow-up to cervical risk assessment, triage, and treatment when needed. In settings with limited specialist access, that linkage may be the difference between detecting infection while it is still manageable and discovering invasive cancer only after symptoms develop.
The predominance of non-16/18 genotypes adds a second policy layer. Broader HPV vaccine coverage may be needed if Sierra Leone wants its prevention strategy to match local genotype patterns rather than imported assumptions about strain prevalence. A vaccine strategy that ignores genotype diversity risks underprotecting the very women most likely to benefit from prevention.
A clinic-based study with clear public health relevance
This was a single-center cross-sectional study conducted at Connaught Teaching Hospital, so the findings should not be generalized beyond the enrolled cohort without caution. Cross-sectional sampling also cannot determine whether HPV positivity preceded contraceptive use history, followed it, or shared a common driver. Still, the study provides rare local data from Sierra Leone, where women with HIV face a cervical cancer risk environment shaped by limited integrated screening and likely constrained access to preventive services.
Ethical approval came from the Sierra Leone Ethics and Scientific Review Committee of the Ministry of Health, and all participants gave written informed consent. Data were anonymized and secured, and the study followed standard ethical safeguards.
The central message is hard to ignore: high-risk HPV is common in this HIV clinic population, multiple infections are frequent, and the genotype pattern extends well beyond HPV 16 and 18. In a country where cervical screening is not yet built into HIV services, that combination leaves too much preventable disease hidden in plain sight.