HPV is a common viral infection, and the immune system controls most infections. However, persistent infection with high-risk HPV types can lead to cellular changes and eventually contribute to cancers of the cervix, anus, genitals, mouth and throat. The review argues that HIV-related immune dysfunction can interfere with the body’s ability to clear HPV, creating conditions that favor persistent infection and cancer development.
The authors conducted a narrative review of research identified through major scientific databases, including PubMed, Scopus, and Web of Science. They considered studies published through December 2024 addressing HPV-HIV coinfection, immune dysregulation, viral persistence, and cancer development. Unlike a systematic review or meta-analysis, the study uses a narrative approach to synthesize findings across molecular, immunological, and clinical research.
One of the major findings is the strong association between HIV-related immune suppression and persistent HPV infection. According to the reviewed evidence, HPV persistence can be up to six times greater among people with HIV, while the risk of HPV infection may be as much as 18 times higher among people with low CD4+ T-cell levels. Oral HPV infection is also substantially more common among people living with HIV, with reported prevalence two to six times higher than in HIV-negative populations in the studies reviewed.
The biological explanation centers on impaired immune surveillance. HIV can reduce both the number and function of CD4+ T cells and disrupt dendritic cell activity, weakening immune responses at mucosal surfaces. This can make it more difficult for the body to eliminate HPV. Persistent infection may then create opportunities for abnormal cells to accumulate genetic and cellular changes.
The review also describes how high-risk HPV contributes directly to cancer development. Viral proteins known as E6 and E7 interfere with important tumor-suppressor pathways, including those involving p53 and retinoblastoma protein. In people with HIV, chronic inflammation, disruption of epithelial barriers, and altered cytokine signaling may further create an environment that supports malignant transformation.
The clinical implications are significant. The authors emphasize that people living with HIV require particular attention to HPV prevention and cancer screening. They recommend strong implementation of HPV vaccination, increased screening for cervical and anal HPV-related disease, and monitoring for oral and oropharyngeal HPV in higher-risk populations.
The review acknowledges important limitations. Because it is a narrative review rather than a quantitative meta-analysis, study selection and interpretation may be subject to bias, and the findings cannot necessarily establish causal relationships.
The evidence reviewed suggests that HPV-HIV coinfection represents an important intersection between infectious disease, immune dysfunction, and cancer. Strengthening vaccination, screening, HIV management and surveillance could help reduce the burden of HPV-related cancers among people living with HIV.