Helminth infection shows repeated signals of association with HPV and cervical neoplasia
Cervical cancer remains unevenly distributed across the world, and the burden falls hardest on people living in low- and middle-income countries. Limited access to screening, vaccination, and treatment explains part of that gap, but the clinical question addressed in this scoping review is more biologically specific: could chronic helminth infection also contribute to the persistence of HPV and the development of cervical cancer?
The review, published in PLoS Neglected Tropical Diseases, examined epidemiologic studies published between 1990 and 2022 that evaluated associations between helminth infection and HPV prevalence, HPV persistence, or cervical cancer progression. Chronic helminth infection is not a neutral background exposure. These parasites can alter host immunity in ways that suppress anti-viral responses, creating a plausible pathway through which HPV may persist longer or progress more easily toward neoplasia.
Eight studies met eligibility criteria out of 93 reports screened for inclusion. The evidence base is small, but its direction is remarkably consistent.
The strongest recurring signal involved schistosomiasis
Six of the eight studies found a positive trend between schistosomiasis and cervical neoplasia. In a field where the available literature is sparse and heterogeneous, repeated directional agreement carries weight even without pooled effect estimates. Schistosomiasis is common in many of the same settings where cervical cancer screening and treatment access are already limited, so the overlap between infection burden and cancer risk is clinically important.
A plausible mechanism exists. Helminths can skew immune responses away from the kind of antiviral surveillance needed to suppress HPV, and that immune diversion may make the cervix more vulnerable to persistent infection and progressive epithelial changes. In practical terms, a host already managing chronic parasitic immune modulation may have less effective clearance of oncogenic HPV types.
The signal is not proof of causation, but it is too consistent to dismiss as random noise.
HPV prevalence also tracked with hookworm in two studies
Two studies found a positive association between hookworm infection and HPV prevalence. The review also identified one study linking Ascaris, Trichuris, and Strongyloides with HPV prevalence. Those findings broaden the concern beyond schistosomiasis alone and point toward a wider interaction between helminth burden and susceptibility to HPV infection.
This matters because HPV is the upstream driver of cervical cancer. If helminth infection raises the likelihood that HPV is present, or makes persistent infection more likely, then the downstream cancer risk becomes a second-order consequence of a parasitic disease that is often treated as separate from gynecologic oncology. The biology is coherent: immune dysregulation from chronic helminth infection could weaken mucosal antiviral defenses, tilt local immune signaling, and reduce the host’s ability to control HPV at the cervical epithelium.
A small evidence base still points in one direction
The review identified only eight relevant studies from an initial pool of 93 reports. That narrow base limits certainty, but it also exposes the gap in clinical knowledge with unusual clarity. The available studies did not point in conflicting directions. Every included report suggested a possible positive association between helminth infection and HPV or cervical cancer.
Because the review focused on epidemiologic association rather than mechanistic experiments, it cannot establish whether helminth infection directly increases cancer risk, whether shared social and environmental exposures explain part of the relationship, or whether the association is stronger in some parasite species than others. Still, the pattern is biologically plausible and epidemiologically relevant, especially in regions where both infections are common. Women and girls in these settings may be exposed simultaneously to two infectious conditions that interact through the immune system rather than through direct tissue invasion.
The clinical consequence is not abstract. If chronic helminth infection contributes even modestly to HPV persistence or cervical neoplasia, then deworming strategies, parasitic disease control, and cervical cancer prevention cannot be treated as isolated public health silos.
Why this association matters in low-resource settings
The review was driven by a broader concern: cervical cancer burden is not explained fully by access disparities alone. In low- and middle-income countries, helminth infection remains common, and HPV exposure is widespread. Where those burdens overlap, the probability of immune interaction rises as well.
For clinicians and public health teams, the finding argues for a more integrated view of cervical cancer prevention. HPV vaccination, screening, treatment of precancerous lesions, and control of endemic helminth infections may all be part of the same prevention ecosystem. Even without definitive causal proof, the repeated association seen across these studies supports the idea that parasitic infection could be one contributor to differential cervical cancer risk.
A single sentence captures the state of the evidence: the association is plausible, repeated, and unresolved.
What the literature still cannot answer
The review also makes clear how much remains unknown. The included studies were few, and the abstract does not provide effect sizes, uniform diagnostic methods, or enough detail to compare species-specific risks across populations. The evidence spans different helminths, different HPV-related outcomes, and different study settings, which makes synthesis difficult and leaves open questions about which infection, if any, carries the strongest signal.
Future research will need to separate parasite species, clarify temporality, and determine whether treatment of helminth infection changes HPV persistence or cervical neoplasia risk. Until then, the most defensible interpretation is cautious but clinically serious: chronic helminth infection may be one of the biological threads linking infectious disease burden to cervical cancer disparities in LMICs, and the published evidence has begun to point in that direction.