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The pooled prevalence of HHV infection among women with cervical cancer is notably higher at 56% compared to 34% in women with normal cervix, identifying an overall 2.74-fold increase in CC risk associated with HHV infection, signaling a significant epidemiological relevance of herpesviruses as cofactors.
The significant and consistent association of HSV-2 infection with both CC (OR = 3.01) and PCL (OR = 2.14), corroborated by adjusted effect estimates, supports its role as a potential risk factor that operates beyond mere co-infection with HPV, which has implications for research and preventative strategies.
EBV infection shows an even stronger association with CC (OR = 4.89) and PCL (OR = 3.55), with risk escalating alongside lesion severity, indicating EBV’s possible oncogenic cofactor role and suggesting pathways involving immunosuppression and synergy with HPV that warrant targeted investigations.
No significant associations were found between HSV-1 or cytomegalovirus (HCMV) and cervical lesions, clarifying the specificity of herpesvirus subtypes in cervical carcinogenesis risk.
Meta-regression analyses revealed that infection risk estimates vary with viral detection methods and HDI levels, with markedly higher risks in low and medium HDI regions, underscoring the need to consider socio-economic and methodological contexts when interpreting viral oncogenesis data.
The limited but suggestive data on HHV-6, HHV-7, and Kaposi sarcoma–associated herpesvirus (KSHV) underscore potential novel cofactors requiring further study, indicating the complexity of viral interactions in cervical lesion development.
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