Abstract

Background: Cervical cancer remains a significant health concern worldwide and the primary cause of cancerous cervical lesions is the infection with high-risk human papillomavirus (HR-HPV). However, emerging evidence suggests that HR-HPV infection alone is insufficient for cancer development, and other co-factors may contribute to cervical carcinogenesis. Human cytomegalovirus (HCMV), a common herpesvirus frequently detected in cervical cancer samples, has demonstrated oncogenic potential. Objectives: This review aims to explore the molecular interactions between HR-HPV and HCMV in promoting cervical cancer progression. Methods. A comprehensive search was conducted in PubMed and Google Scholar, focusing on articles examining the role of HCMV in cervical tissues and/or cells, selected based on relevance and significance. Results: The reviewed literature indicates that HCMV and HR-HPV share several oncogenic mechanisms that could drive cervical cell transformation. Conclusions. Both viruses may synergistically promote cervical epithelial transformation and tumor progression in multiple ways. HR-HPV may facilitate HCMV entry by increasing host cell receptors essential for viral attachment. Additionally, HR-HPV and HCMV may cooperatively disrupt cellular processes, enhancing carcinogenesis. Both viruses may also modulate the local immune environment, enabling immune evasion and lesion persistence. However, further in vitro and in vivo studies are required to validate these hypotheses.