Cellular redox, cancer and human papillomavirus

Area of Science:

• Oncology
• Virology
• Molecular Biology

Background:

• High-risk Human Papillomavirus (HR-HPV) causes various human cancers.
• Persistent HR-HPV infection disrupts cellular processes like proliferation, apoptosis, immune evasion, and genomic stability.
• HR-HPV proteins are increasingly associated with oxidative stress (OS), a proposed risk factor for cancer.

Purpose of the Study:

• To review the association between oxidative stress (OS) and HR-HPV proteins.
• To elucidate the interplay between viral proteins and cellular antioxidant and DNA damage response (DDR) systems.
• To highlight mechanisms potentially crucial for viral lifecycle and oncogenic DNA integration.

Main Methods:

• Literature review of existing studies on HR-HPV, oxidative stress, and DNA damage response.
• Analysis of the role of reactive oxygen and nitrogen species (RONS) in cellular processes.
• Focus on the molecular interactions between viral oncoproteins and host cellular machinery.

Main Results:

• Oxidative stress arises from an imbalance in redox systems, damaging DNA, proteins, and lipids.
• This damage leads to mutations and genomic instability, contributing to cancer development.
• OS is implicated as a co-factor in cervical cancer and other malignancies.

Conclusions:

• HR-HPV proteins interact with cellular antioxidant and DNA damage response pathways.
• These interactions may facilitate viral persistence, replication, and DNA integration.
• Understanding this interplay is crucial for comprehending HR-HPV-induced carcinogenesis.