Increased human papillomavirus viral load is correlated to higher severity of cervical disease and poorer clinical outcome: A systematic review

Author:

Fobian Seth‐Frerich1234ORCID,Mei Xionge123ORCID,Crezee Johannes13ORCID,Snoek Barbara C.123ORCID,Steenbergen Renske D. M.5ORCID,Hu Jiafen6ORCID,ten Hagen Timo L. M.4ORCID,Vermeulen Louis237ORCID,Stalpers Lukas J. A.123ORCID,Oei Arlene L.123ORCID

Affiliation:

1. Department of Radiation Oncology, Amsterdam UMC University of Amsterdam Amsterdam The Netherlands

2. Center for Experimental and Molecular Medicine (CEMM) Laboratory for Experimental Oncology and Radiobiology (LEXOR) Amsterdam The Netherlands

3. Cancer Center Amsterdam Cancer Biology and Immunology Amsterdam The Netherlands

4. Precision Medicine in Oncology (PrMiO), Department of Pathology Erasmus MC Cancer Institute Rotterdam The Netherlands

5. Department of Pathology, Amsterdam UMC Vrije University Amsterdam The Netherlands

6. Jake Gittlen Laboratories of Cancer Research, Department of Pathology Pennsylvania State University College of Medicine Hershey Pennsylvania USA

7. Oncode Institute Amsterdam The Netherlands

Abstract

AbstractCervical cancer is the fourth most common cancer in women worldwide and is caused by persistent infection with high‐risk types of human papillomavirus (HPV). HPV viral load, the amount of HPV DNA in a sample, has been suggested to correlate with cervical disease severity, and with clinical outcome of cervical cancer. In this systematic review, we searched three databases (EMBASE, PubMed, Web of Science) to examine the current evidence on the association between HPV viral load in cervical samples and disease severity, as well as clinical outcome. After exclusion of articles not on HPV, cervical cancer, or containing clinical outcomes, 85 original studies involving 173 746 women were included. The vast majority (73/85 = 85.9%) reported that a higher viral load was correlated with higher disease severity or worse clinical outcome. Several studies reported either no correlation (3/85 = 3.5%), or the opposite correlation (9/85 = 10.6%); possible reasons being different categorization of HPV viral load levels, or the use of specific sampling methods. Despite variations in study design and populations, the above findings suggest that HPV viral load is correlated to clinical outcome, and may become an important biomarker for treatment selection and response monitoring for cervical cancer.

Funder

China Scholarship Council

Publisher

Wiley

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