Chlamydia trachomatis and human herpesvirus 6 infections in ovarian cancer-Casual or causal?

About the Authors: Nitish Gulve Current Address: Program in Gene Expression and Regulation, The Wistar Institute, Philadelphia, Pennsylvania, United States of America Affiliation: Department of Microbiology, Biocenter, University of Wuerzburg, Wuerzburg, Germany ORCID logo http://orcid.org/0000-0001-8511-1065 Thomas Rudel * E-mail: thomas.rudel@biozentrum.uni-wuerzburg.de Affiliation: Department of Microbiology, Biocenter, University of Wuerzburg, Wuerzburg, Germany ORCID logo http://orcid.org/0000-0003-4740-6991 Citation: Gulve N, Rudel T (2019) Chlamydia trachomatis and human herpesvirus 6 infections in ovarian cancer—Casual or causal? In this brief review, we endeavor to highlight the role that coinfection of human herpesvirus 6 (HHV-6) and Chlamydia trachomatis may play in initiation and progression of ovarian cancer and propose a theory that may justify their presence in ovarian cancer tissues, thus enabling a directed therapeutic approach. During C. trachomatis infection, the host cell encounters DNA damage and suffers impaired repair thereby giving rise to the underlying foundation of the prominent cancer hallmark—genomic instability. C. trachomatis has been known to be an important factor in determining the course of Human Papillomavirus (HPV) infection and C. trachomatis/HPV coinfection may cause cervical cancer [24–26].