KSHV co-infection down-regulates HPV16 E6 and E7 from cervical cancer cells
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Lu Dai1,2,4, Yueyu Cao2, Wei Jiang3, Jovanny Zabaleta5, Zhongmin Liu2, Jing Qiao1, Zhiqiang Qin1,2,4
1Department of Pediatrics, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
2Research Center for Translational Medicine and Key Laboratory of Arrhythmias, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
3Department of Microbiology and Immunology, Division of Infectious Diseases, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA
4Departments of Genetics Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
5Pediatrics, Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
Jing Qiao, email: email@example.com
Zhiqiang Qin, email: firstname.lastname@example.org
Keywords: HPV, KSHV, E6, E7, microRNA
Received: February 14, 2017 Accepted: March 07, 2017 Published: March 15, 2017
High-risk human papillomavirus (HPV) infection is the etiological agent of some malignancies such as cervical, oral and oropharyngeal cancers. Kaposi sarcoma-associated herpesvirus (KSHV) represents a principal causative agent of several human cancers arising in those immunocompromised patients. Interestingly, KSHV DNA has been detected in the oral cavity and the female genital tract, although its detection rate in cervical samples is very low and few reports are about KSHV/HPV co-infection. Therefore, it remains unclear about the role of KSHV co-infection in the development of HPV-related neoplasias. In the current study, we report that HPV16-integrated cervical cancer cell-line SiHa is susceptible to KSHV latent infection and replication. We also have found that KSHV infection or viral latent proteins are capable of reducing HPV16 E6/E7 expression through the manipulation of cellular microRNA function. Array analysis indicates that KSHV infection induces some inflammatory cytokines/chemokines production as well as up-regulates a series of interferon-induced genes expression, which may facilitate host immune defense system attacking these co-infected cells and clearance of viruses. Together, our data have provided possible explanations for very low detection rate of KSHV shedding as well as of KSHV/HPV co-infection in cervical samples and/or cervical cancer cells.
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