Journal
ONCOTARGET
Volume 8, Issue 22, Pages 35792-35803Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.16207
Keywords
HPV; KSHV; E6; E7; microRNA
Categories
Funding
- DOD Career Development Award [CA140437]
- Leukemia Research Foundation
- Louisiana Clinical and Translational Science Center Pilot grant (NIH) [U54GM104940]
- NIH RO1s [AI091526, AI128864]
- National Natural Science Foundation of China [81472547, 81400164, 81672924]
- Health Industry Project from Pudong Health Bureau of Shanghai, China [PW2013E-1]
- CDMRP [CA140437, 793839] Funding Source: Federal RePORTER
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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 interferoninduced 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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