Infect Agent Cancer. 2014 Aug 24;9:28. doi: 10.1186/1750-9378-9-28. eCollection 2014.
Oncogenic viruses associated with vulva cancer in HIV-1 patients in Botswana.
Infectious agents and cancer
Kenneth O Simbiri, Hem C Jha, Mukendi K Kayembe, Carrie Kovarik, Erle S Robertson
Affiliations
Affiliations
- Department of Microbiology and Immunology, Upstate Medical University, R2120A, Weiskotten Hall, 750 East Adams Street, Syracuse, NY 13210, USA.
- Department of Microbiology, Abramson Cancer Center, Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, 202A Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104-6076, USA.
- National Health Laboratory, Gaborone, Botswana.
- Botswana-University of Pennsylvania Partnership, Gaborone, Botswana ; Department of Dermatology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
PMID: 25225572
PMCID: PMC4164322 DOI: 10.1186/1750-9378-9-28
Abstract
BACKGROUND: Oncoviruses such as HPV, KSHV, and EBV have been reported in patients with HIV infection and AIDS. How oncovirus-associated cancers rise in AIDS patients has not been fully established. The purpose of our study was to identify the viral agents in vulvar cancer and to assess their contribution to pathogenesis.
METHOD: We retrospectively identified a total of 13 vulva tissue samples from HIV-1 positive and 9 vulvar samples from HIV-1 negative patients from the Botswana National Health Laboratory in Gaborone, Botswana, a Southern African country with a high incidence of HIV. We utilized PCR and IHC to identify HPV, EBV, KSHV, and JC virus in FFPE preserved tissue samples.
RESULTS: Using the GP5(+)/GP6(+) primer set we detected several HPV types in tissue samples. EBV was detected in all of the positive cases (100%) and in most of the negative cases (89%). KSHV was detected in 39% of the HIV-1 positive samples and in 11% of the negative samples, and no JC virus was detected in any of the samples. Using IHC we demonstrated that LANA was expressed in 61% of the positive samples and in 44% of the negative samples. The ubiquitous EBV was more consistently expressed in negative cases (100%) than in positive cases (69%). Interestingly, the HPV-16 E6 transcript was detected in 56% of the negative samples compared to 31% of the positive samples. However, the cell cycle protein P21 used as a surrogate marker for HPV was detected in 77% of the positive samples and in 44% of the negative samples, while VEGF signals were similar in both positive (92%) and negative samples (89%).
CONCLUSION: Our study, suggests that in Botswana, vulvar squamous cell carcinoma (VSCC) is associated with oncogenic viruses present in the niche but the contribution and progression may be regulated by HPV and other immunosuppressive infections that include HIV-1.
Keywords: EBV; HIV-1; HPV; KSHV; OSSN
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