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J Infect Dis. 2019 May 17. pii: jiz249. doi: 10.1093/infdis/jiz249. [Epub ahead of print]

KSHV and Staphylococcus aureus co-infection in oral cavities of HIV+ patients: a unique niche for oncogenic virus lytic reactivation.

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Department of Pathology, Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Department of Pediatrics, Research Center for Translational Medicine and Key Laboratory of Arrhythmias, East Hospital, Tongji University School of Medicine, Shanghai, China.
Departments of Diagnostic Sciences, School of Dentistry, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Departments of Biostatistics, School of Public Health, Louisiana State University Health Sciences Center, , New Orleans, LA, USA.


Collectively, viruses are the principal cause of cancers arising in patients with immune dysfunction, including HIV+ patients. Kaposi's Sarcoma (KS) etiologically linked to KSHV continues to be the most common AIDS-associated tumor. The involvement of oral cavity represents one of the most common clinical manifestations of this tumor. HIV infection incurs an increased risk for periodontal diseases and oral carriage from a variety of pathogenic bacteria. However, whether interactions involving periodontal bacteria and oncogenic viruses in local environment facilitate replication or maintenance of these viruses in oral cavity of HIV+ patients remain largely unknown. We previously showed that pathogen-associated molecular patterns (PAMPs) molecules from specific periodontal bacteria promoted KSHV entry into oral cells and subsequent latency establishment. In the current study, we demonstrate that Staphylococcus aureus, one of common pathogens causing infection in HIV+ patients, and its PAMPs can effectively induce KSHV lytic reactivation from infected oral cells, through the TLR-ROS and Cyclin D1-Dicer-viral microRNAs axis. We have further provided clinical evidence and relevance of these two pathogens co-infection in oral cavities of cohort HIV+ patients. Our studies have revealed novel mechanisms through which these pathogens co-infection potentially promote virus-associated cancer development in the unique niche of immunocompromised patients.


HIV; KSHV; Kaposi’s Sarcoma; Staphylococcus aureus; microRNA


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