2014
DOI: 10.1371/journal.pone.0101326
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Lipoteichoic Acid (LTA) and Lipopolysaccharides (LPS) from Periodontal Pathogenic Bacteria Facilitate Oncogenic Herpesvirus Infection within Primary Oral Cells

Abstract: Kaposi’s sarcoma (KS) remains the most common tumor arising in patients with HIV/AIDS, and involvement of the 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 of a variety of bacteria. Whether interactions involving pathogenic bacteria and oncogenic viruses in the local environment facilitate replication or maintenance of these viruses in the oral cavity remains unknown. In the current study, o… Show more

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Cited by 32 publications
(33 citation statements)
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“…Also, Epstein–Barr virus reactivation may trigger overgrowth of P. gingivalis and, bidirectionally, P. gingivalis has the potential to reactivate Epstein–Barr virus with the risk of generating and disseminating infectious virions . Porphyromonas gingivalis lipopolysaccharide may facilitate herpesviral entry into periodontal fibroblasts and activate intracellular signaling pathways, such as nuclear factor‐kappaB , and butyric acid and other products of P. gingivalis may reactivate Epstein–Barr virus by acetylation of histone proteins and by other means of epigenetic changes . The vicious cycle of increased pathogenicity of both herpesviruses and pathogenic bacteria may lead to periodontal breakdown if the herpesvirus–bacterial collaboration is not swiftly controlled by host defenses or by therapy.…”
Section: Herpesvirus Pathogenicitymentioning
confidence: 99%
“…Also, Epstein–Barr virus reactivation may trigger overgrowth of P. gingivalis and, bidirectionally, P. gingivalis has the potential to reactivate Epstein–Barr virus with the risk of generating and disseminating infectious virions . Porphyromonas gingivalis lipopolysaccharide may facilitate herpesviral entry into periodontal fibroblasts and activate intracellular signaling pathways, such as nuclear factor‐kappaB , and butyric acid and other products of P. gingivalis may reactivate Epstein–Barr virus by acetylation of histone proteins and by other means of epigenetic changes . The vicious cycle of increased pathogenicity of both herpesviruses and pathogenic bacteria may lead to periodontal breakdown if the herpesvirus–bacterial collaboration is not swiftly controlled by host defenses or by therapy.…”
Section: Herpesvirus Pathogenicitymentioning
confidence: 99%
“…Moreover, interaction between EBV and Porphyromonas gingivalis may also be bidirectional [123]. Herpesviral proteins on infected cells may serve as a new attachment sites for bacteria [124], while some bacterial products may facilitate herpesviral entry into cells and activate intracellular signalling pathways [125].…”
Section: Discussionmentioning
confidence: 99%
“…*, P Ͻ 0.05; **, P Ͻ 0.01. with 20% fetal bovine serum. Primary human umbilical vein endothelial cells (HUVEC) were cultured as described previously (7). All the cells were cultured at 37°C in 5% CO 2 .…”
Section: Fig 5 Legend (Continued)mentioning
confidence: 99%