ArticleRetrovirology2008
Porphyromonas gingivalis induces CCR5-dependent transfer of infectious HIV-1 from oral keratinocytes to permissive cells.
Article in Retrovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Macrophage activation and invasion byJournal of oral microbiology · 2026Article
- Antimicrobial peptides: Defending the mucosal epithelial barrier.Frontiers in oral health · 2022Review
- COVID-19: A Recommendation to Examine the Effect of Mouthrinses with β-Cyclodextrin Combined with Citrox in Preventing Infection and Progression.Journal of clinical medicine · 2020Article
- Current trends and new developments in HIV research and periodontal diseases.Periodontology 2000 · 2020Review
- Activation of Notch-1 in oral epithelial cells by P. gingivalis triggers the expression of the antimicrobial protein PLAMucosal immunology · 2018Article
- Role of Porphyromonas gingivalis outer membrane vesicles in oral mucosal transmission of HIV.Scientific reports · 2018Article
- Oral microbiome and health.AIMS microbiology · 2018Review
- [Promotion of Porphyromonas gingivalis to viral disease].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2016Review
- Autonomous immunity in mucosal epithelial cells: fortifying the barrier against infection.Microbes and infection · 2016Review
- Oral innate immunity in HIV infection in HAART era.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2016Review
- Porphyromonas gingivalis-mediated Epithelial Cell Entry of HIV-1.Journal of dental research · 2014Article
- Interaction between endogenous bacterial flora and latent HIV infection.Clinical and vaccine immunology : CVI · 2013Review
- Short communication: HIV type 1 escapes inactivation by saliva via rapid escape into oral epithelial cells.AIDS research and human retroviruses · 2012Article
- Mucosal co-infections and HIV-1 transmission and pathogenesis.Current HIV research · 2012Article
- Potential mechanisms for increased HIV-1 transmission across the endocervical epithelium during C. trachomatis infection.Current HIV research · 2012Review
- Plausibility of HIV-1 Infection of Oral Mucosal Epithelial Cells.Advances in dental research · 2011Review
- Innate immunity including epithelial and nonspecific host factors: workshop 1B.Advances in dental research · 2011Article
- Contrasting roles for TLR ligands in HIV-1 pathogenesis.PloS one · 2010Article
- The oral microbiota: living with a permanent guest.DNA and cell biology · 2009Review
- Oral keratinocytes support non-replicative infection and transfer of harbored HIV-1 to permissive cells.Retrovirology · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSystemic infection with HIV occurs infrequently through the oral route. The frequency of occurrence may be increased by concomitant bacterial infection of the oral tissues, since co-infection and inflammation of some cell types increases HIV-1 replication. A putative periodontal pathogen, Porphyromonas gingivalis selectively up-regulates expression of the HIV-1 coreceptor CCR5 on oral keratinocytes. We, therefore, hypothesized that P. gingivalis modulates the outcome of HIV infection in oral epithelial cells.
resultsOral and tonsil epithelial cells were pre-incubated with P. gingivalis, and inoculated with either an X4- or R5-type HIV-1. Between 6 and 48 hours post-inoculation, P. gingivalis selectively increased the infectivity of R5-tropic HIV-1 from oral and tonsil keratinocytes; infectivity of X4-tropic HIV-1 remained unchanged. Oral keratinocytes appeared to harbor infectious HIV-1, with no evidence of productive infection. HIV-1 was harbored at highest levels during the first 6 hours after HIV exposure and decreased to barely detectable levels at 48 hours. HIV did not appear to co-localize with P. gingivalis, which increased selective R5-tropic HIV-1 trans infection from keratinocytes to permissive cells. When CCR5 was selectively blocked, HIV-1 trans infection was reduced.
conclusionP. gingivalis up-regulation of CCR5 increases trans infection of harbored R5-tropic HIV-1 from oral keratinocytes to permissive cells. Oral infections such as periodontitis may, therefore, increase risk for oral infection and dissemination of R5-tropic HIV-1.
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Registered trials
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