Periodontopathic Bacteria in English HIV-Seropositive Persons

Scully, Crispian; Porter, Stephen; Mutlu, Serdar; Epstein, Joel B.; Glover, S. C.; Kumar, Navdeep

doi:10.1089/apc.1999.13.369

Cited by 29 publications

(34 citation statements)

References 32 publications

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“…Previous studies have consistently shown that P. gingivalis was significantly more prevalent in both supra-and subgingival plaque samples from periodontitis subjects compared to those from healthy individuals (10,31). Results from independent studies indicate that periodontopathogens, including P. gingivalis, were detected more frequently and were found at higher levels in HIV-infected patients than in noninfected control subjects with similar periodontal statuses (5,20,26,33). On the contrary, recent results from Patel et al (23) showed a significant prevalence of Porphyromonas gingivalis and Treponema denticola among HIV-negative patients compared to that among HIV-positive patients.…”

Section: Discussionmentioning

confidence: 93%

Inhibition of Human Immunodeficiency Virus Type 1 Entry by a Binding Domain of Porphyromonas gingivalis Gingipain

Xie

Belogortseva

et al. 2006

Antimicrob Agents Chemother

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Human immunodeficiency virus (HIV) transmission through saliva is extremely low. Several oral components, including secretory immunoglobulin A and secretory leukocyte protease inhibitor, are known as potential inhibitory agents of HIV oral transmission. Here we examined anti-HIV activity of oral bacterial components. We showed that recombinant protein HGP44 derived from Porphyromonas gingivalis, one of the primary infectious agents of periodontitis, was capable of inhibiting HIV type 1 (HIV-1) replication. HGP44 bound specifically to HIV-1 gp120 and blocked HIV-1 envelope-mediated membrane fusion. These findings suggest that HGP44 of P. gingivalis can inhibit HIV-1 infection by blocking HIV-1 entry.The predominant mode of human immunodeficiency virus (HIV) transmission is by sexual contact through broken mucosal or epidermal epithelia. It is rather clear that oral transmission of HIV is a rare event relative to vaginal and rectal transmission (3,32). It has been reported that fewer infectious HIV particles are in saliva than in other body fluids, such as blood, semen, and vaginal and cervical secretions (25). However, hyperexcretion of HIV type 1 (HIV-1) RNA in saliva has been reported previously (27). It appears that 87% of HIVinfected patients had plasma titers exceeding those in saliva, and 7% of the 67 tested individuals had a fourfold or higher viral load in saliva relative to that than in plasma (27).Several endogenous oral components are proposed to contribute to inactivating HIV, either alone or in combination (28). Among them, the secretory leukocyte protease inhibitor has been extensively studied. The secretory leukocyte protease inhibitor was first described by Thompson and Ohlsson (30) as a potent inhibitor of leukocyte elastase. Since then, studies from many independent laboratories have confirmed its anti-HIV-1 activity in in vitro assays (17,19,28). Recently, a novel mechanism of anti-HIV activity has been proposed; this mechanism involves the unique hypotonicity of saliva (2, 3). The tonicity of saliva is approximately 14% of that of blood and other mucosal secretions. Peripheral blood mononuclear cells were rapidly disrupted in saliva in an in vitro study. The hypothesis is that cell-associated HIV is released due to saliva disruption, and cell-free HIV is mostly neutralized by a specific antibody or inhibited by other macromolecular inhibitors in saliva.Despite the great effort that has been made to search for oral inhibitors of HIV, little information is available on the interaction of HIV and bacteria in the oral cavity, an environment harboring over 30 genera representing more than 500 species of bacteria (21). We speculated that oral bacteria may contain anti-HIV activity and create a microenvironment unfavorable for HIV infection. In this study, members of a group of oral bacteria were examined for their abilities to inhibit HIV-1. We demonstrated that Porphyromonas gingivalis, an organism frequently detected in the mouths of adult periodontitis patients, produced an antiviral molecule(s)...

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Section: Discussionmentioning

confidence: 93%

Inhibition of Human Immunodeficiency Virus Type 1 Entry by a Binding Domain of Porphyromonas gingivalis Gingipain

Xie

Belogortseva

et al. 2006

Antimicrob Agents Chemother

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“…In addition, there was a significant correlation between the clinical stage of periodontitis and the HIV-1 proviral DNA load in gingival crevicular fluid as well as the HIV-1 RNA viral load in plasma (33,34) and saliva (34). More P. gingivalis organisms were found in the HIV-1-positive individuals than in the otherwise healthy controls (35,36).…”

Section: Reactivation Of Latent Hiv-1 Infection By the Periodontopathmentioning

confidence: 94%

Reactivation of Latent HIV-1 Infection by the Periodontopathic Bacterium Porphyromonas gingivalis Involves Histone Modification

Imai

Ochiai

Okamoto

2009

The Journal of Immunology

121

139

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Latently infected cells harbor the HIV-1 proviral DNA genome primarily integrated into heterochromatin, allowing the persistence of transcriptionally silent proviruses. Hypoacetylation of histone proteins by histone deacetylases (HDAC) is involved in the maintenance of HIV-1 latency by repressing viral transcription. In addition, periodontal diseases, caused by polymicrobial subgingival bacteria including Porphyromonas gingivalis, are among the most prevalent infections of mankind. Here we demonstrate the effects of P. gingivalis on HIV-1 replication. This activity could be ascribable to the bacterial culture supernatant but not to other bacterial components such as fimbriae or LPS. We found that this HIV-1-inducing activity was recovered in the lower molecular mass (<3 kDa) fraction of the culture supernatant. We also demonstrated that P. gingivalis produces high concentrations of butyric acid, acting as a potent inhibitor of HDACs and causing histone acetylation. Chromatin immunoprecipitation assays revealed that the corepressor complex containing HDAC1 and AP-4 was dissociated from the HIV-1 long terminal repeat promoter upon stimulation with bacterial culture supernatant concomitantly with the association of acetylated histone and RNA polymerase II. We thus found that P. gingivalis could induce HIV-1 reactivation via chromatin modification and that butyric acid, one of the bacterial metabolites, is responsible for this effect. These results suggest that periodontal diseases could act as a risk factor for HIV-1 reactivation in infected individuals and might contribute to the systemic dissemination of the virus.

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“…(Zambon et al, 1990;Brady et al, 1996;Nakou et al, 1997;Tsang & Samaranayake, 2001;Teanpaisan et al, 2001). Other studies have shown a higher prevalence of putative periodontal pathogens such Treponema denticola, in HIV-positive patients, in comparison to HIVnegative patients, (Murray et al, 1989;Cross & Smith, 1995;Scully et al, 1999;Alpagot et al, 2004) Data from studies in the HAART era, which apply culture-independent molecular techniques are displayed in Table 3. These techniques as well as other approaches such as proteomics and the study of biofilms will allow an extensive investigation of the microbiota in HIV-infected individuals and the pathogenetic role of "unusual" species.…”

Section: )mentioning

confidence: 99%

HIV infection and periodontal diseases: an overview of the post-HAART era

2011

Br Dent J

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Periodontopathic Bacteria in English HIV-Seropositive Persons

Cited by 29 publications

References 32 publications

Inhibition of Human Immunodeficiency Virus Type 1 Entry by a Binding Domain of Porphyromonas gingivalis Gingipain

Inhibition of Human Immunodeficiency Virus Type 1 Entry by a Binding Domain of Porphyromonas gingivalis Gingipain

Reactivation of Latent HIV-1 Infection by the Periodontopathic Bacterium Porphyromonas gingivalis Involves Histone Modification

HIV infection and periodontal diseases: an overview of the post-HAART era

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