Periodontal pathogens in subgingival plaque of HIV‐positive subjects with chronic periodontitis

Patel, Michele; Coogan, Maeve M.; Galpin, Jacqueline S.

doi:10.1034/j.1399-302x.2003.00064.x

Cited by 41 publications

(56 citation statements)

References 20 publications

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“…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. Thus, it is possible that P. gingivalis and HIV infections might coexist in the oral cavity, especially in HIV-positive periodontitis patients.…”

Section: Discussionmentioning

confidence: 41%

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: 41%

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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“…It has been suggested that the loss of CD4+ T-lymphocytes and subsequent immunosuppression in HIV-infected individuals could compromise normal mucosal responses to oral microorganisms, resulting in an elevated colonization of cariogenic and periodontal pathogens or an alteration of the oral microbial community (Patel et al, 2003;Gonçalves et al, 2004Gonçalves et al, , 2007Aas et al, 2007;Saxena et al, 2012). Those changes could be contributing factors for the development of HIV-associated oral diseases, including increased prevalence of dental caries.…”

Section: Discussionmentioning

confidence: 99%

HIV Infection Affects Streptococcus mutans Levels, but Not Genotypes

et al. 2012

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We report a clinical study that examines whether HIV infection affects Streptococcus mutans colonization in the oral cavity. Whole stimulated saliva samples were collected from 46 HIV-seropositive individuals and 69 HIV-seronegative control individuals. The level of S. mutans colonization was determined by conventional culture methods. The genotype of S. mutans was compared between 10 HIV-positive individuals before and after highly active antiretroviral therapy (HAART) and 10 non-HIV-infected control individuals. The results were analyzed against viral load, CD4+ and CD8+ T-cell counts, salivary flow rate, and caries status. We observed that S. mutans levels were higher in HIV-infected individuals than in the non-HIV-infected control individuals (p = 0.013). No significant differences in S. mutans genotypes were found between the two groups over the six-month study period, even after HAART. There was a bivariate linear relationship between S. mutans levels and CD8+ counts ( r = 0.412; p = 0.007), but not between S. mutans levels and either CD4+ counts or viral load. Furthermore, compared with non-HIV-infected control individuals, HIV-infected individuals experienced lower salivary secretion (p = 0.009) and a positive trend toward more decayed tooth surfaces (p = 0.027). These findings suggest that HIV infection can have a significant effect on the level of S. mutans, but not genotypes.

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“…HIV-positive individuals are at greater risk of dental caries and periodontal diseases than are HIV-negative individuals (71)(72)(73). The increased risk may be caused by depletion of CD4 ϩ and CD8 ϩ lymphocytes and resultant decreased host immune responses (16,74), increased S. mutans colonization (16), reduced salivary secretion (75,76), and/or poor oral hygiene (77).…”

Section: Discussionmentioning

confidence: 99%

HIV Infection and Microbial Diversity in Saliva

et al. 2014

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f Limited information is available about the effects of HIV and subsequent antiretroviral treatment on host-microbe interactions. This study aimed to determine the salivary microbial composition for 10 HIV-seropositive subjects, before and 6 months after highly active antiretroviral therapy (HAART), compared with that for 10 HIV-seronegative subjects. A conventional culture and two culture-independent analyses were used and consistently demonstrated differences in microbial composition among the three sets of samples. HIV-positive subjects had higher levels of total cultivable microbes, including oral streptococci, lactobacilli, Streptococcus mutans, and Candida, in saliva than did HIV-negative subjects. The total cultivable microbial levels were significantly correlated with CD4 ؉ T cell counts. Denaturing gradient gel electrophoresis (DGGE), which compared the overall microbial profiles, showed distinct fingerprinting profiles for each group. The human oral microbe identification microarray (HOMIM) assay, which compared the 16S rRNA genes, showed clear separation among the three sample groups. Veillonella, Synergistetes, and Streptococcus were present in all 30 saliva samples. Only minor changes or no changes in the prevalence of Neisseria, Haemophilus, Gemella, Leptotrichia, Solobacterium, Parvimonas, and Rothia were observed. Seven genera, Capnocytophaga, Slackia, Porphyromonas, Kingella, Peptostreptococcaceae, Lactobacillus, and Atopobium, were detected only in HIVnegative samples. The prevalences of Fusobacterium, Campylobacter, Prevotella, Capnocytophaga, Selenomonas, Actinomyces, Granulicatella, and Atopobium were increased after HAART. In contrast, the prevalence of Aggregatibacter was significantly decreased after HAART. The findings of this study suggest that HIV infection and HAART can have significant effects on salivary microbial colonization and composition.

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Periodontal pathogens in subgingival plaque of HIV‐positive subjects with chronic periodontitis

Cited by 41 publications

References 20 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

HIV Infection Affects Streptococcus mutans Levels, but Not Genotypes

HIV Infection and Microbial Diversity in Saliva

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