Porphyromonas gingivalis induces CCR5-dependent transfer of infectious HIV-1 from oral keratinocytes to permissive cells

Rodrigo A. Giacaman, Anil C. Asrani, Kristin H. Gebhard, Elizabeth A. Dietrich, Anjalee Vacharaksa, Karen F. Ross, Mark C. Herzberg

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27 Scopus citations

Abstract

Background: Systemic 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. Results: Oral 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. Conclusion: P. 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.

Original languageEnglish (US)
Article number29
JournalRetrovirology
Volume5
DOIs
StatePublished - Mar 27 2008

Bibliographical note

Funding Information:
These studies were supported by NIH grants-in-aid DE015503 (to MCH), DE15506 (KFR), the Veterans Affairs Research Service, and the Mucosal and Vaccine Research Center. The expert technical support and advice of Claudine Fasching is greatly appreciated. This manuscript was submitted in partial fulfillment of the requirements for the PhD degree by RAG.

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