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

Giacaman RA; Asrani, AC; Gebhard, KH; Dietrich, EA; Vacharaksa, A; Ross, KF; Herzberg, MC

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. © 2008 Giacaman et al; licensee BioMed Central Ltd.

Más información

Título de la Revista: Retrovirology
Volumen: 5
Editorial: Springer Nature
Fecha de publicación: 2008-01-01
Idioma: English
DOI/URL:

10.1186/1742-4690-5-29

Identificador: 10.1186/1742-4690-5-29
Notas: ISI, SCOPUS