title: Plausibility of HIV-1 Infection of Oral Mucosal Epithelial Cells.
abstract: The AIDS pandemic continues. Little is understood about how HIV gains access to permissive cells across mucosal surfaces, yet such knowledge is crucial to the development of successful topical anti-HIV-1 agents and mucosal vaccines. HIV-1 rapidly internalizes and integrates into the mucosal keratinocyte genome, and integrated copies of HIV-1 persist upon cell passage. The virus does not appear to replicate, and the infection may become latent. Interactions between HIV-1 and oral keratinocytes have been modeled in the context of key environmental factors, including putative copathogens and saliva. In keratinocytes, HIV-1 internalizes within minutes; in saliva, an infectious fraction escapes inactivation and is harbored and transferable to permissive target cells for up to 48 hours. When incubated with the common oral pathogen Porphyromonas gingivalis, CCR5- oral keratinocytes signal through protease-activated receptors and Toll-like receptors to induce expression of CCR5, which increases selective uptake of infectious R5-tropic HIV-1 into oral keratinocytes and transfer to permissive cells. Hence, oral keratinocytes-like squamous keratinocytes of other tissues-may be targets for low-level HIV-1 internalization and subsequent dissemination by transfer to permissive cells.
authors: Department of Diagnostic and Biological Sciences, School of Dentistry, University of Minnesota, Minneapolis, Minnesota, USA. mcherzb@umn.edu
authors: M C
authors: MC
authors: Herzberg
authors: A
authors: A
authors: Vacharaksa
authors: K H
authors: KH
authors: Gebhard
authors: R A
authors: RA
authors: Giacaman
authors: K F
authors: KF
authors: Ross
mesh_terms: D000818:Animals; D003713:Dendritic Cells / Q000821:virology; D015658:HIV Infections / Q000503:physiopathology*; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D018928:Immunity, Mucosal; D015603:Keratinocytes / Q000821:virology*; D009061:Mouth Mucosa / Q000166:cytology / Q000821:virology*; D016966:Porphyromonas gingivalis / Q000502:physiology; D019713:Receptors, CCR5 / Q000502:physiology; D054387:Receptors, CXCR / Q000502:physiology; D015163:Superinfection / Q000503:physiopathology; D014566:Urogenital System / Q000821:virology; D053586:Virus Internalization; D017735:Virus Latency; D014779:Virus Replication
chemical_list: D019713:Receptors, CCR5; D054387:Receptors, CXCR