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Plausibility of HIV-1 Infection of Oral Mucosal Epithelial Cells

Advances in dental research, 2011-04, Vol.23 (1), p.38-44

2011 International & American Associations for Dental Research ;2011 International & American Associations for Dental Research 2011 International & American Associations for Dental Research ;ISSN: 0895-9374 ;EISSN: 1544-0737 ;DOI: 10.1177/0022034511399283 ;PMID: 21441479

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Title:
Plausibility of HIV-1 Infection of Oral Mucosal Epithelial Cells
Author: Herzberg, M.C. ; Vacharaksa, A. ; Gebhard, K.H. ; Giacaman, R.A. ; Ross, K.F.
Challacombe, Stephen J ; Xu, Tao ; Coogan, Maeve M ; Yu, Guang-yan ; Greenspan, John
Subjects: Animals ; Dendritic Cells - virology ; Dentistry ; HIV Infections - physiopathology ; HIV-1 - physiology ; Humans ; Immunity, Mucosal ; Keratinocytes - virology ; Mouth Mucosa - cytology ; Mouth Mucosa - virology ; Porphyromonas gingivalis - physiology ; Receptors, CCR5 - physiology ; Receptors, CXCR - physiology ; Superinfection - physiopathology ; Urogenital System - virology ; Virus Internalization ; Virus Latency ; Virus Replication
Is Part Of: Advances in dental research, 2011-04, Vol.23 (1), p.38-44
Description: 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.
Publisher: Los Angeles, CA: SAGE Publications
Language: English
Identifier: ISSN: 0895-9374
EISSN: 1544-0737
DOI: 10.1177/0022034511399283
PMID: 21441479
Source: MEDLINE
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Plausibility of HIV-1 Infection of Oral Mucosal Epithelial Cells

2011 International & American Associations for Dental Research ;2011 International & American Associations for Dental Research 2011 International & American Associations for Dental Research ;ISSN: 0895-9374 ;EISSN: 1544-0737 ;DOI: 10.1177/0022034511399283 ;PMID: 21441479

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