Detection of HIV in oral mucosal cells

Qureshi, M N; Ce, Barr; Hewlitt, I; Boorstein, Robert J.; Kong, Fanrong; Bagasra, Omar; Bobroski, Lisa; Joshi, Bharat

doi:10.1111/j.1601-0825.1997.tb00380.x

Cited by 43 publications

(43 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The virus was localized in the interepithelial space bound by tight junctions, suggesting epithelial cell to epithelial cell contact as a route of transmission of HIV in mucosal linings. Consistent with this hypothesis, Qureshi et al (32) reported histological studies of primary tissue samples indicating that epithelial cells were infected at the basal layer, migrated toward the superficial layers, and were then sloughed off into the oral cavity. Such results are consistent with in vitro data showing that epithelial cell lines can be productively infected with HIV-1 (9,31,43).…”

supporting

confidence: 53%

“…Studies of clinical specimens have identified HIV DNA and RNA in oral epithelial cells obtained from saliva (33). In mucosal tissue biopsies from HIV-infected patients, HIV-positive lymphocytes were localized in both submucosal and mucosal layers in the vicinity of epithelial cells bearing HIV-1 DNA sequences (32). By electron microscopy, HIV was detected in two-thirds of the buccal mucosal scrapings obtained from HIVseropositive patients.…”

mentioning

confidence: 98%

See 1 more Smart Citation

Human Immunodeficiency Virus Type 1 Infection and Replication in Normal Human Oral Keratinocytes

Li¹,

Zha

Chen³

et al. 2003

J Virol

View full text Add to dashboard Cite

Recent epidemiologic studies show increasing human immunodeficiency virus type 1 (HIV-1) transmission through oral-genital contact. This paper examines the possibility that normal human oral keratinocytes (NHOKs) might be directly infected by HIV or might convey infectious HIV virions to adjacent leukocytes. PCR analysis of proviral DNA constructs showed that NHOKs can be infected by CXCR4-tropic (NL4-3 and ELI) and dualtropic (89.6) strains of HIV-1 to generate a weak but productive infection. CCR5-tropic strain Ba-L sustained minimal viral replication. Antibody inhibition studies showed that infection by CXCR4-tropic viral strains is mediated by the galactosylceramide receptor and the CXCR4 chemokine coreceptor. Coculture studies showed that infectious HIV-1 virions can also be conveyed from NHOKs to activated peripheral blood lymphocytes, suggesting a potential role of oral epithelial cells in the transmission of HIV infection.

show abstract

supporting

confidence: 53%

mentioning

confidence: 98%

Human Immunodeficiency Virus Type 1 Infection and Replication in Normal Human Oral Keratinocytes

Li¹,

Zha

Chen³

et al. 2003

J Virol

View full text Add to dashboard Cite

show abstract

“…In studies in which HIV-infected cells were detected at the lymphoepithelial interface of the tonsil and adenoids, most of the virusbearing cells were colabeled for viral RNA and S100, a DC marker (29,68). In buccal biopsy samples from HIV-infected individuals, provirus was identified in lymphocytes, LC, and epithelial cells (66). As early as 3 days after application of SIV to macaque tonsillar mucosa, rare SIV-infected CD4 ϩ T cells abutting the antigen-transporting epithelium of the tonsillar crypts were identified (76).…”

Section: Vaginal Transmission (I) Tsa-ish Fiv Rna Was Detected In Cmentioning

confidence: 99%

Early Pathogenesis of Transmucosal Feline Immunodeficiency Virus Infection

Obert

Hoover

2002

J Virol

View full text Add to dashboard Cite

To identify the early target cells and tissues in transmucosal feline immunodeficiency virus (FIV) infection, cats were exposed to a clade C FIV isolate via the oral-nasal or vaginal mucosa and multiple tissues were examined by virus isolation coculture (VI), DNA PCR, catalyzed tyramide signal-amplified in situ hybridization (TSA-ISH), and immunohistochemistry between days 1 and 12 postinoculation (p.i.). FIV RNA was detected in tonsil and oral or vaginal mucosa as early as 1 day p.i. by TSA-ISH and in retropharyngeal, tracheobronchial, or external iliac lymph nodes and sometimes in spleen or blood mononuclear cells by day 2, indicating that regional and distant spread of virus-infected cells occurred rapidly after mucosal exposure. By day 8, viral RNA, DNA, and culturable virus were uniformly detected in regional and distant tissues, connoting systemic infection. TSA-ISH proved more sensitive than DNA PCR in detecting early FIV-infected cells. In mucosal tissues, the earliest demonstrable FIV-bearing cells were either within or subjacent to the mucosal epithelium or were in germinal centers of regional lymph nodes. The FIV ؉ cells were of either of two morphological types, large stellate or small round. Those FIV RNA ؉ cells which could be colabeled for a phenotype marker, were labeled for either dendritic-cell-associated protein p55 or T-lymphocyte receptor antigen CD3. These studies indicate that FIV crosses mucous membranes within hours after exposure and rapidly traffics via dendritic and T cells to systemic lymphoid tissues, a pathway similar to that thought to occur in the initial phase of infection by the human and simian immunodeficiency viruses.

show abstract

“…Therefore, there is no evidence of appreciable changes in levels of Candida-specific Oral epithelial keratinocytes play a critical role in the pathogenesis of OPC because of their close interaction with C. albicans in the superficial epithelium. Because oral epithelial keratinocytes from HIV-infected patients contain integrated HIV proviral DNA and HIV Tat/Rev RNA (347,348), possibly acquired through contact with submucosal HIV-positive lymphocytes and/or Langerhans' cells, the anticandidal properties of these cells could be potentially impaired. However, although HIV-positive patients with OPC had a significant decrease in oral epithelial cell-mediated growth inhibition of C. albicans in vitro compared to those without OPC, there was no difference in epithelial cell activity between HIV-noninfected and -infected persons without OPC (411).…”

Section: Perturbed Mucosal Immune Defense Mechanisms Against C Albicmentioning

confidence: 99%

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

2004

View full text Add to dashboard Cite

Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal

show abstract

Detection of HIV in oral mucosal cells

Cited by 43 publications

References 31 publications

Human Immunodeficiency Virus Type 1 Infection and Replication in Normal Human Oral Keratinocytes

Human Immunodeficiency Virus Type 1 Infection and Replication in Normal Human Oral Keratinocytes

Early Pathogenesis of Transmucosal Feline Immunodeficiency Virus Infection

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Contact Info

Product

Resources

About