HIV-associated disruption of mucosal epithelium facilitates paracellular penetration by human papillomavirus

Tugizov, Sharof M.; Herrera, Rossana; Chin‐Hong, Peter; Veluppillai, Piri; Greenspan, Deborah; Berry, J. Michael; Pilcher, Christopher D.; Shiboski, Caroline H.; Jay, Naomi; Rubin, Mary; Chein, Aung; Palefsky, Joel M.

doi:10.1016/j.virol.2013.08.018

Cited by 100 publications

(122 citation statements)

References 86 publications

(165 reference statements)

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“…This study also supports a modest role for immunosuppression (low CD4 cell count) prior to cancer diagnosis. This supports evidence from other studies [7,31], that immunosuppression from HIV may impact the head and neck carcinogenesis process.…”

Section: Discussionsupporting

confidence: 92%

Incidence and risk factors of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma in HIV-infected individuals

et al. 2014

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Objectives To examine the risk and trends of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma (HNSCC) in HIV-infected individuals and assess whether immunosuppression (measured through CD4 cell count) and other risk factors impact HNSCC risk. Materials and methods Incident HNSCCs at HPV-related and HPV-unrelated anatomic sites were detected in HIV-infected participants from pooled data from 17 prospective studies in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) between 1996 and 2009. HNSCC cases were validated using chart review or cancer registry matching. Risk factors for incident HPV-related and HPV-unrelated HNSCC were explored using mixed effects Poisson regression in a full prospective analysis, and the effect of CD4 prior to cancer diagnosis was examined in a nested case control analysis. Results 66 HPV-related and 182 HPV-unrelated incident HNSCCs were detected among 82,375 HIV-infected participants. Standardized incidence ratios (SIRs) for both HPV-related (SIR = 3.2, 95%CI = 2.5–3.4) and HPV-unrelated (SIR = 3.0, 95%CI = 2.5–4.1) HNSCC were significantly elevated in HIV-infected individuals compared with the US general population. Between 1996 and 2009, the age-standardized HPV-related HNSCC incidence increased non-significantly from 6.8 to 11.4 per 100,000 person-years (p-trend = 0.31) while the age-standardized incidence of HPV-unrelated HNSCC decreased nonsignificantly from 41.9 to 29.3 per 100,000 person-years (p-trend = 0.16). Lower CD4 cell count prior to cancer diagnosis was significantly associated with increased HPV-related and HPV-unrelated HNSCC risk. Conclusion The standardized incidence of HPV-related and HPV-unrelated HNSCC are both elevated in HIV-infected individuals. Immunosuppression may have a role in the development of both HPV-related and HPV-unrelated HNSCC.

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Section: Discussionsupporting

confidence: 92%

Incidence and risk factors of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma in HIV-infected individuals

et al. 2014

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“…Polarized cells were established in 12-well Transwell two-chamber permeable filter inserts with 3-μm pore size, as described in our previous work (Tugizov et al, 2003, 2013a, 2013b, 2011; Yasen et al, 2017). The polarity of epithelial cells was verified by immunodetection of the tight junction protein ZO-1 and measurement of TER using a Millicell-ERS voltohmmeter, as described (Tugizov et al, 2003, 2013a, b, 2011).…”

Section: Methodsmentioning

confidence: 99%

“…The polarity of epithelial cells was verified by immunodetection of the tight junction protein ZO-1 and measurement of TER using a Millicell-ERS voltohmmeter, as described (Tugizov et al, 2003, 2013a, b, 2011). …”

Section: Methodsmentioning

confidence: 99%

HIV internalization into oral and genital epithelial cells by endocytosis and macropinocytosis leads to viral sequestration in the vesicles

et al. 2018

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Recently, we showed that HIV-1 is sequestered, i.e., trapped, in the intracellular vesicles of oral and genital epithelial cells. Here, we investigated the mechanisms of HIV-1 sequestration in vesicles of polarized tonsil, foreskin and cervical epithelial cells. HIV-1 internalization into epithelial cells is initiated by multiple entry pathways, including clathrin-, caveolin/lipid raft-associated endocytosis and macropinocytosis. Inhibition of HIV-1 attachment to galactosylceramide and heparan sulfate proteoglycans, and virus endocytosis and macropinocytosis reduced HIV-1 sequestration by 30–40%. T-cell immunoglobulin and mucin domain 1 (TIM-1) were expressed on the apical surface of polarized tonsil, cervical and foreskin epithelial cells. However, TIM-1-associated HIV-1 macropinocytosis and sequestration were detected mostly in tonsil epithelial cells. Sequestered HIV-1 was resistant to trypsin, pronase, and soluble CD4, indicating that the sequestered virus was intracellular. Inhibition of HIV-1 intraepithelial sequestration and elimination of vesicles containing virus in the mucosal epithelium may help in the prevention of HIV-1 mucosal transmission.

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“…ASCC commonly occurs at the transformation zone, where the squamous epithelium of the anal canal transitions in the columnar epithelium of the distal rectum 58. HIV might facilitate initial HPV infection through the disruption of epithelial tight junction 59. Decreased immunity due to HIV infection might hinder spontaneous HPV viral clearance, cause reactivation of latent HPV infection and/or result in faster progression to HPV-associated cancerous lesions 60.…”

Section: Introductionmentioning

confidence: 99%

Emerging viral STIs among HIV-positive men who have sex with men: the era of hepatitis C virus and human papillomavirus

Laar

Richel

2016

Sex Transm Infect

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The number of infectious disease outbreaks and the number of unique pathogens responsible have significantly increased since the 1980s. HIV-positive men who have sex with men (MSM) are a vulnerable population with regards to the introduction, spread and clinical consequences of (newly introduced) STIs. After the introduction of combination antiretroviral treatment (cART), the incidence of sexually acquired hepatitis C virus (HCV) infection and human papillomavirus (HPV)-induced anal cancers have significantly increased among HIV-positive MSM. The introduction and expansion of HCV is the result of increased sexual risk behaviour and sexually acquired mucosal trauma within large interconnected networks of HIV-positive MSM in particular. With the availability of cART, postexposure and pre-exposure prophylaxis (PEP and PrEP) and direct-acting antivirals (DAAs) for HCV, less concern for HIV and HCV might require a new approach to develop effective behavioural intervention strategies among MSM. The marked rise in HPV-induced anal cancers can be ascribed to the long-term immunologic defects in an ageing population affected by HIV. More evidence with regards to effective treatment options for anal dysplastic lesions and the usefulness of anal malignancy screening programmes is urgently needed. Most anal cancers in the future generation of HIV-positive MSM could be prevented with the inclusion of boys in addition to girls in current HPV vaccination programmes.

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HIV-associated disruption of mucosal epithelium facilitates paracellular penetration by human papillomavirus

Cited by 100 publications

References 86 publications

Incidence and risk factors of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma in HIV-infected individuals

Incidence and risk factors of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma in HIV-infected individuals

HIV internalization into oral and genital epithelial cells by endocytosis and macropinocytosis leads to viral sequestration in the vesicles

Emerging viral STIs among HIV-positive men who have sex with men: the era of hepatitis C virus and human papillomavirus

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