Risk Factors for Oral Human Papillomavirus in Adults Infected and Not Infected With Human Immunodeficiency Virus

Coutlée, François; Trottier, Anne-Marie; Ghattas, Georges; Leduc, Raymond; Toma, Emil; Sanche, Gilbert; Rodrigues, Isabel; Turmel, Bruno; Allaire, Guy; Ghadirian, Parvis

doi:10.1097/00007435-199701000-00006

Cited by 95 publications

(84 citation statements)

References 40 publications

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“…8,9 This data is also consistent with prior longitudinal studies that attributed the elevated prevalence of cervical HPV infection among HIV-infected women to both an increased risk of incident and persistent infection as severity of immunosuppression increased. 10,[18][19][20][21][22][23][24][25] Strickler and colleagues recently reported a strong interaction between serum HIV viral load and CD4 cell count on cervical HPV natural history in the WIHS study cohort. 24 Because of sample size constraints, a larger study will be needed to evaluate the interaction of HIV viral load and CD4 cell count on oral HPV natural history.…”

Section: Discussionmentioning

confidence: 99%

“…Tobacco-related immune dysfunction might facilitate an incident HPV infection among exposed individuals, impede the ability to clear an infection, or facilitate reactivation of a latent infection. Tobacco smoking has been inconsistently associated with cervical HPV infection prevalence 10,[29][30][31] and clearance. 10,32 Highly active antiretroviral therapy (HAART) was surprisingly associated with increased risk of oral HPV infection persistence.…”

Section: Discussionmentioning

confidence: 99%

“…Tobacco smoking has been inconsistently associated with cervical HPV infection prevalence 10,[29][30][31] and clearance. 10,32 Highly active antiretroviral therapy (HAART) was surprisingly associated with increased risk of oral HPV infection persistence. Confounding by indication is unlikely to entirely account for this finding, because HAART therapy remained associated with risk of persistence even after adjustment for current or nadir CD4 cell count, HIV viral load, or time on HAART therapy.…”

Section: Discussionmentioning

confidence: 99%

“…7 These methods were applied to a well-studied, longitudinal cohort of HIV-positive and at-risk HIV-negative individuals, the Women's Interagency HIV Study (WIHS), 8 chosen because of the high risk for oral HPV infection previously reported among individuals with HIV infection. 9,10 This is the first study to estimate incidence rates for oral HPV infection, to evaluate factors that influence infection persistence, and to compare these measures to those for cervical infection. A concurrent comparison of the natural history of oral to cervical HPV infection allowed for the investigation of potential differences at the 2 sites, while minimizing the possibility that observed differences would be attributed entirely to study population or laboratory methodology.…”

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confidence: 99%

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Six‐month natural history of oral versus cervical human papillomavirus infection

D’Souza

Fakhry

Sugar

et al. 2007

Intl Journal of Cancer

157

138

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Human papillomavirus (HPV) infection is etiologically associated with a subset of oral cancers, and yet, the natural history of oral HPV infection remains unexplored. The feasibility of studying oral HPV natural history was evaluated by collecting oral rinse samples on 2 occasions at a 6-month interval from 136 HIV-positive and 63 HIV-negative participants. Cervical vaginal lavage samples were concurrently collected for comparison. HPV genomic DNA was detected in oral and cervical samples by consensus primer PCR and type-specified for 37 HPV types. The sixmonth cumulative prevalence of oral HPV infection was significantly less than for cervical infection (p < 0.0001). HIV-positive women were more likely than HIV-negative women to have an oral (33 vs. 15%, p 5 0.016) or cervical (78 vs. 51%, p < 0.001) infection detected. Oral HPV infections detected at baseline were as likely as cervical infections to persist to 6 months among HIVnegative (60% vs. 51%, p 5 0.70) and HIV-positive (55% vs. 63%, p 5 0.27) women. Factors that independently elevated odds for oral HPV persistence differed from cervical infection and included current smoking (OR 5 8, 95% CI 5 1.3-53), age above 44 years (OR 5 20, 95% CI 5 4.1-83), CD4 < 500 (OR 5 6, 95% CI 5 1.1-26), use of HAART therapy (OR 5 12, 95% CI 5 1.0-156), and time on HAART therapy (trend p 5 0.04). The rate of oral HPV infections newly detected at follow-up was significantly lower than cervical infection among HIV-positive (p < 0.001) and HIV-negative women (p < 0.001). Our study not only demonstrates that it is feasible to study the natural history of oral HPV infection with oral rinse sampling, but also indicates that oral and cervical HPV natural history may differ. ' 2007 Wiley-Liss, Inc.Key words: oral; HPV; natural history; comparison; cervical; human papillomavirus; infectionThe majority of oral cancers are attributable to alcohol and tobacco use, however a subset are etiologically associated with human papillomavirus (HPV) infection.1 Case-control studies have shown that oral HPV infection elevates risk of oral cancer, 2,3 and therefore is likely a prerequisite for cancer development. Although natural history studies of oral infection are yet to be performed, seropositivity to HPV16 increases risk for incident oral cancer, supporting a temporal association between infection and cancer risk. While the natural history of cervical HPV infection is well studied, it is unclear whether it is appropriate to extrapolate data from the cervical literature to oral HPV infection. Unfortunately, 2 studies with consecutive measures of oral HPV infection provide limited insight into its natural history. One study evaluated persistence of oral HPV infection at baseline and a subsequent two and a half year time-point among only 4 subjects. 5 In a study of husband-wife pairs, only overall HPV infection status was considered.6 Because analysis of type-specific HPV infection was not performed, meaningful estimates of incidence and clearance could not be obtained. Our study was designed ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Six‐month natural history of oral versus cervical human papillomavirus infection

D’Souza

Fakhry

Sugar

et al. 2007

Intl Journal of Cancer

157

138

View full text Add to dashboard Cite

show abstract

“…40 One study, for example, demonstrates that HIV-seropositive individuals have a significantly increased risk of contracting oncogenic oral human papillomavirus through unprotected oral sex. 74 Prevention of STDs, which are more prevalent than HIV, remains an extremely important public health concern that health care professionals can address directly with patients.…”

Section: Discussionmentioning

confidence: 99%

Counseling patients about HIV risk from oral sex

1997

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nprotected oral sex is not well recognized as a risk factor for transmitting the human immunodeficiency virus, yet as evidence of its potential risk accrues, physicians must confront the question of how to counsel patients about oral sex risk. How do health care professionals feel about broaching this topic with their patients? Can the psychological literature help physicians understand their patients' risk perceptions and motivate healthful behaviors? In this article, we review the literature on oral sex risk, discuss barriers to communicating caution to patients, and propose recommendations and specific counseling strategies based on risk perception and behavior change theory that we believe will help physicians effectively intervene in the prevention of HIV transmission. REVIEW OF THE LITERATURESince the advent of the AIDS epidemic, researchers have sought to define categories of risk for transmission of HIV in sexual behavior. Although receptive anal and vaginal intercourse have been clearly classified as the highest-risk behaviors, and kissing and masturbation as behaviors with the lowest risk, 1 the level of risk for oral sex remains a matter of debate. A variety of research methods-human and animal, epidemiologic studies and case reports, in vitro and in vivo-have yielded a growing literature addressing the question of oral sex risk. The comparative riskiness of oral sex in epidemiologic studies attempting to relate behavior to HIV seroconversion has been difficult to assess. These studies attempt the nearimpossible task of isolating specific sexual practices in research subjects, who usually engage in more than one type of risk behavior, and rely on retrospective self-report data, which can involve recall bias and responses tainted by social desirability (for commentary on problems in sexual behavior research, see R. C. Lewontin, Sex, lies and social science, The New York Review , April 20, 1995:24-9).Subsamples of subjects engaging only in oral sex are likely to be too small to provide adequate statistical power to assess the relative risk. 2,3 Some investigators have asked subjects only about oral sex practices or have lumped oral sex together with other behaviors. 4 In addition, a myriad of uncontrolled factors-dates of infection, number of oral sex events, whether or not oral cuts or abrasions were present-prevent the clear quantification of risk. Most of these epidemiologic studies have sampled homosexual or bisexual men exclusively; accordingly, even less is known about the relative risk of oral sex in the context of lesbian or heterosexual practices.Results from epidemiologic studies have generally been interpreted as evidence against oral sex risk, relative to other behaviors. 3,[5][6][7][8] These studies are based on retrospective self-report data from questionnaires or interviews about risk behaviors over a previous time period, and are also longitudinal in that they follow initially HIV-negative men and test these men over time to see whether or not they undergo seroconversion. Laboratory stud...

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Transmission and clearance of human papillomavirus infection in the oral cavity and its role in oropharyngeal carcinoma – A review

Wierzbicka

Giorgi

Dikkers

2022

Reviews in Medical Virology

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The majority of sexually active individuals becomes infected with human papillomavirus (HPV) at least once in their lifetime. Pathways for HPV transmission vary across different mucosal sites per individual. They include autoinoculation within one host, direct transmission between individuals (including perinatal transmission and transmission during sexual activity), and indirect transmission through contact with hands. The authors aim to clarify the prevalence and route of transmission per anatomic site, inter-and intra-individually, using a narrative review of the literature.In conclusion, transmission of HPV to the oral cavity and oropharynx is hypothesised to occur mainly through sexual contact. Transmission of particles through saliva has not been proven and daily living activities are not a documented source of HPV infection. Oropharyngeal HPV related cancer survivors and their partners do not show increased risk of infection during sexual intercourse. Transmission of HPV to the oral cavity (autoinoculation with fingers or transmission through saliva in deep kissing) is probably of limited importance. K E Y W O R D S extragenital → extragenital, extragenital → genital, genital → extragenital, genital → genital, human papilloma virus, mucosal squamous cell carcinomas, orogenital transmission concerns 1 | INTRODUCTION This article will review the known pathways of transmission and clearance of oral human papilloma virus (HPV) infection. The problem of orogenital transmission concerns very sensitive personal spheres of life and is therefore often unexplored in literature. Furthermore, the literature data on the upper airway clearance mechanisms are still scarce and scattered. In this article we describe the risk of HPV transmission to the oropharynx per pathway (autoinoculation, perinatal transmission, inter-site transmission between individuals) as well as the prevalence of simultaneous occurrence of the same type of HPV in different anatomical sites in sexual partners (concordance).A significant proportion of mucosal squamous cell carcinomas of the head and neck, particularly of the oropharynx, are directly attributable to the HPV. 1,2 HPV infection is considered the most common sexually transmitted disease among both males and Abbreviations: DNA, deoxyribonucleic acid; HIV, human immunodeficiency virus; HPV, human papilloma virus; HPV-OPC, human papilloma virus associated oropharyngeal carcinoma; HR-HPV, high-risk human papilloma virus; LR-HPV, low-risk human papilloma virus; MHC, major histocompatibility complex; MMP-8, matrix metallo-proteinase-8; OPC, oropharyngeal carcinoma; RRP, recurrent respiratory papilloma.

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Risk Factors for Oral Human Papillomavirus in Adults Infected and Not Infected With Human Immunodeficiency Virus

Cited by 95 publications

References 40 publications

Six‐month natural history of oral versus cervical human papillomavirus infection

Six‐month natural history of oral versus cervical human papillomavirus infection

Counseling patients about HIV risk from oral sex

Transmission and clearance of human papillomavirus infection in the oral cavity and its role in oropharyngeal carcinoma – A review

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