Diversity and uncommon HPV types in HIV seropositive and seronegative women attending an STI clinic

Mattos, Adriana Tonani de; Freitas, Luciana Bueno de; Lima, Bettina Moulin Coelho; Miranda, Angélica Espinosa; Spano, Liliana Cruz

doi:10.1590/s1517-83822011000200047

Cited by 11 publications

(11 citation statements)

References 35 publications

(43 reference statements)

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“…1). These studies were reported from Rwanda [36,37], Brazil [38][39][40], Nigeria [41,42] Thailand [43], South Africa [44][45][46][47], Zambia [48], Burkinafaso [35,49], Senegal [23] and Colombia [50,51]. There was one study conducted in two countries Burkinafaso and South Africa [52].…”

Section: Study Characteristicsmentioning

confidence: 99%

“…The maximum sample size was 1371 [44] and the minimum was 98 [41]. The age of participants ranged from 14 to 73 years [39,50]. Three studies didn't mention the upper age range of the participants [23,36,42] (Table 1).…”

Section: Study Characteristicsmentioning

confidence: 99%

“…The pooled prevalence of high risk HPV genotypes was also estimated in the studies (i.e. HPV genotypes 16,18,26,31,33,35,39,45,51,52,53,56,58,59, 66, 67, 68, 69, 70, 73, and 82). The highest prevalence was observed for genotype 16 (20%) followed by 18 (15%) and 52 (13%).…”

Section: Pooled Prevalence Of Hpvmentioning

confidence: 99%

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Molecular epidemiology of human papillomavirus among HIV infected women in developing countries: systematic review and meta-analysis

Bogale

Belay

Medhin

et al. 2020

Virol J

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Background Although, there is a variable burden of human papillomavirus (HPV) in women infected with HIV in developing countries, there are few studies that attempted to surmise such variable evidences. This review aimed to estimate the pooled prevalence of HPV genotype distribution and risk factors contributing to HPV infection among women infected with HIV in low- and middle-income countries. Methods We conducted a systematic review and meta-analysis of studies conducted in developing countries and reported HPV prevalence. We searched electronic databases: PubMed/Medline, SCOPUS, ScienceDirect, Excerpta Medical Database from Elsevier, Web of science, Cumulative Index of Nursing and allied Health Sciences and Google scholar databases to retrieve primary studies published in English language till 11th August 2019. We used random-effects model to estimate the pooled prevalence of HPV genotypes, and funnel plot to assess publication bias. The registration number of this review study protocol is CRD42019123549. Results We included nineteen studies with a total of 8,175 participants in this review. The prevalence of HPV was extremely heterogeneous across the studies (χ2= 3782.80, p value < 0.001, I2 = 99.6%). The estimated pooled prevalence of all HPV genotypes was 63.0% (95% CI: 48.0–78.0) while the pooled prevalence of high risk and low risk HPV genotypes were 51.0% (95% CI: 38.0–63.0) and 28.0% (95% CI: 12.0–43.0), respectively. The pooled prevalence of HPV genotype 16 was 20%, while genotype 18 and 52 were 15% and 13%, respectively. Different risk factors reported for HPV infection and the frequently reported were low CD4 count below 200 cells/mm3 and high HIV viral load. Conclusion The pooled prevalence of HPV among HIV infected women in low- and middle-income countries was considerable and the proportion of high risk HPV genotypes were high when compared with low risk genotypes. Therefore, it is essential for the HPV prevention program to prevent the double burden of HPV and HIV in women.

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Section: Study Characteristicsmentioning

confidence: 99%

Section: Study Characteristicsmentioning

confidence: 99%

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Molecular epidemiology of human papillomavirus among HIV infected women in developing countries: systematic review and meta-analysis

Bogale

Belay

Medhin

et al. 2020

Virol J

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“…Therefore, there is a continuing need for the identification of viral and host factors that modulate the risk of disease progression (11). Possible agents included Herpes viruses among which more recently Epstein-Barr Virus (EBV), have been suspected to participate in cervical carcinogenesis (15, 33, 31, 13). For example, latent infection with EBV has been shown to act as a carcinogenic cofactor in several epithelial cell malignancies (38).…”

Section: Introductionmentioning

confidence: 99%

Correlation between ebv co-infection and HPV16 genome integrity in Tunisian cervical cancer patients

Kahla¹,

Oueslati²,

Achour³

et al. 2012

Braz. J. Microbiol.

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Infection with high risk Human papillomavirus (HR-HPV) is necessary but not sufficient to cause cervical carcinoma. This study explored whether multiple HR-HPV or coinfection with Epstein-Barr virus (EBV) influence the integration status of HPV16 genome. The presence and typing of HPV in a series of 125 cervical specimens were assessed by polymerase chain reaction (PCR) using the specific primers for the HPV L1 region. As for EBV infection, the viral EBNA1 gene was used for its detection through PCR amplification. Disruption of the HPV E2 gene was assessed by amplification of the entire E2 gene with single set of primers, while E2 transcripts were evaluated by a reverse transcription PCR method (RT-PCR). The overall prevalence of HPVDNA was of 81.8% in cervical cancers versus 26.9% in benign lesions. In HPV positive cases, HPV16 and HPV18 were the most prevalent types, followed by HPV types 33, 31. EBV EBNA1 prevalence was statistically more frequent in cervical carcinomas than in benign lesions (29.5%, vs 9.6%; P=0.01). No viral infection was detected in healthy control women. The uninterrupted E2 gene was correlated with the presence of E2 transcripts originating from the HPV episomal forms. It was observed that integration was more common in HPV18 and EBV coinfection. The presence of EBV caused a five-fold [OR= 5; CI= 1.15-21.8; P = 0.04] increase in the risk of HPV16 genome integration in the host genome. This study indicates that EBV infection is acting as a cofactor for induction of cervical cancer by favoring HPVDNA integration.

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“…Genotypes 6 and 11, although common at anogenital sites, are considered to be low risk for development of carcinoma, as based on studies of cervical SCC . The prevalence of HPV 6 and/or 11 in the anal canal of men who have sex with men (MSM) has been shown to be 15% in HIV‐negative men and as high as 60% in HIV‐positive men, which is significantly higher than the prevalence observed in the female cervix of ∼10% in both HIV‐positive and ‐negative populations . Therefore, HPV 6 and/or 11 genotypes may be more likely to be present in anal and perianal SCC than in cervical SCC.…”

mentioning

confidence: 99%

Anal and perianal squamous carcinomas and high‐grade intraepithelial lesions exclusively associated with “low‐risk” HPV genotypes 6 and 11

Cornall

Roberts

Garland

et al. 2013

Intl Journal of Cancer

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Anal squamous cell carcinomas are predominantly associated with high-risk human papillomaviruses (HPVs), particularly HPV 16, similar to cervical, vaginal and vulvar cancers. Although the presence of "low-risk" HPVs, in particular genotypes 6 and 11, have occasionally been reported in various HPV-related anogenital cancers, the overall distribution of these genotypes in the anal canal and perianal tissue may differ to that in the cervix. In addition, although the majority of anal and perianal cancers are associated with HPV, some are not; hence, confirmation of direct association of the virus within a lesion is important. Using laser capture microdissection, anal and perianal invasive carcinomas and high-grade squamous intraepithelial lesions (HSILs) in biopsies previously associated with HPV 6 or 11 alone were isolated from tissue sections and HPV genotype tested. Of seven cases tested, four invasive carcinomas were positive for HPV 6 only, one invasive carcinoma was negative for HPV and two HSILs were positive for HPV 11 only. All samples were confirmed as HPV 16/18 negative using two different DNA targets (E6 and L1). From these results, we confirm that HPV 6 and 11 can occasionally be associated with high-grade lesion and anal cancer.The rate of anal squamous cell carcinoma (SCC) has been steadily increasing in Australia since the mid-1980s in both men and women, and 90% of cases are associated with human papillomavirus (HPV) infection.1 At greatest risk of developing anal SCC are sexually active homosexual men who demonstrate very high rates of HPV infection, HIV-positive individuals, women with previous HPV-related anogenital disease and solid-organ transplant recipients. 2,3A limited number of studies on HPV genotypes potentially associated with anal SCC in Australia 4 have shown similar results to studies conducted in Europe, Asia and the United States, 5-7 which indicate that 70-90% of intra-anal SCC in men are associated with "high-risk" HPV genotypes (HRHPV), predominantly HPV 16. The prevalence of "lowrisk" HPV (LRHPV) genotypes has also occasionally been reported. 6 A study of 110 Australian cases of anal SCC who underwent HPV genotyping (Hillman, personal communication) identified HPV 6 and/or 11 infections in the absence of other HPV genotypes in nine (8.5%) cases; significantly higher than estimates of up to 1% of cervical cancers associated only with HPV 6 or 11.8 Genotypes 6 and 11, although common at anogenital sites, 2 are considered to be low risk for development of carcinoma, as based on studies of cervical SCC. 8 The prevalence of HPV 6 and/or 11 in the anal canal of men who have sex with men (MSM) has been shown to

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Diversity and uncommon HPV types in HIV seropositive and seronegative women attending an STI clinic

Cited by 11 publications

References 35 publications

Molecular epidemiology of human papillomavirus among HIV infected women in developing countries: systematic review and meta-analysis

Molecular epidemiology of human papillomavirus among HIV infected women in developing countries: systematic review and meta-analysis

Correlation between ebv co-infection and HPV16 genome integrity in Tunisian cervical cancer patients

Anal and perianal squamous carcinomas and high‐grade intraepithelial lesions exclusively associated with “low‐risk” HPV genotypes 6 and 11

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