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Anal and oral human papillomavirus (HPV) infection in HIV-infected subjects in northern Italy: a longitudinal cohort study among men who have sex with men.

Parisi SG, Cruciani M, Scaggiante R, Boldrin C, Andreis S, Dal Bello F, Pagni S, Barelli A, Sattin A, Mengoli C, Palù G - BMC Infect. Dis. (2011)

Bottom Line: The overall prevalence of HPV did not vary significantly between the baseline and the follow-up, either in the oral (20.1 and 21.3%, respectively) or the anal specimens (88.6 and 86.3%).A significant correlation was found between the persistence of HHV-8 shedding and HIV viral load by logistic bivariate analysis (Odds Ratio of HHV-8 persistence for 1-log increase of HIV viral load = 1.725 ± 0.397, p = 0.018).A high prevalence of HPV infection was found in our cohort of HIV-infected MSM, with a negative correlation between anal HPV infection and CD4 cell count.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Histology, Microbiology and Medical Biotechnology, Padua University, Via Gabelli 63, 35100 Padova, Italy. saverio.parisi@unipd.it

ABSTRACT

Background: A study including 166 subjects was performed to investigate the frequency and persistence over a 6-month interval of concurrent oral and anal Human Papillomavirus (HPV) infections in Human Immunodeficiency Virus (HIV)-infected men who have sex with men (MSM).

Methods: Patients with no previously documented HPV-related anogenital lesion/disease were recruited to participate in a longitudinal study. Polymerase chain reaction (PCR) was performed to detect HPV from oral and anal swabs and to detect Human Herpes Virus 8 (HHV-8) DNA in saliva on 2 separate specimen series, one collected at baseline and the other collected 6 months later. A multivariate logistic analysis was performed using anal HPV infection as the dependent variable versus a set of covariates: age, HIV plasma viral load, CD4+ count, hepatitis B virus (HBV) serology, hepatitis C virus (HCV) serology, syphilis serology and HHV-8 viral shedding. A stepwise elimination of covariates with a p-value > 0.1 was performed.

Results: The overall prevalence of HPV did not vary significantly between the baseline and the follow-up, either in the oral (20.1 and 21.3%, respectively) or the anal specimens (88.6 and 86.3%). The prevalence of high-risk (HR) genotypes among the HPV-positive specimens was similar in the oral and anal infections (mean values 24.3% and 20.9%). Among 68 patients with either a HR, low-risk (LR) or undetermined genotype at baseline, 75% had persistent HPV and the persistence rates were 71.4% in HR infections and 76.7% in LR infections. There was a lack of genotype concordance between oral and anal HPV samples. The prevalence of HR HPV in anus appeared to be higher in the younger patients, peaking (> 25%) in the 43-50 years age group. A decrease of the high level of anal prevalence of all genotypes of HPV in the patients > 50 years was evident. HHV-8 oral shedding was positively related to HPV anal infection (p = 0.0046). A significant correlation was found between the persistence of HHV-8 shedding and HIV viral load by logistic bivariate analysis (Odds Ratio of HHV-8 persistence for 1-log increase of HIV viral load = 1.725 ± 0.397, p = 0.018).

Conclusions: A high prevalence of HPV infection was found in our cohort of HIV-infected MSM, with a negative correlation between anal HPV infection and CD4 cell count.

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HPV genotype distribution of all oral and anal infections detected among paired oral and anal swabs. A: HPV genotype distribution at baseline; B: HPV genotype distribution in subsequent specimens (6 months after study entry). n.t.: non-typeable HPV strains. The genotype is indicated on the abscissa. Genotypes 10, 32, 34, 38, 90, (anal swabs) and 10, 97 (oral swabs) are of undefined oncogenic risk; genotypes 6, 11, 40, 53, 54, 61, 62, 66, 70, 71, 72, 81, 83, 84 (anal swabs) and 6, 66, 81 (oral swabs) are low-risk; genotypes 16, 18, 33, 35, 58 (anal swabs) and 16, 18, 33, 35, 56, 58, 73 (oral swabs) are high-risk.
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Figure 1: HPV genotype distribution of all oral and anal infections detected among paired oral and anal swabs. A: HPV genotype distribution at baseline; B: HPV genotype distribution in subsequent specimens (6 months after study entry). n.t.: non-typeable HPV strains. The genotype is indicated on the abscissa. Genotypes 10, 32, 34, 38, 90, (anal swabs) and 10, 97 (oral swabs) are of undefined oncogenic risk; genotypes 6, 11, 40, 53, 54, 61, 62, 66, 70, 71, 72, 81, 83, 84 (anal swabs) and 6, 66, 81 (oral swabs) are low-risk; genotypes 16, 18, 33, 35, 58 (anal swabs) and 16, 18, 33, 35, 56, 58, 73 (oral swabs) are high-risk.

Mentions: A total of 166 men were enrolled in this study. The characteristics of the study population are listed in Table 1. Paired concurrent anal and oral swabs were collected from all 166 of the patients at baseline. There were 49 withdrawals from the study, meaning that specimens at the 6 month follow-up were available from only 117 patients. Moreover, 41 oral swabs (thirty-two at baseline: 19%, nine at follow-up: 7.7%) were not able to be evaluated by PCR due to inadequate sampling revealed by the inability to detect beta-globin in the DNA sample. All anal swabs were adequate for sampling. Therefore, 283 anal swabs and 242 oral swabs were available for analysis. The HPV detection in oral and anal swabs is indicated in Table 2. The overall prevalence of HPV did not vary significantly between the baseline and follow-up time points and was 20.1 vs. 21.3% in oral specimens ((p-value = 0.8266) and 88.6 vs. 86.3% in anal specimens (p-value = 0.5748). The prevalence of HR genotypes among HPV-positive specimens was similar in oral and anal infections (mean values 24.3% and 20.9%, p-value = 0.6417). Among the 68 patients with HR, LR, or undetermined genotypes at the baseline in their anus who provided two consecutive anal samples, 75% (51/68) had persistent HPV six months after enrolment. Persistence rates of 71.4% (10/14) in patients with high-risk infections and 76.7% (33/43) in patients with low-risk infections were found. Rates of persistence of HPV according to the level of risk associated with the HPV genotype are shown in Table 3. The HPV genotype distribution in oral and anal swabs is depicted in Figure 1. There was no genotype concordance between oral and anal HPV types, with the exception of non-typeable strains in 3 paired oral and anal swabs (in a single patient at baseline and in two patients at follow-up). Genotype identification was not performed when multiple co-infecting HPV strains were obtained (Table 2).


Anal and oral human papillomavirus (HPV) infection in HIV-infected subjects in northern Italy: a longitudinal cohort study among men who have sex with men.

Parisi SG, Cruciani M, Scaggiante R, Boldrin C, Andreis S, Dal Bello F, Pagni S, Barelli A, Sattin A, Mengoli C, Palù G - BMC Infect. Dis. (2011)

HPV genotype distribution of all oral and anal infections detected among paired oral and anal swabs. A: HPV genotype distribution at baseline; B: HPV genotype distribution in subsequent specimens (6 months after study entry). n.t.: non-typeable HPV strains. The genotype is indicated on the abscissa. Genotypes 10, 32, 34, 38, 90, (anal swabs) and 10, 97 (oral swabs) are of undefined oncogenic risk; genotypes 6, 11, 40, 53, 54, 61, 62, 66, 70, 71, 72, 81, 83, 84 (anal swabs) and 6, 66, 81 (oral swabs) are low-risk; genotypes 16, 18, 33, 35, 58 (anal swabs) and 16, 18, 33, 35, 56, 58, 73 (oral swabs) are high-risk.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3119070&req=5

Figure 1: HPV genotype distribution of all oral and anal infections detected among paired oral and anal swabs. A: HPV genotype distribution at baseline; B: HPV genotype distribution in subsequent specimens (6 months after study entry). n.t.: non-typeable HPV strains. The genotype is indicated on the abscissa. Genotypes 10, 32, 34, 38, 90, (anal swabs) and 10, 97 (oral swabs) are of undefined oncogenic risk; genotypes 6, 11, 40, 53, 54, 61, 62, 66, 70, 71, 72, 81, 83, 84 (anal swabs) and 6, 66, 81 (oral swabs) are low-risk; genotypes 16, 18, 33, 35, 58 (anal swabs) and 16, 18, 33, 35, 56, 58, 73 (oral swabs) are high-risk.
Mentions: A total of 166 men were enrolled in this study. The characteristics of the study population are listed in Table 1. Paired concurrent anal and oral swabs were collected from all 166 of the patients at baseline. There were 49 withdrawals from the study, meaning that specimens at the 6 month follow-up were available from only 117 patients. Moreover, 41 oral swabs (thirty-two at baseline: 19%, nine at follow-up: 7.7%) were not able to be evaluated by PCR due to inadequate sampling revealed by the inability to detect beta-globin in the DNA sample. All anal swabs were adequate for sampling. Therefore, 283 anal swabs and 242 oral swabs were available for analysis. The HPV detection in oral and anal swabs is indicated in Table 2. The overall prevalence of HPV did not vary significantly between the baseline and follow-up time points and was 20.1 vs. 21.3% in oral specimens ((p-value = 0.8266) and 88.6 vs. 86.3% in anal specimens (p-value = 0.5748). The prevalence of HR genotypes among HPV-positive specimens was similar in oral and anal infections (mean values 24.3% and 20.9%, p-value = 0.6417). Among the 68 patients with HR, LR, or undetermined genotypes at the baseline in their anus who provided two consecutive anal samples, 75% (51/68) had persistent HPV six months after enrolment. Persistence rates of 71.4% (10/14) in patients with high-risk infections and 76.7% (33/43) in patients with low-risk infections were found. Rates of persistence of HPV according to the level of risk associated with the HPV genotype are shown in Table 3. The HPV genotype distribution in oral and anal swabs is depicted in Figure 1. There was no genotype concordance between oral and anal HPV types, with the exception of non-typeable strains in 3 paired oral and anal swabs (in a single patient at baseline and in two patients at follow-up). Genotype identification was not performed when multiple co-infecting HPV strains were obtained (Table 2).

Bottom Line: The overall prevalence of HPV did not vary significantly between the baseline and the follow-up, either in the oral (20.1 and 21.3%, respectively) or the anal specimens (88.6 and 86.3%).A significant correlation was found between the persistence of HHV-8 shedding and HIV viral load by logistic bivariate analysis (Odds Ratio of HHV-8 persistence for 1-log increase of HIV viral load = 1.725 ± 0.397, p = 0.018).A high prevalence of HPV infection was found in our cohort of HIV-infected MSM, with a negative correlation between anal HPV infection and CD4 cell count.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Histology, Microbiology and Medical Biotechnology, Padua University, Via Gabelli 63, 35100 Padova, Italy. saverio.parisi@unipd.it

ABSTRACT

Background: A study including 166 subjects was performed to investigate the frequency and persistence over a 6-month interval of concurrent oral and anal Human Papillomavirus (HPV) infections in Human Immunodeficiency Virus (HIV)-infected men who have sex with men (MSM).

Methods: Patients with no previously documented HPV-related anogenital lesion/disease were recruited to participate in a longitudinal study. Polymerase chain reaction (PCR) was performed to detect HPV from oral and anal swabs and to detect Human Herpes Virus 8 (HHV-8) DNA in saliva on 2 separate specimen series, one collected at baseline and the other collected 6 months later. A multivariate logistic analysis was performed using anal HPV infection as the dependent variable versus a set of covariates: age, HIV plasma viral load, CD4+ count, hepatitis B virus (HBV) serology, hepatitis C virus (HCV) serology, syphilis serology and HHV-8 viral shedding. A stepwise elimination of covariates with a p-value > 0.1 was performed.

Results: The overall prevalence of HPV did not vary significantly between the baseline and the follow-up, either in the oral (20.1 and 21.3%, respectively) or the anal specimens (88.6 and 86.3%). The prevalence of high-risk (HR) genotypes among the HPV-positive specimens was similar in the oral and anal infections (mean values 24.3% and 20.9%). Among 68 patients with either a HR, low-risk (LR) or undetermined genotype at baseline, 75% had persistent HPV and the persistence rates were 71.4% in HR infections and 76.7% in LR infections. There was a lack of genotype concordance between oral and anal HPV samples. The prevalence of HR HPV in anus appeared to be higher in the younger patients, peaking (> 25%) in the 43-50 years age group. A decrease of the high level of anal prevalence of all genotypes of HPV in the patients > 50 years was evident. HHV-8 oral shedding was positively related to HPV anal infection (p = 0.0046). A significant correlation was found between the persistence of HHV-8 shedding and HIV viral load by logistic bivariate analysis (Odds Ratio of HHV-8 persistence for 1-log increase of HIV viral load = 1.725 ± 0.397, p = 0.018).

Conclusions: A high prevalence of HPV infection was found in our cohort of HIV-infected MSM, with a negative correlation between anal HPV infection and CD4 cell count.

Show MeSH
Related in: MedlinePlus