scholarly journals Differences and changes in human papillomavirus type 16 variant status in human immunodeficiency virus-positive adults are not uncommon

2010 ◽  
Vol 91 (8) ◽  
pp. 2068-2072 ◽  
Author(s):  
Martin Steinau ◽  
David C. Swan ◽  
Juanita M. Onyekwuluje ◽  
John T. Brooks ◽  
Claudia Vellozzi ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Papillomavirus ◽  
Anatomical Site ◽  
Hpv 16 ◽  
Cervical Sample ◽  
Human Papillomavirus Type 16 ◽  
Immunodeficiency Virus ◽  
Serial Samples ◽  
Study Participants ◽  
Over Time

Human papillomavirus type 16 (HPV-16) genotype variants have been the subject of several investigations, but study participants have rarely been sampled more than once. In this study, among a cohort of human immunodeficiency virus (HIV)-infected adults, HPV-16 variants were investigated in samples collected concurrently from the anus and cervix, as well as in serial samples collected from the same anatomical site at 12-month intervals. HPV-16 variants in stored extracts of cervical and anal samples were determined from subjects with multiple visits and at least one sample positive for HPV-16. Seven polymorphic nucleotide positions within the E6 region were analysed by pyrosequencing to determine genotype variants. Of 364 samples examined, 176 anal and 39 cervical swabs from 84 different subjects yielded unequivocal sequences of eight major HPV-16 variants. Eight samples contained probable novel HPV-16 variants and in one sample two variants were detected. In eight out of 29 (27.6 %) anal–cervical sample pairs positive for HPV-16, discordant variants were found. From 57 anal and nine cervical sample series of HPV-16-positive samples, a change in HPV-16 variant status over time was seen in nine (13.6 %) instances (seven anal and two cervical) from eight different participants. Changes in HPV-16 variants in HIV-infected adults were seen most frequently when different anatomical sites were sampled, but were also observed over time.

scholarly journals Association of serum and mucosal neutralizing antibodies to human papillomavirus type 16 (HPV-16) with HPV-16 infection and cervical disease

2008 ◽  
Vol 89 (4) ◽  
pp. 910-914 ◽  
Author(s):  
Zizipho Z. A. Mbulawa ◽  
Anna-Lise Williamson ◽  
Debbie Stewart ◽  
Jo-Ann S. Passmore ◽  
Lynette Denny ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Neutralizing Antibodies ◽  
Antibody Responses ◽  
Normal Cytology ◽  
Hpv 16 ◽  
Human Papillomavirus Type 16 ◽  
Immunodeficiency Virus ◽  
Cervical Disease ◽  
Hpv Types

We investigated neutralizing antibodies to human papillomavirus type 16 (HPV-16) in serum and cervical washes from 84 women with normal cytology or cervical disease. Serum neutralizing antibodies were detected in 78 % of women infected at the cervix with HPV-16, compared with 35 % (P=0.002) of women infected with HPV-16-related types (α9 HPV types), 14 % (P<0.0001) of women infected with HPV-16 non-related types and none of HPV-uninfected women. A significant correlation between HPV-16 infection and serum HPV-16-neutralizing antibodies was observed (r s=0.97; P=0.032). Cervical neutralizing antibodies were detected in 38 % of women with HPV-16 infection and in 17 % of women infected with the HPV-16-related type HPV-31. Cervical neutralizing antibodies correlated with HPV-16 infection (r s=0.95; P=0.08), but not with cervical disease. Serum and cervical HPV-16 antibody responses were not affected significantly by human immunodeficiency virus type 1 infection. In conclusion, serum and cervical HPV-16-neutralizing antibodies were found to correlate with HPV-16 infection, but not with cervical disease.

scholarly journals Human papillomavirus type-specific risk of cervical cancer in a population with high human immunodeficiency virus prevalence: case–control study

2011 ◽  
Vol 92 (12) ◽  
pp. 2784-2791 ◽  
Author(s):  
Pontus Naucler ◽  
Flora Mabota da Costa ◽  
Joao Leopoldo da Costa ◽  
Otto Ljungberg ◽  
Antonio Bugalho ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Immunodeficiency Virus ◽  
Human Papillomavirus ◽  
Effect Modification ◽  
Hiv Positive ◽  
Hpv 16 ◽  
Cervical Cancer Risk ◽  
Hiv Positive Women ◽  
Immunodeficiency Virus ◽  
Hiv Negative

There are limited data on human papillomavirus (HPV) type-specific cervical cancer risk among human immunodeficiency virus (HIV)-positive women. Previous studies have suggested that HPV 16 would be relatively less important as a causative agent among HIV-positive compared with HIV-negative women. This study investigates HPV type-specific cervical cancer risk in a population in which HIV is endemic. At the Central Hospital, Maputo, Mozambique, 221 cervical cancer cases and 203 hospital-based controls were consecutively enrolled. HPV typing from cervical samples, HIV testing and recording of socio-demographic factors were performed. Logistic regression modelling was used to assess HPV type-specific risk and effect modification between HIV and HPV infection. Infection with HPV 16, 18 and ‘high-risk non-HPV 16/18 types’ (HPV 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59) was associated with cervical cancer in both crude and adjusted analyses. HPV 16 and 18 were the most common types detected in cancer biopsies among both HIV-negative and HIV-positive women. There was no significant evidence of effect modification between any HPV type and HIV infection, and there were no significant differences in the HPV type-specific prevalence when cervical cancers among HIV-positive and HIV-negative women were compared. Within the limitations of the study, the relative importance of different HPV types in cervical carcinogenesis appears not to be modified greatly by HIV infection, suggesting that HPV vaccines might not need to be type-specifically modified to be suitable for populations where HIV is endemic.

scholarly journals Human Papillomavirus-Specific Antibody Status in Oral Fluids Modestly Reflects Serum Status in Human Immunodeficiency Virus-Positive Individuals

2003 ◽  
Vol 10 (3) ◽  
pp. 431-438 ◽  
Author(s):  
Jennifer E. Cameron ◽  
Isaac V. Snowhite ◽  
Anil K. Chaturvedi ◽  
Michael E. Hagensee
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Papillomavirus ◽  
Oral Fluid ◽  
Human Papillomaviruses ◽  
Antibody Detection ◽  
Prevalence Rates ◽  
Hpv 16 ◽  
Oral Fluids ◽  
Immunodeficiency Virus ◽  
Serum Testing

ABSTRACT Serological assays are valuable tools for studies of the epidemiology of human papillomaviruses (HPVs). The efficacy of a less invasive oral-fluid assay for detection of HPV antibodies was examined. Matched serum, saliva, and oral mucosal transudate (OMT) specimens collected from 150 human immunodeficiency virus-seropositive patients were tested for immunoglobulin G antibodies against HPV-6 and HPV-11 combined (HPV-6/11) and HPV-16 capsids. Antibodies to HPV were detected in both types of oral specimens. Seroprevalence rates were 55% for HPV-6/11 and 37% for HPV-16, whereas oral prevalence rates were significantly lower (for HPV-6/11 in saliva, 31%, and in OMT, 19%; for HPV-16 in saliva, 19%, and in OMT, 17%). HPV antibody detection in OMT more accurately reflected the presence of antibodies in serum than did HPV antibody detection in saliva. More stringent saliva assay cutpoints yielded stronger associations between oropositivity and seropositivity; less stringent OMT cutpoints yielded stronger associations between oropositivity and seropositivity. Although HPV antibodies were detected in oral fluids, further optimization of the assay is necessary before oral-fluid testing can be implemented as a reliable alternative to serum testing for HPV.

scholarly journals Increasing hepatitis C virus RNA levels in hemophiliacs: relationship to human immunodeficiency virus infection and liver disease. Multicenter Hemophilia Cohort Study

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1020-1023 ◽  
Author(s):  
ME Eyster ◽  
MW Fried ◽  
AM Di Bisceglie ◽  
JJ Goedert
Keyword(s):  
Immune Deficiency ◽  
Human Immunodeficiency Virus ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hcv Rna ◽  
Immunodeficiency Virus ◽  
Hiv Seroconversion ◽  
Serial Samples ◽  
Over Time ◽  
Rna Levels

Abstract We have previously observed an increased frequency of liver failure in human immunodeficiency virus (HIV)-infected hemophiliacs. The purpose of this study was to quantitate hepatitis C virus (HCV) RNA levels in serial samples from HIV-seropositive (HIV+) and HIV-seronegative (HIV-) hemophiliacs before and after HIV seroconversion, and to examine the relationship of HCV RNA levels to CD4 cell counts and to hepatic dysfunction over time. HCV RNA levels were measured on serial samples of serum stored frozen from 17 HCV+/HIV+ and 17 HCV+/HIV- subjects matched within 5 years of their birth dates. All were HCV+ before study entry. HCV RNA levels were quantitated by a branched DNA-enhanced label amplification (bDNA) assay. For samples less than the cut off, HCV RNA was measured by the nested polymerase chain reaction. Individual changes over time, clinical groups, and mean values within predetermined time windows were compared with Wilcoxon rank sum tests. Mean HCV RNA levels increased from 2.76 (standard error [SE] 1.33) x 10(5) to 2.84 (SE 1.39) x 10(6) eq/mL during the first 2 years after HIV seroconversion (P = .006). Baseline HCV RNA levels in the pre-HIV seroconversion group were not significantly different from the baseline levels in those who remained HIV (P = .79). Over the entire period of study, HCV RNA levels increased nearly threefold in those who remained HIV- (mean 9.47 [SE 4.78] x 10(5) to 2.81 [SE 1.13] x 10(6)/mL; P = .02). Among those who became HIV+, HCV RNA levels increased 58-fold (mean 2.85 [SE 1.26] x 10(5) to 1.66 [SE 0.57] x 10(7) eq/mL; P = .0001). The rate of increase in HCV RNA levels was eightfold faster for HIV+ subjects than for subjects who remained HIV- (P = .009). HCV RNA levels increased twofold higher in 5 subjects who developed liver failure compared with the 12 who did not (P = .43). HCV RNA levels correlated significantly with CD4 counts (R = -.33, P = .01) and serum aspartate aminotransferase levels (AST) (R = .36, P = .007). We conclude that HCV RNA levels are significantly higher in HIV+ than in HIV- multitransfused hemophiliacs. HCV load increases over time, is enhanced by HIV, and further increases as immune deficiency progresses. HCV RNA levels are directly associated with high AST levels. These findings suggest that HIV-induced immune deficiency may promote increased HCV replication.

scholarly journals Incidence and Clearance of Anal Human Papillomavirus (HPV)-16 and HPV-18 Infection, and Their Determinants, Among Human Immunodeficiency Virus-Infected Men Who Have Sex With Men in France

2019 ◽  
Vol 221 (9) ◽  
pp. 1488-1493 ◽  
Author(s):  
Catharina J Alberts ◽  
Isabelle Heard ◽  
Ana Canestri ◽  
Lucie Marchand ◽  
Jean-François Fléjou ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Papillomavirus ◽  
Hpv Infection ◽  
High Grade ◽  
Hpv 16 ◽  
Human Papillomavirus 16 ◽  
Immunodeficiency Virus ◽  
Adjusted Incidence Rate ◽  
Sex With Men ◽  
Hpv 18

Abstract Background Prospective data on the natural history of anal human papillomavirus (HPV) infection are scarce in human immunodeficiency virus (HIV)-infected men who have sex with men (MSM). Methods We analyzed incidence and clearance of HPV-16 and HPV-18 in a French cohort of HIV-infected MSM, aged ≥35 years, followed-up annually (n = 438, 2014–2018). Results Human papillomavirus-16 and HPV-18 incidence were similar (~10% incident infections at 24 months). Human papillomavirus-16 incidence was higher among high-grade versus no lesion at baseline (adjusted incidence rate ratio = 3.0; 95% confidence interval, 1.07–8.18). Human papillomavirus-16 cleared significantly slower than HPV-18 (32% versus 54% by 24 months). Conclusions In conclusion, anal HPV-16 is more persistent than HPV-18, and its incidence correlates with a prior detection of high-grade lesions.

scholarly journals Influence of human papillomavirus type 16 (HPV-16) E2 polymorphism on quantification of HPV-16 episomal and integrated DNA in cervicovaginal lavages from women with cervical intraepithelial neoplasia

2008 ◽  
Vol 89 (7) ◽  
pp. 1716-1728 ◽  
Author(s):  
Naoufel Azizi ◽  
Jessica Brazete ◽  
Catherine Hankins ◽  
Deborah Money ◽  
Julie Fontaine ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Viral Load ◽  
Cervical Intraepithelial Neoplasia ◽  
Asian American ◽  
Intraepithelial Neoplasia ◽  
Hpv 16 ◽  
Viral Loads ◽  
Human Papillomavirus Type 16 ◽  
Immunodeficiency Virus ◽  
Intraepithelial Lesion

Integrated human papillomavirus type 16 (HPV-16) viral loads are currently estimated by quantification with real-time PCR of HPV-16 E6 (RT-E6 and HPV-16 PG) and E2 (RT-E2-1) DNA. We assessed the influence of HPV-16 E2 polymorphism on quantification of integrated HPV-16 DNA in anogenital specimens. HPV-16 E2 was sequenced from 135 isolates (123 from European and 12 from non-European lineages). An assay targeting conserved HPV-16 E2 sequences (RT-E2-2) was optimized and applied with RT-E6 and RT-E2-1 on 139 HPV-16-positive cervicovaginal lavages collected from 74 women [58 human immunodeficiency virus (HIV)-seropositive and 16 HIV-seronegative]. Ratios of HPV-16 copies measured with RT-E2-2 and RT-E2-1 obtained with African 2 (median=3.23, range=1.92–3.49) or Asian–American (median=3.78, range=1.47–37) isolates were greater than those obtained with European isolates (median=1.02, range=0.64–1.80; P<0.02 for each comparison). The distribution of HPV-16 E2 copies measured in 139 samples with RT-E2-2 (median=6150) and RT-E2-1 (median=8960) were different (P<0.0001). The risk of high-grade cervical intraepithelial neoplasia (CIN-2,3) compared with women without CIN was increased with higher HPV-16 total [odds ratio (OR)=2.17, 95 % confidence interval (CI)=1.11–4.23], episomal (OR=2.14, 95 % CI=1.09–4.19), but not for HPV-16 integrated viral load (OR=1.71, 95 % CI=0.90–3.26), after controlling for age, race, CD4 count, HIV and HPV-16 polymorphism. The proportion of samples with an E6/E2 ratio >2 in women without squamous intraepithelial lesion (7 of 35) was similar to that of women with CIN-2,3 (5 of 11, P=0.24) or CIN-1 (5 of 14, P=0.50). HPV-16 E2 polymorphism was a significant factor that influenced measures of HPV-16 integrated viral load.

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