Abstract:B-cell and T-cell memory did not significantly differ after either three or four doses of QHPV in HIV-infected children. The clinical consequences of decreasing global T-cell function and HPV B-cell memory over time in HIV-infected children requires further investigation.
“…Counseling of girls and young women and improved access to clinics and other health-care facilities may be important in reducing oncogenic HPV infections. Because vaccination against HPV is effective in preventing infection with oncogenic HPV types, it is important that all women are vaccinated, whether they are HIV-infected or HIV-uninfected [34,35].…”
Section: Discussionmentioning
confidence: 99%
“…(HPV 16,18,26,31,33,35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 67, 68, 69, 70, 73, 82, IS39). One or more HR-HPV types defined by IARC (HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66) were detected in 70 of 220 (31.8%) participants.…”
Background: Cervical cancer is caused by oncogenic human papillomaviruses (HPV) and is one of the most common malignancies in women living in sub-Saharan Africa. Women infected with the human immunodeficiency virus (HIV) have a higher incidence of cervical cancer, but the full impact on HPV detection is not well understood, and associations of biological and behavioral factors with oncogenic HPV detection have not been fully examined. Therefore, a study was initiated to investigate factors that are associated with oncogenic HPV detection in Kenyan women. Methods: Women without cervical dysplasia were enrolled in a longitudinal study. Data from enrollment are presented as a cross-sectional analysis. Demographic and behavioral data was collected, and HPV typing was performed on cervical swabs. HIV-uninfected women (n = 105) and HIV-infected women (n = 115) were compared for demographic and behavioral characteristics using t-tests, Chi-square tests, Wilcoxon sum rank tests or Fisher's exact tests, and for HPV detection using logistic regression or negative binomial models adjusted for demographic and behavioral characteristics using SAS 9.4 software. Results: Compared to HIV-uninfected women, HIV-infected women were older, had more lifetime sexual partners, were less likely to be married, were more likely to regularly use condoms, and were more likely to have detection of HPV 16, other oncogenic HPV types, and multiple oncogenic types. In addition to HIV, more lifetime sexual partners was associated with a higher number of oncogenic HPV types (aIRR 1.007, 95% CI 1.007-1.012). Greater travel distance to the clinic was associated with increased HPV detection (aOR for detection of ≥ 2 HPV types: 3.212, 95% CI 1. 206-8.552). Older age (aOR for HPV 16 detection: 0.871, 95% CI 0.764-0.993) and more lifetime pregnancies (aOR for detection of oncogenic HPV types: 0.706, 95% CI, 0.565-0.883) were associated with reduced detection. Conclusion: HIV infection, more lifetime sexual partners, and greater distance to health-care were associated with a higher risk of oncogenic HPV detection, in spite of ART use in those who were HIV-infected. Counseling of women about sexual practices, improved access to health-care facilities, and vaccination against HPV are all potentially important in reducing oncogenic HPV infections.
“…Counseling of girls and young women and improved access to clinics and other health-care facilities may be important in reducing oncogenic HPV infections. Because vaccination against HPV is effective in preventing infection with oncogenic HPV types, it is important that all women are vaccinated, whether they are HIV-infected or HIV-uninfected [34,35].…”
Section: Discussionmentioning
confidence: 99%
“…(HPV 16,18,26,31,33,35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 67, 68, 69, 70, 73, 82, IS39). One or more HR-HPV types defined by IARC (HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66) were detected in 70 of 220 (31.8%) participants.…”
Background: Cervical cancer is caused by oncogenic human papillomaviruses (HPV) and is one of the most common malignancies in women living in sub-Saharan Africa. Women infected with the human immunodeficiency virus (HIV) have a higher incidence of cervical cancer, but the full impact on HPV detection is not well understood, and associations of biological and behavioral factors with oncogenic HPV detection have not been fully examined. Therefore, a study was initiated to investigate factors that are associated with oncogenic HPV detection in Kenyan women. Methods: Women without cervical dysplasia were enrolled in a longitudinal study. Data from enrollment are presented as a cross-sectional analysis. Demographic and behavioral data was collected, and HPV typing was performed on cervical swabs. HIV-uninfected women (n = 105) and HIV-infected women (n = 115) were compared for demographic and behavioral characteristics using t-tests, Chi-square tests, Wilcoxon sum rank tests or Fisher's exact tests, and for HPV detection using logistic regression or negative binomial models adjusted for demographic and behavioral characteristics using SAS 9.4 software. Results: Compared to HIV-uninfected women, HIV-infected women were older, had more lifetime sexual partners, were less likely to be married, were more likely to regularly use condoms, and were more likely to have detection of HPV 16, other oncogenic HPV types, and multiple oncogenic types. In addition to HIV, more lifetime sexual partners was associated with a higher number of oncogenic HPV types (aIRR 1.007, 95% CI 1.007-1.012). Greater travel distance to the clinic was associated with increased HPV detection (aOR for detection of ≥ 2 HPV types: 3.212, 95% CI 1. 206-8.552). Older age (aOR for HPV 16 detection: 0.871, 95% CI 0.764-0.993) and more lifetime pregnancies (aOR for detection of oncogenic HPV types: 0.706, 95% CI, 0.565-0.883) were associated with reduced detection. Conclusion: HIV infection, more lifetime sexual partners, and greater distance to health-care were associated with a higher risk of oncogenic HPV detection, in spite of ART use in those who were HIV-infected. Counseling of women about sexual practices, improved access to health-care facilities, and vaccination against HPV are all potentially important in reducing oncogenic HPV infections.
“…Better immunogenicity is seen when HIV viral replication is controlled, and when there is no overt immunodeficiency [2,12]. Longitudinal data suggests somewhat reduced antibody persistence [13,14], although modest memory B cell responses after G4 out to 4–5 years have been reported [13], and vaccinated HIV + ve subjects respond to late boosting with a 4th dose [14,15].…”
Persons with HIV are at increased risk of HPV infection, HPV disease, and HPV-related cancers compared to HIV negative persons. In persons with HIV, immune responses to vaccination are often sub-optimal, and while these improve with ART, they often remain lower and decline more rapidly than in HIV-negative individuals. Although the evidence base to support the
immunogenicity
of HPV vaccines in HIV + ve persons is reasonable, the evidence base to support the
efficacy
of HPV vaccines in HIV + ve individuals is inconsistent. There is one study in HIV + ve men who have sex with men (MSM) which showed
no effect
, and two other studies, one in HIV + ve women and one in HIV + ve adolescents that showed
reduced effectiveness
. All these effectiveness studies used Gardasil 4 (G4). Two studies in HIV + ve persons have shown superior immunogenicity of Cervarix (which uses a TLR4 agonist adjuvant) compared to G4. Studies of Hepatitis B vaccines in HIV + ve persons have shown that either (i) increased number of doses (ii) increased vaccine dose, or (iii) TLR agonist adjuvanted vaccines, all produce increased immunogenicity compared to standard vaccine regimes. Therefore, questions remain as to optimal HPV vaccine regimes in HIV and further clinical trials with different HPV vaccine regimes are needed.
“…Then we used the systematic literature search strategy, and 1369 potential relevant studies were identified. After duplication checking, title and abstract screening and full-text review, 24 full-text studies 20–43 were included in the final analysis (see Figure 1), involving 11 RCTs, 12 non-RCTs and 1 cohort study, among which, 9 studies reached high quality. The main characteristics of the 24 studies were described in Table 1.…”
Section: Resultsmentioning
confidence: 99%
“…55 Therefore, a few studies suggested PLWH should receive a four-dose regimen of HPV vaccine. 39,41 The current meta-analysis has the following limitations which should be taken into account. First, due to insufficient data, the occurrence of HPV-related cancers such as cervical cancer were not taken into account as the outcome indicator, so it could not provide evidence for HPV vaccine to reduce HPV-related cancer incidence and mortality.…”
The current evidence regarding the safety and immunogenicity of human papillomavirus (HPV) vaccinations for people living with HIV (PLWH) is unclear. We searched PubMed, Embase, Cochrane Library and Web of Science databases from inception to 23 November 2018. The pooled proportion, relative risk (RR) and the standardized mean difference (SMD) with 95% confidence intervals (CIs) were calculated. Twenty-four studies consisting of 7507 participants were identified. The pooled proportion of adverse events in HIV-infected vaccinees was 60% and the antibody seroconversion rates in HPV-6, -11, -16, -18 subtypes were all above 90%. When compared with the placebo groups, the risk of adverse events was not different except for the injection site reactions (RR: 2.63, 95% CI: 1.72–4.01, p < 0.001), and the level of CD4 was relatively lower (SMD: −0.17, 95% CI: −0.29 to −0.04, p = 0.01) in the HIV-positive vaccinees groups. When compared with HIV-negative vaccinees, the risk of adverse events was not different, but the pooled RR and SMD indicated that antibody seroconversion and geometric mean titer for HPV-18 in HIV-positive groups was lower (RR: 0.91, 95% CI: 0.87–0.95, p < 0.001; SMD: −0.43, 95% CI: −0.62 to −0.24, p < 0.001). The study proves that HPV vaccine is safe and efficacious for PLWH and has important implications for international guidelines and strategies for HPV vaccination.
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