Search

BackgroundUnderstanding the natural history of anal high-risk human papillomavirus (hrHPV) infection is key for designing anal cancer prevention programs but has not been systematically characterized.MethodsWe reanalyzed data from 34 studies including 16 164 individuals in 6 risk groups defined by human immunodeficiency virus (HIV) status, sex, and male sexuality: men who have sex with men (MSM) and people with HIV (MSMWH), HIV-negative MSM, women with HIV (WWH), HIV-negative women, men who have sex with women (MSW) with HIV (MSWWH), and HIV-negative MSW. We used Markov models to estimate incidence and clearance of 13 hrHPV types and their determinants.ResultsHuman papillomavirus (HPV) 16 had the highest incidence-clearance ratio of the hrHPV types. MSMWH had the highest hrHPV incidence (eg, 15.5% newly HPV-16 infected within 2 years), followed by HIV-negative MSM (7.5%), WWH (6.6%), HIV-negative women (2.9%), MSWWH (1.7%), and HIV-negative MSW (0.7%). Determinants of HPV-16 incidence included HIV status and number of sexual partners for MSM, women, and MSW, and anal sex behavior for MSM only. HPV-16 clearance was lower for people with HIV (PWH) and lower for prevalent than incident infection. Among MSM, increasing age was associated with lower clearance of prevalent, but not incident, HPV-16 infection.ConclusionsThis robust and unifying analysis of anal hrHPV natural history is essential to designing and predicting the impact of HPV vaccination and HPV-based screening programs on anal cancer prevention, particularly in MSM and PWH. Importantly, it demonstrates the higher carcinogenic potential of longstanding anal prevalent hrHPV infection than more recent incident infection.

BackgroundAge-specific data on anal, and corresponding cervical, human papillomavirus (HPV) infection are needed to inform female anal cancer prevention.MethodsWe centrally reanalyzed individual-level data from 26 studies reporting HPV prevalence in paired anal and cervical samples by human immunodeficiency virus (HIV) status and age. For women with HIV (WWH) with anal high-grade squamous intraepithelial lesions or worse (HSIL+), we also investigated concurrent cervical cytopathology.ResultsIn HIV-negative women, HPV16 prevalence decreased significantly with age, both at anus (4.3% at 15-24 years to 1.0% at ≥55 years; ptrend = 0.0026) and cervix (7.4% to 1.7%; ptrend < 0.0001). In WWH, HPV16 prevalence decreased with age at cervix (18.3% to 7.2%; ptrend = 0.0035) but not anus (11.5% to 13.9%; ptrend = 0.5412). Given anal HPV16 positivity, concurrent cervical HPV16 positivity also decreased with age, both in HIV-negative women (ptrend = 0.0005) and WWH (ptrend = 0.0166). Among 48 WWH with HPV16-positive anal HSIL+, 27 (56%) were cervical high-risk HPV-positive, including 8 with cervical HPV16, and 5 were cervical HSIL+.ConclusionsAge-specific shifts in HPV16 prevalence from cervix to anus suggest that HPV infections in the anus persist longer, or occur later in life, than in the cervix, particularly in WWH. This is an important consideration when assessing the utility of cervical screening results to stratify anal cancer risk.

Understanding the proportion of invasive cervical cancer (ICC) caused by different human papillomavirus (HPV) genotypes can inform primary (ie, vaccination) and secondary (ie, screening) prevention efforts that target specific HPV genotypes. However, using the global literature to estimate population attributable fractions (AFs) requires a methodological framework to address HPV genotype-specific causality from aggregated data. We aimed to estimate the proportion of ICC caused by different HPV genotypes at the global, regional, and national level. This systematic review identified studies reporting HPV genotype-specific prevalence in ICC or people with normal cervical cytology. We searched PubMed, Embase, Scopus, and Web of Science up to Feb 29, 2024, using the search terms "cervix" and "HPV", with no language restrictions. Odds ratios (ORs) were estimated by comparing HPV genotype-specific prevalence between HPV-positive ICC and normal cervical cytology with logistic regression models, adjusting for region, year of paper publication, and HPV primer or test. HPV genotypes with a lower bound to the 95% CI of the OR greater than 1·0 were judged as causal to ICC. Corresponding regional genotype-specific AFs were calculated as regional HPV prevalence in ICC multiplied by (1 – [1 / OR]) and were proportionally adjusted to total 100%. Global AFs were calculated from regional AFs weighted by number of regional ICC cases in 2022 (GLOBOCAN). The systematic review identified 1174 studies with 111 902 cases of HPV-positive ICC and 2 755 734 of normal cervical cytology. 17 HPV genotypes were considered causal to ICC, with ORs ranging widely from 48·3 (95% CI 45·7–50·9) for HPV16 to 1·4 (1·2–1·7) for HPV51. HPV16 had the highest global AF (61·7%), followed by HPV18 (15·3%), HPV45 (4·8%), HPV33 (3·8%), HPV58 (3·5%), HPV31 (2·8%), and HPV52 (2·8%). Remaining causal genotypes (HPV35, 59, 39, 56, 51, 68, 73, 26, 69, and 82) had a combined global AF of 5·3%. AFs for HPV16 and 18 and HPV16, 18, 31, 33, 45, 52, and 58 combined were lowest in Africa (71·9% and 92·1%, respectively) and highest in central, western, and southern Asia (83·2% and 95·9%, respectively). HPV35 had a higher AF in Africa (3·6%) than other regions (0·6–1·6%). This study provides a comprehensive global picture of HPV genotype-specific AFs in ICC, before the influence of HPV vaccination. These data can inform HPV genotype-specific vaccination and screening strategies to reduce the burden of ICC. EU Horizon 2020 Research and Innovation Programme. [ABSTRACT FROM AUTHOR]

While previous reviews found a positive association between pre‐existing cancer diagnosis and COVID‐19‐related death, most early studies did not distinguish long‐term cancer survivors from those recently diagnosed/treated, nor adjust for important confounders including age. We aimed to consolidate higher‐quality evidence on risk of COVID‐19‐related death for people with recent/active cancer (compared to people without) in the pre‐COVID‐19‐vaccination period. We searched the WHO COVID‐19 Global Research Database (20 December 2021), and Medline and Embase (10 May 2023). We included studies adjusting for age and sex, and providing details of cancer status. Risk‐of‐bias assessment was based on the Newcastle‐Ottawa Scale. Pooled adjusted odds or risk ratios (aORs, aRRs) or hazard ratios (aHRs) and 95% confidence intervals (95% CIs) were calculated using generic inverse‐variance random‐effects models. Random‐effects meta‐regressions were used to assess associations between effect estimates and time since cancer diagnosis/treatment. Of 23 773 unique title/abstract records, 39 studies were eligible for inclusion (2 low, 17 moderate, 20 high risk of bias). Risk of COVID‐19‐related death was higher for people with active or recently diagnosed/treated cancer (general population: aOR = 1.48, 95% CI: 1.36‐1.61, I2 = 0; people with COVID‐19: aOR = 1.58, 95% CI: 1.41‐1.77, I2 = 0.58; inpatients with COVID‐19: aOR = 1.66, 95% CI: 1.34‐2.06, I2 = 0.98). Risks were more elevated for lung (general population: aOR = 3.4, 95% CI: 2.4‐4.7) and hematological cancers (general population: aOR = 2.13, 95% CI: 1.68‐2.68, I2 = 0.43), and for metastatic cancers. Meta‐regression suggested risk of COVID‐19‐related death decreased with time since diagnosis/treatment, for example, for any/solid cancers, fitted aOR = 1.55 (95% CI: 1.37‐1.75) at 1 year and aOR = 0.98 (95% CI: 0.80‐1.20) at 5 years post‐cancer diagnosis/treatment. In conclusion, before COVID‐19‐vaccination, risk of COVID‐19‐related death was higher for people with recent cancer, with risk depending on cancer type and time since diagnosis/treatment. [ABSTRACT FROM AUTHOR]

This result appears to be somewhat inconsistent with another important finding of Liu et al [[3]] (and of previous analyses [[5]]), namely that cervical HPV infection is a strong predictor of anal HPV infection and aHSIL. So, if not cervical screening results, then could perhaps routinely available HIV-related immune suppression be used to triage WLH (as well as other PLH) for anal cancer screening? In this respect, anal HPV16 infection was by far the strongest predictor of histological aHSIL, of which approximately one-third were diagnosed among WLH with HPV16-positive anal swabs in the report by Liu et al [[3]]. [Extracted from the article]

HIV substantially worsens human papillomavirus (HPV) carcinogenicity and contributes to an important population excess of cervical cancer, particularly in sub‐Saharan Africa (SSA). We estimated HIV‐ and age‐stratified cervical cancer burden at a country, regional and global level in 2020. Proportions of cervical cancer (a) diagnosed in women living with HIV (WLHIV), and (b) attributable to HIV, were calculated using age‐specific estimates of HIV prevalence (UNAIDS) and relative risk. These proportions were validated against empirical data and applied to age‐specific cervical cancer incidence (GLOBOCAN 2020). HIV was most important in SSA, where 24.9% of cervical cancers were diagnosed in WLHIV, and 20.4% were attributable to HIV (vs 1.3% and 1.1%, respectively, in the rest of the world). In all world regions, contribution of HIV to cervical cancer was far higher in younger women (as seen also in empirical series). For example, in Southern Africa, where more than half of cervical cancers were diagnosed in WLHIV, the HIV‐attributable fraction decreased from 86% in women ≤34 years to only 12% in women ≥55 years. The absolute burden of HIV‐attributable cervical cancer (approximately 28 000 cases globally) also shifted toward younger women: in Southern Africa, 63% of 5341 HIV‐attributable cervical cancer occurred in women <45 years old, compared to only 17% of 6901 non‐HIV‐attributable cervical cancer. Improved quantification of cervical cancer burden by age and HIV status can inform cervical cancer prevention efforts in SSA, including prediction of the impact of WLHIV‐targeted vs general population approaches to cervical screening, and impact of HIV prevention. What's new? The cancer‐causing potential of human papillomavirus (HPV) is amplified in patients infected with HIV. This is a particular consideration in sub‐Saharan Africa. Here, the authors developed an age‐specific method to determine the global burden of cervical cancer cases attributable to HIV. They found that around 20% of cervical cancer cases in sub‐Saharan Africa were attributable to HIV. Most of these occurred in women under age 45. These data can inform design of cervical cancer prevention programs, particularly in settings hit by a double burden of HPV and HIV. [ABSTRACT FROM AUTHOR]