Background: In 2011, Rwanda became the first African nation to implement a national human papillomavirus (HPV) vaccination program, conceived to protect girls aged <15 years (i.e. born ≥1997). After an initial school-grade-targeted catch-up campaign, there was a transition to routine vaccination of 12 year-olds only. We aimed to produce population-level vaccine coverage estimates.
Methods: The Rwandan Expanded Program on Immunization (EPI) collected data on number of eligible girls and HPV vaccines delivered, stratified by calendar year (2011-2018), girl's age, district and vaccination round. HPV vaccine coverage was estimated by birth cohort (reconstituted using calendar year and age), as a proportion of (1) eligible target, and (2) the 2012 Rwandan census population.
Results: 1,156,863 girls received first dose of HPV vaccine between 2011 and 2018, corresponding to 98% of the eligible target. Median vaccination age was 15 years (interquartile range [IQR] 13-16) in 2011-2013 (school grade-targeted catch-up), 13 years (IQR 12-14) in 2014 (transition) and 12 years in 2015-2018 (routine). Population-level coverage versus the census increased from 10 to 40% for girls born in 1993-1995 (median vaccination age = 17 years) to 50-65% for 1996-2000 birth cohorts (14 years), and 80-90% for 2001-2006 birth cohorts (12 years). Coverage trends were similar across provinces and in the capital, Kigali. Second and third round coverage suggested most vaccinated girls completed their recommended dosing regimen (which reduced from 3 to 2 doses in 2015).
Conclusions: Birth cohorts provide a clear picture of population-level HPV vaccine coverage after a pragmatic catch-up campaign, particularly in Rwanda where eligible school grades included wide age ranges. Whilst the catch-up campaign resulted in some coverage gaps in out-of-school teenagers, coverage remains high in cohorts routinely targeted as 12 year-olds.
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http://dx.doi.org/10.1016/j.vaccine.2020.04.021 | DOI Listing |
Tumour Virus Res
March 2025
School of Biological Sciences, University of Oklahoma, Norman, OK, USA; College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Cancers caused by high-risk human papillomavirus (HPV) remain a significant health threat resulting in more than 300,000 deaths, annually. Persistent expression of two HPV oncogenes, E6 and E7, are necessary for cancer development and progression. E6 has several functions contributing to tumorigenesis one of which is blocking programmed cell death, apoptosis.
View Article and Find Full Text PDFJAMA Netw Open
March 2025
Center for Health Decision Science, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Importance: Cervical screening guidelines in the US recommend that most females can exit routine screening at age 65 years following 2 recent consecutive negative cotest results (concurrent human papillomavirus and cytology tests). However, empirical data on the subsequent risks of cancer and cancer death in this subgroup of females are limited.
Objective: To estimate the risks of cervical cancer and cervical cancer death among females who meet the cotesting criteria to exit screening.
J Allergy Clin Immunol
March 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minn. Electronic address:
Background: The few reported patients with pathogenic IRF8 variants have manifested 2 distinct phenotypes: (1) an autosomal recessive severe immunodeficiency with significant neutrophilia and absence of or significant decrease in monocytes and dendritic cells and (2) a dominant-negative form with only a decrease in conventional type 2 dendritic cells (cDC2s) and susceptibility to mycobacterial disease.
Objectives: Genetic testing of a child with persistent EBV viremia identified a novel IRF8 variant: c.1279dupT (p.
Int J Cancer
March 2025
Anal Neoplasia Clinic, Research, and Education Center, University of California, San Francisco, California, USA.
J Med Virol
March 2025
Biosensors Laboratory, Department of Biomedical Engineering, Faculty of Engineering, Mahidol University, Nakhon Pathom, Thailand.
Human papillomavirus type 16 (HPV-16) is a key driver in the development of cervical carcinoma, with the integration of its genome into the host DNA marking a critical step in disease progression. Monitoring the physical state of HPV-16, particularly the transition from episomal to integrated forms, is essential for evaluating the risk of malignancy development in cervix. This study presents the development of a duplex electrochemical biosensor for the simultaneous detection of the E2 and E6 genes of HPV-16.
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