ArticleJournal of clinical microbiology2022
A Prolonged Outbreak of Human Adenovirus A31 (HAdV-A31) Infection on a Pediatric Hematopoietic Stem Cell Transplantation Ward with Whole Genome Sequencing Evidence of International Linkages.
Article in Journal of clinical microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Hidden Circulation and Socio-Sanitary Vulnerability: Rotavirus A and Human Adenovirus Prevalence in Symptomatic and Asymptomatic Children in Central Brazil Post-COVID-19.Pathogens (Basel, Switzerland) · 2025Article
- The seroprevalence of adenoviruses since 2000Emerging microbes & infections · 2025Review
- Adenovirus Types in US Children Hospitalized or Seen in the Emergency Department With Acute Respiratory Illness, 2016-2019.Open forum infectious diseases · 2025Article
- Whole-Genome Sequencing of Adenovirus Genotypes and Clinical Implications in Pediatric Patients.Viruses · 2025Article
- Next-Generation Sequencing for Infectious Disease Diagnostics in Pediatric Patients with Malignancies or After Hematopoietic Cell Transplantation: A Systematic Review.Journal of clinical medicine · 2025Review
- Genetic Evolution and Variation of Human Adenovirus Serotype 31 Epidemic Strains in Beijing, China, during 2010-2022.Viruses · 2023Article
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Authors and funding
15 authors.
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Abstract
A surge in hematopoietic stem cell transplantation (HSCT) human adenovirus A31 (HAdV-A31) infections was initially observed in late 2014/2015 at SickKids (SK) Hospital, Toronto, Canada. In response, enhanced laboratory monitoring for all adenovirus infections was conducted. Positive samples underwent genotyping, viral culture, and, in selected cases, whole-genome sequencing (WGS). HAdV-A31 specimens/DNA obtained from four international pediatric HSCT centers also underwent WGS. During the SK outbreak period (27 October 2014 to 31 October 2018), 17/20 HAdV-A31 isolates formed a distinct clade with 0 to 8 mutations between the closest neighbors. Surveillance before and after the outbreak detected six additional HAdV-A31 HSCT cases; three of the four sequenced cases clustered within the outbreak clade. Two SK outbreak isolates were identical to sequences from two patients in an outbreak in England. Three SK non-outbreak sequences also had high sequence similarity to strains from three international centers. Environmental PCR testing of the HSCT ward showed significant adenovirus contamination. Despite intense infection control efforts, we observed re-occurrence of infection with the outbreak strain. Severe but nonfatal infection was observed more commonly with HAdV-A31 compared to other genotypes, except HAdV-C1. Our findings strongly implicate nosocomial spread of HAdV-A31 over 10 years on a HSCT unit and demonstrate the value of WGS in defining and mapping the outbreak. Close linkages among strains in different countries suggest international dissemination, though the mechanism is undetermined. This large, extended outbreak emphasizes the pre-eminent role of HAdV-A31 in causing intractable pediatric HSCT outbreaks of severe illness worldwide.
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