Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human adenovirus F (HAdV-F) is one of the major causative species detected in acute gastroenteritis in children worldwide. HAdV-F is composed of serotypes 40 and 41. Most studies have reported the prevalence of HAdV-41 and focused on its epidemiologic characteristics. In this study, seventeen samples were identified as HAdV-41 out of 273 fecal specimens from children with acute diarrhea in Shanghai. Five isolates were isolated and subjected to whole genome sequencing and analysis to characterize the genetic variation and evolution. Full genome analysis revealed low genetic variation (99.07-99.92% identity) among the isolates, and InDels are observed in the E2A gene and the hexon gene compared to the reference strain NIVD103. Phylogenetic analysis showed that all isolates mainly formed two genome-type clusters but with incongruence in the trees of whole genomes and individual genes. The recombination breakpoints of the five isolates were inferred by the Recombination Detection Program (RDP) and varied in the number and location of the recombination events, indicating different evolution origins. Overall, our study highlights the genetic diversity of HAdV-41 isolates circulating in Shanghai, which may have evolved from inter-strain recombination.
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PMID:Circulation of HAdV-41 with diverse genome types and recombination in acute gastroenteritis among children in Shanghai. 2861 24

Human adenoviruses (HAdV) are associated with clinical symptoms such as gastroenteritis, keratoconjunctivitis, pneumonia, hepatitis, and encephalitis. In the absence of protective immunity, as in allogeneic bone marrow transplant patients, HAdV infections can become lethal. Alarmingly, various outbreaks of highly pathogenic, pneumotropic HAdV types have been recently reported, causing severe and lethal respiratory diseases. Effective drugs for treatment of HAdV infections are still lacking. The repurposing of drugs approved for other indications is a valuable alternative for the development of new antiviral therapies and is less risky and costly than de novo development. Arsenic trioxide (ATO) is approved for treatment of acute promyelocytic leukemia. Here, it is shown that ATO is a potent inhibitor of HAdV. ATO treatment blocks virus expression and replication by reducing the number and integrity of promyelocytic leukemia (PML) nuclear bodies, important subnuclear structures for HAdV replication. Modification of HAdV proteins with small ubiquitin-like modifiers (SUMO) is also key to HAdV replication. ATO reduces levels of viral SUMO-E2A protein, while increasing SUMO-PML, suggesting that ATO interferes with SUMOylation of proteins crucial for HAdV replication. It is concluded that ATO targets cellular processes key to HAdV replication and is relevant for the development of antiviral intervention strategies.
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PMID:ATO (Arsenic Trioxide) Effects on Promyelocytic Leukemia Nuclear Bodies Reveals Antiviral Intervention Capacity. 3232 11