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Susceptibility to Viral Infections v0.126 RNASEL Zornitza Stark Marked gene: RNASEL as ready
Susceptibility to Viral Infections v0.126 RNASEL Zornitza Stark Gene: rnasel has been classified as Amber List (Moderate Evidence).
Susceptibility to Viral Infections v0.126 RNASEL Zornitza Stark Phenotypes for gene: RNASEL were changed from MIS-C to Multisystem inflammatory syndrome, MONDO:0035375, RNASEL-related
Susceptibility to Viral Infections v0.125 RNASEL Zornitza Stark Classified gene: RNASEL as Amber List (moderate evidence)
Susceptibility to Viral Infections v0.125 RNASEL Zornitza Stark Gene: rnasel has been classified as Amber List (Moderate Evidence).
Susceptibility to Viral Infections v0.124 RNASEL Zornitza Stark reviewed gene: RNASEL: Rating: AMBER; Mode of pathogenicity: None; Publications: ; Phenotypes: Multisystem inflammatory syndrome, MONDO:0035375, RNASEL-related; Mode of inheritance: BIALLELIC, autosomal or pseudoautosomal
Susceptibility to Viral Infections v0.117 RNASEL Peter McNaughton gene: RNASEL was added
gene: RNASEL was added to Susceptibility to Viral Infections. Sources: Literature
Mode of inheritance for gene: RNASEL was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: RNASEL were set to PMID: 36538032
Phenotypes for gene: RNASEL were set to MIS-C
Review for gene: RNASEL was set to AMBER
Added comment: Single patient presenting with similar presentation and functional findings to OAS1 and OAS2
Sources: Literature
Susceptibility to Viral Infections v0.117 OAS2 Peter McNaughton gene: OAS2 was added
gene: OAS2 was added to Susceptibility to Viral Infections. Sources: Literature
Mode of inheritance for gene: OAS2 was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: OAS2 were set to PMID: 36538032
Phenotypes for gene: OAS2 were set to MIS-C
Review for gene: OAS2 was set to GREEN
Added comment: 3x unrelated patients with MIS-C after COVID infection. Patients displayed excessive inflammatory responses to intracellular dsRNA, SARS-CoV-2, SARS-CoV-2–infected cells, and their RNA, providing a plausible mechanism for MIS-C. Similar presentation to OAS1 and RNASEL.
Sources: Literature