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Age-dependent pathogenic characteristics of SARS-CoV-2 infection in ferrets

While the seroprevalence of SARS-CoV-2 in healthy people does not differ significantly among age groups, those aged 65 years or older exhibit strikingly higher COVID-19 mortality compared to younger individuals. To further understand differing COVID-19 manifestations in patients of different ages, t...

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Detalles Bibliográficos
Autores principales: Kim, Young-Il, Yu, Kwang-Min, Koh, June-Young, Kim, Eun-Ha, Kim, Se-Mi, Kim, Eun Ji, Casel, Mark Anthony, Rollon, Rare, Jang, Seung-Gyu, Song, Min-Suk, Park, Su-Jin, Jeong, Hye Won, Kim, Eung-Gook, Lee, Ok-Jun, Choi, Younho, Lee, Shin-Ae, Park, Su-Hyung, Jung, Jae U., Choi, Young Ki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Journal Experts 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8020987/
https://www.ncbi.nlm.nih.gov/pubmed/33821260
http://dx.doi.org/10.21203/rs.3.rs-131380/v2
Descripción
Sumario:While the seroprevalence of SARS-CoV-2 in healthy people does not differ significantly among age groups, those aged 65 years or older exhibit strikingly higher COVID-19 mortality compared to younger individuals. To further understand differing COVID-19 manifestations in patients of different ages, three age groups of ferrets were infected with SARS-CoV-2. Although SARS-CoV-2 was isolated from all ferrets regardless of age, aged ferrets (≥ 3 years old) showed higher viral loads, longer nasal virus shedding, and more severe lung inflammatory cell infiltration and clinical symptoms compared to juvenile (≤ 6 months) and young adult (1–2 years) groups. Transcriptome analysis of aged ferret lungs revealed strong enrichment of gene sets related to type I interferon, activated T cells, and M1 macrophage responses, mimicking the gene expression profile of severe COVID-19 patients. Thus, SARS-CoV-2-infected aged ferrets highly recapitulate COVID-19 patients with severe symptoms and are useful for understanding age-associated infection, transmission, and pathogenesis of SARS-CoV-2.