SARS‐CoV‐2 Omicron (B.1.1.529) infection in rhesus macaques, hamsters, and BALB/c mice with severe lung histopathological damage

Author:

Yu Wenhai1ORCID,Wang Junbin1,Yang Yun1,Tang Cong1ORCID,Yang Chengyun1,Li Bai1,Wang Haixuan1,Zhou Yanan1,Huang Qing1,Yang Hao1,Wu Daoju1,Luo Zhiwu1,Gao Jiahong1,Kuang Dexuan1,Long Haiting1,Peng Xiaozhong12,Xie Zhongping1,Lu Shuaiyao1

Affiliation:

1. National Kunming High‐level Biosafety Primate Research Center Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College Kunming Yunnan China

2. State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College Beijing China

Abstract

AbstractSince the first SARS‐CoV‐2 outbreak in late 2019, the SARS‐CoV‐2 genome has harbored multiple mutations, especially spike protein mutations. The currently fast‐spreading Omicron variant that manifests without symptoms or with upper respiratory diseases has been recognized as a serious global public health problem. However, its pathological mechanism is largely unknown. In this work, rhesus macaques, hamsters, and BALB/C mice were employed as animal models to explore the pathogenesis of Omicron (B.1.1.529). Notably, Omicron (B.1.1.529) infected the nasal turbinates, tracheae, bronchi, and lungs of hamsters and BALB/C mice with higher viral loads than in those of rhesus macaques. Severe histopathological damage and inflammatory responses were observed in the lungs of Omicron (B.1.1.529)‐infected animals. In addition, viral replication was found in multiple extrapulmonary organs. Results indicated that hamsters and BALB/c mice are potential animal models for studies on the development of drugs/vaccines and therapies for Omicron (B.1.1.529).

Publisher

Wiley

Subject

Infectious Diseases,Virology

Cited by 4 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3