Integrated gut virome and bacteriome dynamics in COVID-19 patients
SARS-CoV-2 is the cause of the current global pandemic of COVID-19; this virus infects multiple organs, such as the lungs and gastrointestinal tract. The microbiome in these organs, including the bacteriome and virome, responds to infection and might also influence disease progression and treatment...
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Published in | Gut microbes Vol. 13; no. 1; p. 1 |
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Main Authors | , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Taylor & Francis
01.01.2021
Taylor & Francis Group |
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Abstract | SARS-CoV-2 is the cause of the current global pandemic of COVID-19; this virus infects multiple organs, such as the lungs and gastrointestinal tract. The microbiome in these organs, including the bacteriome and virome, responds to infection and might also influence disease progression and treatment outcome. In a cohort of 13 COVID-19 patients in Beijing, China, we observed that the gut virome and bacteriome in the COVID-19 patients were notably different from those of five healthy controls. We identified a bacterial dysbiosis signature by observing reduced diversity and viral shifts in patients, and among the patients, the bacterial/viral compositions were different between patients of different severities, although these differences are not entirely distinguishable from the effect of antibiotics. Severe cases of COVID-19 exhibited a greater abundance of opportunistic pathogens but were depleted for butyrate-producing groups of bacteria compared with mild to moderate cases. We replicated our findings in a mouse COVID-19 model, confirmed virome differences and bacteriome dysbiosis due to SARS-CoV-2 infection, and observed that immune/infection-related genes were differentially expressed in gut epithelial cells during infection, possibly explaining the virome and bacteriome dynamics. Our results suggest that the components of the microbiome, including the bacteriome and virome, are affected by SARS-CoV-2 infections, while their compositional signatures could reflect or even contribute to disease severity and recovery processes. |
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AbstractList | SARS-CoV-2 is the cause of the current global pandemic of COVID-19; this virus infects multiple organs, such as the lungs and gastrointestinal tract. The microbiome in these organs, including the bacteriome and virome, responds to infection and might also influence disease progression and treatment outcome. In a cohort of 13 COVID-19 patients in Beijing, China, we observed that the gut virome and bacteriome in the COVID-19 patients were notably different from those of five healthy controls. We identified a bacterial dysbiosis signature by observing reduced diversity and viral shifts in patients, and among the patients, the bacterial/viral compositions were different between patients of different severities, although these differences are not entirely distinguishable from the effect of antibiotics. Severe cases of COVID-19 exhibited a greater abundance of opportunistic pathogens but were depleted for butyrate-producing groups of bacteria compared with mild to moderate cases. We replicated our findings in a mouse COVID-19 model, confirmed virome differences and bacteriome dysbiosis due to SARS-CoV-2 infection, and observed that immune/infection-related genes were differentially expressed in gut epithelial cells during infection, possibly explaining the virome and bacteriome dynamics. Our results suggest that the components of the microbiome, including the bacteriome and virome, are affected by SARS-CoV-2 infections, while their compositional signatures could reflect or even contribute to disease severity and recovery processes. SARS-CoV-2 is the cause of the current global pandemic of COVID-19; this virus infects multiple organs, such as the lungs and gastrointestinal tract. The microbiome in these organs, including the bacteriome and virome, responds to infection and might also influence disease progression and treatment outcome. In a cohort of 13 COVID-19 patients in Beijing, China, we observed that the gut virome and bacteriome in the COVID-19 patients were notably different from those of five healthy controls. We identified a bacterial dysbiosis signature by observing reduced diversity and viral shifts in patients, and among the patients, the bacterial/viral compositions were different between patients of different severities, although these differences are not entirely distinguishable from the effect of antibiotics. Severe cases of COVID-19 exhibited a greater abundance of opportunistic pathogens but were depleted for butyrate-producing groups of bacteria compared with mild to moderate cases. We replicated our findings in a mouse COVID-19 model, confirmed virome differences and bacteriome dysbiosis due to SARS-CoV-2 infection, and observed that immune/infection-related genes were differentially expressed in gut epithelial cells during infection, possibly explaining the virome and bacteriome dynamics. Our results suggest that the components of the microbiome, including the bacteriome and virome, are affected by SARS-CoV-2 infections, while their compositional signatures could reflect or even contribute to disease severity and recovery processes.SARS-CoV-2 is the cause of the current global pandemic of COVID-19; this virus infects multiple organs, such as the lungs and gastrointestinal tract. The microbiome in these organs, including the bacteriome and virome, responds to infection and might also influence disease progression and treatment outcome. In a cohort of 13 COVID-19 patients in Beijing, China, we observed that the gut virome and bacteriome in the COVID-19 patients were notably different from those of five healthy controls. We identified a bacterial dysbiosis signature by observing reduced diversity and viral shifts in patients, and among the patients, the bacterial/viral compositions were different between patients of different severities, although these differences are not entirely distinguishable from the effect of antibiotics. Severe cases of COVID-19 exhibited a greater abundance of opportunistic pathogens but were depleted for butyrate-producing groups of bacteria compared with mild to moderate cases. We replicated our findings in a mouse COVID-19 model, confirmed virome differences and bacteriome dysbiosis due to SARS-CoV-2 infection, and observed that immune/infection-related genes were differentially expressed in gut epithelial cells during infection, possibly explaining the virome and bacteriome dynamics. Our results suggest that the components of the microbiome, including the bacteriome and virome, are affected by SARS-CoV-2 infections, while their compositional signatures could reflect or even contribute to disease severity and recovery processes. |
Author | Yan, Jin Shi, Yi Cao, Jiabao Dai, Lianpan Lu, Jingjing Bai, Changqing Gong, Yuhuan Zhao, Na Chen, Zhu Wang, Jun Lei, Guanglin Bi, Yuhai Xu, Kun Meng, Fanping Yu, Linxiang Zhang, Yuqing Yang, Penghui Wang, Cheng Zhang, Shaogeng Zhang, Ning |
Author_xml | – sequence: 1 givenname: Jiabao surname: Cao fullname: Cao, Jiabao email: ypenghuiamms@hotmail.com organization: University of Chinese Academy of Sciences – sequence: 2 givenname: Cheng surname: Wang fullname: Wang, Cheng organization: First Medical Center of Chinese PLA General Hospital – sequence: 3 givenname: Yuqing surname: Zhang fullname: Zhang, Yuqing organization: University of Chinese Academy of Sciences – sequence: 4 givenname: Guanglin surname: Lei fullname: Lei, Guanglin organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 5 givenname: Kun surname: Xu fullname: Xu, Kun organization: School of Tropical Medicine and Laboratory Medicine, the First Affiliated Hospital, Hainan Medical University – sequence: 6 givenname: Na surname: Zhao fullname: Zhao, Na organization: Institute of Microbiology, Chinese Academy of Sciences – sequence: 7 givenname: Jingjing surname: Lu fullname: Lu, Jingjing organization: University of Chinese Academy of Sciences – sequence: 8 givenname: Fanping surname: Meng fullname: Meng, Fanping organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 9 givenname: Linxiang surname: Yu fullname: Yu, Linxiang organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 10 givenname: Jin surname: Yan fullname: Yan, Jin organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 11 givenname: Changqing surname: Bai fullname: Bai, Changqing organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 12 givenname: Shaogeng surname: Zhang fullname: Zhang, Shaogeng organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 13 givenname: Ning surname: Zhang fullname: Zhang, Ning organization: Center for Influenza Research and Early-warning (CASCIRE), CAS-TWAS Center of Excellence for Emerging Infectious Disease (CEEID), Chinese Academy of Sciences – sequence: 14 givenname: Yuhuan surname: Gong fullname: Gong, Yuhuan organization: Institutes of Physical Science and Information Technology, Anhui University – sequence: 15 givenname: Yuhai orcidid: 0000-0002-5595-363X surname: Bi fullname: Bi, Yuhai organization: Center for Influenza Research and Early-warning (CASCIRE), CAS-TWAS Center of Excellence for Emerging Infectious Disease (CEEID), Chinese Academy of Sciences – sequence: 16 givenname: Yi surname: Shi fullname: Shi, Yi organization: Center for Influenza Research and Early-warning (CASCIRE), CAS-TWAS Center of Excellence for Emerging Infectious Disease (CEEID), Chinese Academy of Sciences – sequence: 17 givenname: Zhu surname: Chen fullname: Chen, Zhu organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases – sequence: 18 givenname: Lianpan surname: Dai fullname: Dai, Lianpan organization: Center for Influenza Research and Early-warning (CASCIRE), CAS-TWAS Center of Excellence for Emerging Infectious Disease (CEEID), Chinese Academy of Sciences – sequence: 19 givenname: Jun surname: Wang fullname: Wang, Jun email: ypenghuiamms@hotmail.com organization: Center for Influenza Research and Early-warning (CASCIRE), CAS-TWAS Center of Excellence for Emerging Infectious Disease (CEEID), Chinese Academy of Sciences – sequence: 20 givenname: Penghui surname: Yang fullname: Yang, Penghui email: junwang@im.ac.cn organization: Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33678150$$D View this record in MEDLINE/PubMed |
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Keywords | COVID-19 virome bacteriome genetic mutation dysbiosis |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Jiabao Cao, Cheng Wang, Yuqing Zhang and Guanglin Lei contributed equally to this manuscript. |
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Title | Integrated gut virome and bacteriome dynamics in COVID-19 patients |
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