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MeSH Disease

Human Phenotype

Transmission

Seroprevalence
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    Stepwise anti-inflammatory and anti-SARS-CoV-2 effects following convalescent plasma SERO therapy with full clinical recovery

    Authors: Aurelia Zimmerli; Matteo Monti; Craig Fenwick; Isabella Eckerle; Catherine Beigelman-Aubry; Celine Pellaton; Katia Jaton; Dominique Dumas; Gian-Marco Stamm; Laura Infanti; Heidrun Andreu-Ullrich; Daphne Germann; Marie Mean; Peter Vollenweider; Raphael Stadelmann; Maura Prella; Denis Comte; Benoit Guery; David Gachoud; Nathalie Rufer

    doi:10.21203/rs.3.rs-76799/v1 Date: 2020-09-12 Source: ResearchSquare

    Convalescent plasma SERO to treat coronavirus disease MESHD 2019 (COVID-19) is currently the focus of numerous clinical trials worldwide, but the criteria of treatment efficacy remain largely unknown. Here, we describe a severely immunosuppressed patient following rituximab and chemotherapy for chronic lymphoid leukemia HP lymphoid leukemia MESHD, who became infected by SARS-CoV-2. His prolonged viral disease was successfully cured after four cycles of convalescent plasma SERO. Its immunomodulatory properties led to the rapid improvement of inflammation MESHD, pneumonia HP pneumonia MESHD and blood SERO cell counts, already after the first cycle. Importantly, the cumulative increase in anti- SARS-CoV-2 neutralizing antibodies SERO following each plasma SERO transfusion was associated to progressive viral clearance, resulting in clinical recovery from infection. Our data provide insight into the different modes of action of plasma SERO components. Understanding the underlying mechanisms will help to optimize the treatment of COVID-19 patients.

    Tracheal tube obstruction MESHD due to hemoptysis HP associated with pulmonary infarction MESHD in a patient with severe COVID-19 pneumonia HP pneumonia MESHD: A case report.

    Authors: Takaaki Maruhashi; Yutaro Kurihara; Tatsuhiko Wada; Mayuko Osada; Marina Oi; Tomonari Masuda; Kunihiro Yamaoka; Yasushi Asari

    doi:10.21203/rs.3.rs-75925/v1 Date: 2020-09-11 Source: ResearchSquare

    Background: The incidence of thrombotic complications MESHD is extremely high among severe coronavirus disease MESHD 2019(COVID-19) patients in the intensive care unit. Various factors such as a cytokine storm due to an excessive immune response to inflammation MESHD, hypoxemia HP hypoxemia MESHD, and disseminated intravascular coagulation HP intravascular coagulation MESHD are considered predisposing factors for thrombotic complications MESHD.Case presentation: A 55-year-old Japanese man intubated 8 days previously was referred to our hospital because of a severe COVID-19 pneumonia HP pneumonia MESHD diagnosis after his pharyngeal swab tested positive for severe acute respiratory syndrome MESHD coronavirus 2 using reverse transcription-polymerase chain reaction. The patient continued to remain hypoxic (PaO2/FiO2 ratio <100 mmHg) at the referring hospital. On admission, we initiated veno-venous extracorporeal membrane oxygenation (VV-ECMO). Unfractionated heparin and nafamostat mesylate were used as anticoagulants during VV-ECMO. Despite the adequate anticoagulant therapy, he developed pulmonary infarction MESHD due to pulmonary embolism HP pulmonary embolism MESHD followed by hemoptysis HP. On day 10 following admission, his oxygen saturation dropped from 95% to 88%, with a marked decrease in his ventilator tidal volume, accompanied by an inability to ventilate the patient. Thereafter, we increased the VV-ECMO flow and exchanged his endotracheal tube. The lumen of the removed tracheal tube was found to be occluded by a large-sized blood SERO coagulum. There was no further episode of tube occlusion MESHD. The patient was discharged in a walkable state on day 39 following admission. Conclusions: Endotracheal tube obstruction MESHD secondary to hemoptysis HP should be suggested in patients with COVID-19 requiring ventilator support, as they are not able to perform frequent endotracheal tube suctions owing to the risk of infection TRANS risk of infection TRANS infection MESHD.

    Gastrointestinal involvement attenuates COVID-19 severity and mortality

    Authors: Alexandra E Livanos; Divya Jha; Francesca Cossarini; Ana S Gonzalez-Reiche; Minami Tokuyama; Teresa Aydillo; Tommaso L Parigi; Irene Ramos; Katie Dunleavy; Brian Lee; Rebekah Dixon; Steven T Chen; Gustavo Martinez-Delgado; Satish Nagula; Huaibin M Ko; Jason Reidy; Steven Naymagon; Ari Grinspan; Jawad Ahmad; Michael Tankelevich; Ronald Gordon; Keshav Sharma; Graham J Britton; Alice Chen-Liaw; Matthew P Spindler; Tamar Plitt; Pei Wang; Andrea Cerutti; Jeremiah J Faith; Jean-Frederic Colombel; Ephraim Kenigsberg; Carmen Argmann; Miriam Merad; Sacha Gnjatic; Noam Harpaz; Silvio Danese; Adeeb Rahman; Nikhil A Kumta; Alessio Aghemo; Francesca Petralia; Harm van Bakel; Adolfo Garcia-Sastre; Saurabh Mehandru

    doi:10.1101/2020.09.07.20187666 Date: 2020-09-09 Source: medRxiv

    Given that gastrointestinal ( GI MESHD) symptoms are a prominent extrapulmonary manifestation of coronavirus disease MESHD 2019 (COVID-19), we investigated the impact of GI infection MESHD on disease pathogenesis in three large cohorts of patients in the United States and Europe. Unexpectedly, we observed that GI involvement MESHD was associated with a significant reduction in disease severity and mortality, with an accompanying reduction in key inflammatory proteins including IL-6, CXCL8, IL-17A and CCL28 in circulation. In a fourth cohort of COVID-19 patients in which GI MESHD biopsies were obtained, we identified severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2) within small intestinal enterocytes for the first time in vivo but failed to obtain culturable virus. High dimensional analyses of GI MESHD tissues confirmed low levels of cellular inflammation MESHD in the GI lamina propria MESHD and an active downregulation of key inflammatory genes including IFNG, CXCL8, CXCL2 and IL1B among others. These data draw attention to organ-level heterogeneity in disease pathogenesis and highlight the role of the GI MESHD tract in attenuating SARS-CoV-2-associated inflammation MESHD with related mortality benefit.

    Small molecules inhibit SARS-COV-2 induced aberrant inflammation MESHD and viral replication in mice by targeting S100A8/A9-TLR4 axis

    Authors: Qirui Guo; Yingchi Zhao; Junhong Li; Jiangning Liu; Chuan Qin; Xiangxi Wang; Fuping You; Xuefei Guo; Zeming Zhang; Lili Cao; Yujie Luo; Xiao Wang; Xuemei Wei; Luoying Chen; Linlin Bao; Wei Deng; Hua Zhu; Ran Gao; Ilayda Tolu; Esra Ayan; Busra Yuksel; Ayse Buket Peksen; Oktay Gocenler; Ali Doga Yucel; Ozgur Can; Serena Ozabrahamyan; Alpsu Olkan; Ece Erdemoglu; Fulya Aksit; Gokhan Haci Tanisali; Oleksandr M. Yefanov; Anton Barty; Alexandra Tolstikova; Gihan K. Ketawala; Sabine Botha; E. Han Dao; Brandon Hayes; Mengning Liang; Matthew H Seaberg; Mark S. Hunter; Alex Batyuk; Valerio Mariani; Zhen Su; Frederic Poitevin; Chun Hong Yoon; Christopher J. Kupitz; Raymond G. Sierra; Edward H Snell; Hasan DeMirci

    doi:10.1101/2020.09.09.288704 Date: 2020-09-09 Source: bioRxiv

    The SARS-CoV-2 pandemic poses an unprecedented public health crisis. Accumulating evidences suggest that SARS-CoV-2 infection MESHD causes dysregulation of immune HP system. However, the unique signature of early immune responses remains elusive. We characterized the transcriptome of rhesus macaques and mice infected with SARS-CoV-2. Alarmin S100A8 was robustly induced by SARS-CoV-2 in animal models as well as in COVID-19 patients. Paquinimod, a specific inhibitor of S100A8/A9, could reduce inflammatory response and rescue the pneumonia HP pneumonia MESHD with substantial reduction of viral titers in SASR-CoV-2 infected MESHD animals. Remarkably, Paquinimod treatment resulted in 100% survival of mice in a lethal model of mouse coronavirus (MHV) infection MESHD. A novel group of neutrophils that contributed to the uncontrolled inflammation MESHD and onset of COVID-19 were dramatically induced by coronavirus infections MESHD. Paquinimod treatment could reduce these neutrophils and regain antiviral responses, unveiling key roles of S100A8/A9 and noncanonical neutrophils in the pathogenesis of COVID-19, highlighting new opportunities for therapeutic intervention.

    Cytotoxic lymphocytes are dysregulated in multisystem inflammatory syndrome MESHD in children TRANS

    Authors: Noam D. Beckmann; Phillip H. Comella; Esther Cheng; Lauren Lepow; Aviva G. Beckmann; Konstantinos Mouskas; Nicole W. Simons; Gabriel E. Hoffman; Nancy J. Francoeur; Diane Marie Del Valle; Gurpawan Kang; Emily Moya; Lillian Wilkins; Jessica Le Berichel; Christie Chang; Robert Marvin; Sharlene Calorossi; Alona Lansky; Laura Walker; Nancy Yi; Alex Yu; Matthew Harnett; Melody Eaton; Sandra Hatem; Hajra Jamal; Alara Akyatan; Alexandra Tabachnikova; Lora E. Liharska; Liam Cotter; Brian Fennessey; Akhil Vaid; Guillermo Barturen; Scott R. Tyler; Hardik Shah; Yinh-chih Wang; Shwetha Hara Sridhar; Juan Soto; Swaroop Bose; Kent Madrid; Ethan Ellis; Elyze Merzier; Konstantinos Vlachos; Nataly Fishman; Manying Tin; Melissa Smith; Hui Xie; Manishkumar Patel; Kimberly Argueta; Jocelyn Harris; Neha Karekar; Craig Batchelor; Jose Lacunza; Mahlet Yishak; Kevin Tuballes; Leisha Scott; Arvind Kumar; Suraj Jaladanki; Ryan Thompson; Evan Clark; Bojan Losic; - The Mount Sinai COVID-19 Biobank Team; Jun Zhu; Wenhui Wang; Andrew Kasarskis; Benjamin S. Glicksberg; Girish Nadkarni; Dusan Bogunovic; Cordelia Elaiho; Sandeep Gangadharan; George Ofori-Amanfo; Kasey Alesso-Carra; Kenan Onel; Karen M. Wilson; Carmen Argmann; Marta E. Alarcón-Riquelme; Thomas U. Marron; Adeeb Rahman; Seunghee Kim-Schulze; Sacha Gnjatic; Bruce D. Gelb; Miriam Merad; Robert Sebra; Eric E. Schadt; Alexander W. Charney

    doi:10.1101/2020.08.29.20182899 Date: 2020-09-02 Source: medRxiv

    Multisystem inflammatory syndrome MESHD in children TRANS (MIS-C) presents with fever HP fever MESHD, inflammation MESHD and multiple organ involvement in individuals under 21 years following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD. To identify genes, pathways and cell types driving MIS-C, we sequenced the blood SERO transcriptomes of MIS-C cases, pediatric cases of coronavirus disease MESHD 2019, and healthy controls. We define a MIS-C transcriptional signature partially shared with the transcriptional response to SARS-CoV-2 infection MESHD and with the signature of Kawasaki disease MESHD, a clinically similar condition. By projecting the MIS-C signature onto a co-expression network, we identified disease gene modules and found genes downregulated in MIS-C clustered in a module enriched for the transcriptional signatures of exhausted CD8+ T-cells and CD56dimCD57+ NK cells. Bayesian network analyses revealed nine key regulators of this module, including TBX21, a central coordinator of exhausted CD8+ T-cell differentiation. Together, these findings suggest dysregulated cytotoxic lymphocyte response to SARS-Cov-2 infection in MIS-C.

    The Potential Role of Extracellular Vesicles in COVID-19 Associated Endothelial injury and Pro-inflammation MESHD

    Authors: Balaji Krishnamachary; Christine Cook; Leslie Spikes; Prabhakar Chalise; Navneet K Dhillon; Yuhang Pan; Tanakao Takana; Peiyu Xie; Zhaoguang Wang; Shuocen Liu; George Fu Gao; Guojun He; Maigeng Zhou

    doi:10.1101/2020.08.27.20182808 Date: 2020-09-01 Source: medRxiv

    COVID-19 infection caused by the novel severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2) has resulted in a global pandemic with the number of deaths growing exponentially. Early evidence points to significant endothelial dysfunction, micro-thromboses, pro- inflammation MESHD as well as a dysregulated immune response in the pathogenesis of this disease. In this study, we analyzed the cargo of EVs isolated from the plasma SERO of patients with COVID-19 for the identification of potential biomarkers of disease severity and to explore their role in disease pathogenesis. Plasma SERO-derived EVs were isolated from 53 hospitalized patients with COVID infection MESHD and compared according to the severity of the disease. Analysis of inflammatory and cardiovascular protein cargo of large EVs revealed significantly differentially expressed proteins for each disease sub-group. Notably, members of the TNF superfamily and IL-6 family were up-regulated in patients on oxygen support with severe and moderate disease. EVs from the severe group were also enhanced with pro- thrombotic MESHD/endothelial injury factors (TF, t-PA, vWF) and proteins associated with cardiovascular pathology (MB, PRSS8, REN, HGF). Significantly higher levels of TF, CD163, and EN-RAGE were observed in EVs from severe patients when compared to patients with a moderate disease requiring supplemental O2. Importantly, we also observed increased caspase 3/7 activity and decreased cell survival in human pulmonary microvascular endothelial cells exposed to EVs from the plasma SERO of patients with severe disease compared to healthy controls. In conclusion, our findings indicate alterations in pro-inflammatory, coagulopathy MESHD, and endothelial injury MESHD protein cargo in large EVs in response to SARS-CoV-2 infection MESHD that may be a causative agent in severe illness.

    Temporal Landscape of Human Gut RNA and DNA Viromes in SARS-CoV-2 Infection MESHD and Severity

    Authors: Tao Zuo; Qin Liu; Fen Zhang; Yun Kit Yeoh; Yating Wan; Hui Zhan; Grace C.Y. Lui; Amy Y.L. Li; Chun Pan Cheung; Nan Chen; Wenqi Lv; Rita W.Y. Ng; Eugene Y.K. Tso; Kitty S.C. Fung; Veronica Chan; Lowell Ling; Gavin Joynt; David S.C. Hui; Francis K.L. Chan; Paul K.S. Chan; Siew Ng

    doi:10.21203/rs.3.rs-66879/v1 Date: 2020-08-27 Source: ResearchSquare

    Background: Coronavirus Disease MESHD 2019 (COVID-19) caused by the enveloped RNA virus SARS-CoV-2 primarily affects the respiratory and gastrointestinal tracts. SARS-CoV-2 was isolated from faecal samples and active viral replication was reported in human intestinal cells. The human gut also harbors an enormous amount of resident viruses (collectively known as virome) that play a role in regulating host immunity and pathophysiology. Understanding gut virome perturbation that underlies SARS-CoV-2 infection MESHD and severity is an unmet need.Methods:We enrolled 98 COVID-19 patients with varying disease severity (3 asymptomatic TRANS, 53 mild, 34 moderate, 5 severe, 3 critical) and 78 non-COVID-19 controls matched for gender TRANS and co-morbidities. All study subjects had faecal specimens sampled at inclusion. Blood SERO specimens were sampled for COVID-19 patients at admission to test for inflammatory markers and white cell counts. Among COVID-19 cases, 37 (38%) patients had serially faecal samples collected 2 to 3 times per week from time of hospitalization until after discharge. Using shotgun metagenomics sequencing, we sequenced and profiled the faecal RNA and DNA virome respectively. We investigated alterations and longitudinal dynamics of the gut virome in association with disease severity and blood SERO parameters.Results: Patients with COVID-19 showed underrepresentation of Pepper mild mottle virus (RNA virus) and multiple bacteriophage lineages (DNA viruses) and enrichment of environment-derived eukaryotic DNA viruses in faecal samples, compared to non-COVID-19 subjects. Such gut virome dysbiosis MESHD persisted up to 30 days after disease resolution. Faecal virome in SARS-CoV-2 infection MESHD harboured more stress-, inflammation MESHD- and virulence-associated gene encoding capacities including those pertaining to bacteriophage integration, DNA repair, and metabolism and virulence associated with their bacterial host. Human faecal baseline abundance of 10 virus species (1 RNA virus, Pepper chlorotic spot virus, and 9 DNA virus species) inversely correlated with disease severity of COVID-19. These viruses were also inversely associated with blood SERO levels of pro-inflammatory proteins, white cells and neutrophils. Among the 10 COVID-19 severity-associated DNA virus species, 4 showed inverse correlation with age TRANS; 5 showed persistent lower abundance both during disease course and after disease resolution relative to non-COVID-19 subjects.Conclusions: Both enteric RNA and DNA viromes were perturbed in COVID-19, which prolonged even after disease resolution. Gut virome may calibrate host immunity and regulate severity to SARS-CoV-2 infection MESHD. Our observation that gut viruses inversely correlated with both severity of COVID-19 and host age TRANS partly explains that older subjects are prone to severe and unfavorable COVID-19 outcomes. Our data altogether highlight the significance of human gut virome in COVID-19 disease course and potentially therapeutics.

    Coronavirus Disease MESHD 2019 Induced Inflammatory Response are Associated with Changes in Lipid Profiles

    Authors: Chuanwei Li; Wen Zhang; Chunmei Xu; Hu Tan; Guoqiang Cao; Li Li; Qidi Sun; Gengze Wu; Mingdong Hu; Shuang Wu; Qi Li; Guansong Wang; Xiaohua Zhang; Chunyu Zeng

    doi:10.21203/rs.3.rs-64766/v1 Date: 2020-08-24 Source: ResearchSquare

    Background: Previous studies have found some evidence of association between changes in lipids and lipoprotein and viral pneumonia MESHD pneumonia HP. No data are available about the effect of coronavirus disease MESHD 2019 (Covid-19) on lipids. The aim of this study was to investigate the relationships between lipid profiles and inflammation MESHD markers among patients with Covid-19. Methods: In this retrospective analysis, Covid-19 patients in Jin-yin-tan Hospital and healthy individuals from Daping Hospital were enrolled. The clinical and biochemical characteristics of Covid-19 patients and healthy controls were compared. We correlated lipid parameters to disease severity and inflammatory markers. The severity of Covid-19 for all patients were stipulated according to the diagnostic and treatment guideline for Covid-19 issued by Chinese National Health Committee (the 7th edition).Results: A total of 242 Covid-19 patients and 242 sex- age TRANS matched controls were enrolled. Compared with controls, Covid-19 patients had lower lymphocyte counts as well as total cholesterol (TC), high density lipoprotein (HDL-c), low density lipoprotein cholesterol (LDL-c), non-high density lipoprotein cholesterol (non-HDL-c) and apoA-I levels on admission. Whereas apolipoprotein B (apoB) and apoB/apoA-I ratio were slightly higher in patients with Covid-19. There was no difference in lipid levels between the moderate and severe groups. The total lymphocytes were weakly positively associated with TC, LDL-c and apoA-I. Conclusion: Patients with Covid-19 are associated with decreased lipid and lipoprotein levels. Covid-19 infection MESHD induced inflammation MESHD response and cytokine storm were associated with a shift of lipids, lipoproteins toward a more atherogenic lipid profile.

    The involvement of Central Nervous System and sequence variability of Severe Adult Respiratory Syndrome MESHD Adult TRANS Respiratory Syndrome – Coronavirus-2 revealed in autopsy tissue samples: a case report.

    Authors: Lis Høy Marbjerg; Christina Jacobsen; Jannik Fonager; Claus Bøgelund; Morten Rasmussen; Anders Fomsgaard; Jytte Banner; Veronika Vorobieva Solholm Jensen

    doi:10.21203/rs.3.rs-61471/v1 Date: 2020-08-18 Source: ResearchSquare

    Background: The case presented here illustrates that interdisciplinary teamwork can be essential for the understanding of the COVID-19 disease presentation and enlightening of the pathophysiology. Case presentation: A 60-years-old overweight HP woman without any comorbidities was found dead in her apartment after 14 days of home isolation due to suspicion on the Coronavirus disease MESHD 2019 (COVID-19). She had reported symptoms of tachycardia HP tachycardia MESHD, fever HP fever MESHD, and increasing respiratory difficulty one day before her death MESHD. Due to the Danish legal act on sudden deaths a forensic autopsy was performed including a thorough examination and biosampling. The results of the forensic autopsy displayed sever densified, almost airless, firm lungs, and an unspecific reactive minimal focal perivascular inflammation MESHD consisting of macrophages of the brain tissue. The final diagnosis, COVID-19 with involvement of the central nervous system was established by use of the RT-RNA analysis on cerebrospinal fluid, as well as by serologic detection of the specific antibodies for SARS-CoV-2 SERO in cerebrospinal fluid and serum SERO. The genetic analysis displayed a 2 % variation between SARS-CoV-2 isolates recovered from the tracheal sample, cerebrospinal fluid, and tissues from both lungs.Conclusion: The combination of all available results revealed that the cause of death MESHD was COVID-19 with severe pulmonary disease MESHD and neuroinvasion, as well as renal affection resulting in hyponatremia HP hyponatremia MESHD. To our knowledge, it was not shown previously that neuroinvasion could be confirmed by the detection of specific antibodies for SARS-CoV-2 SERO and SARS-CoV-2 specific RNA in cerebrospinal fluid. This case supports hypotheses that SARS-CoV-2 may cause central nervous system infection MESHD. The genetic distinction between SARS-CoV-2 isolates was done by whole-genome sequencing, where the isolate recovered from the cerebrospinal fluid was the most different. 

    Analysis of the intestinal microbiota in COVID-19 patients and its correlation with the inflammatory factor IL-18 and SARS-CoV-2-specific IgA

    Authors: Wanyin Tao; Shu Zhu; Guorong Zhang; Xiaofang Wang; Meng Guo; Weihong Zeng; Zihao Xu; Lianxin Liu; Kaiguang Zhang; Yucai Wang; Xiaoling Ma; Zhengxu Chen; Tengchuan Jin; Jianping Weng; Rachel Vreeman; Joseph Masci; Nick A Maskell; Shaney Barratt

    doi:10.1101/2020.08.12.20173781 Date: 2020-08-14 Source: medRxiv

    The current global COVID-19 pandemic is caused by beta coronavirus Severe Acute Respiratory Syndrome Coronavirus-2 MESHD (SARS-CoV-2), which already infected over 10 million and caused 500 thousand deaths by June 2020. Overproduction of cytokines triggered by COVID-19 infection MESHD, known as "cytokine storm", is a highly risk factor associated with disease severity. However, how COVID-19 infection MESHD induce cytokine storm is still largely unknown. Accumulating in vitro and in vivo evidence suggests that gut is also susceptible to COVID19 infection MESHD: Human intestinal organoids, an in vitro model which mimic the specific cell type and spatial structure of the intestine, were susceptible to SARS-CoV2 infection MESHD; A significant fraction of patients reported gut symptoms; Viral RNA may persist for more than 30 days and infectious virus could be isolated in fecal samples. The gastrointestinal tract is the primary site of interaction between the host immune system with symbiotic and pathogenic microorganisms. The bacteria resident in our gastrointestinal tract, known as gut microbiota, is important to maintain the homeostasis of our immune system. While imbalance of gut microbiota, or dysbiosis MESHD, is associated with multiple inflammation diseases5 MESHD. It's possible that SARS-CoV-2 infection MESHD may lead to alternation of gut microbiota thus worsen the host symptom. IL-18 is a proinflammatory cytokine produced multiple enteric cells, including intestinal epithelial cells (IECs), immune cells as well as enteric nervous system, and was shown to increase in the serum SERO of COVID-19 patients. Immunoglobin A (IgA) is mainly produced in the mucosal surfaces, in humans 40-60mg kg-1 day-1 than all other immunoglobulin isotypes combined, and at least 80% of all plasma SERO cells are located in the intestinal lamina propria. Recent study showed that SARS-CoV-2 specific IgA in the serum SERO is positively correlate with the disease severity in COVID-19 patients11. Here we investigated the alterations of microbiota in COVID-19 patients, and its correlation with inflammatory factor IL-18 and SARS-CoV2 specific IgA.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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