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1.
J Zhejiang Univ Sci B ; 21(5): 343-360, 2020 May.
Article in English | MEDLINE | ID: covidwho-1352746

ABSTRACT

Pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection emerged in Wuhan City, Hubei Province, China in December 2019. By Feb. 11, 2020, the World Health Organization (WHO) officially named the disease resulting from infection with SARS-CoV-2 as coronavirus disease 2019 (COVID-19). COVID-19 represents a spectrum of clinical manifestations that typically include fever, dry cough, and fatigue, often with pulmonary involvement. SARS-CoV-2 is highly contagious and most individuals within the population at large are susceptible to infection. Wild animal hosts and infected patients are currently the main sources of disease which is transmitted via respiratory droplets and direct contact. Since the outbreak, the Chinese government and scientific community have acted rapidly to identify the causative agent and promptly shared the viral gene sequence, and have carried out measures to contain the epidemic. Meanwhile, recent research has revealed critical aspects of SARS-CoV-2 biology and disease pathogenesis; other studies have focused on epidemiology, clinical features, diagnosis, management, as well as drug and vaccine development. This review aims to summarize the latest research findings and to provide expert consensus. We will also share ongoing efforts and experience in China, which may provide insight on how to contain the epidemic and improve our understanding of this emerging infectious disease, together with updated guidance for prevention, control, and critical management of this pandemic.


Subject(s)
Betacoronavirus/genetics , Coronavirus Infections/epidemiology , Pneumonia, Viral/epidemiology , Amino Acid Motifs , Animals , Antiviral Agents , COVID-19 , COVID-19 Vaccines , China/epidemiology , Communicable Disease Control/methods , Coronavirus Infections/diagnosis , Coronavirus Infections/physiopathology , Coronavirus Infections/prevention & control , Coronavirus Infections/therapy , Humans , Immunization, Passive , Medicine, Chinese Traditional , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/physiopathology , Pneumonia, Viral/therapy , Protein Domains , SARS-CoV-2 , Spike Glycoprotein, Coronavirus/chemistry , Viral Vaccines
2.
Front Immunol ; 12: 708184, 2021.
Article in English | MEDLINE | ID: covidwho-1346403

ABSTRACT

There is a worldwide pandemic of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; yet our understanding remains limited on the characteristic of antibodies, especially for dynamic long-term tracking. Sequential serum samples were collected up to 416 days post onset of symptoms (POS) from 102 patients who were hospitalized with coronavirus disease 2019 (COVID-19). Immunoglobulin (Ig)G, IgM, and IgA levels targeting SARS-CoV-2 spike 1 receptor-binding domain (S1-RBD), spike 2 extracellular domain (S2-ECD), and nucleocapsid protein (N) were quantified as well as neutralizing activity. We were pleasantly surprised to find that the antibody remained detective and effective for more than a year POS. We also found the varied reactions of different antibodies as time passed: N-IgA rose most rapidly in the early stage of infection, while S2-IgG was present at a high level in the long time of observation. This study described the long traceable antibody response of the COVID-19 and offered hints about targets to screen for postinfectious immunity and for vaccination development of SARS-CoV-2.


Subject(s)
Antibodies, Neutralizing/blood , Antibodies, Viral/blood , COVID-19/immunology , SARS-CoV-2/immunology , Aged , Antibodies, Neutralizing/immunology , Antibodies, Viral/immunology , COVID-19/diagnosis , Coronavirus Nucleocapsid Proteins/immunology , Female , Follow-Up Studies , Hospitalization , Humans , Immunoglobulin Isotypes/blood , Immunoglobulin Isotypes/immunology , Kinetics , Male , Middle Aged , Models, Theoretical , Phosphoproteins/immunology , Protein Domains/immunology , SARS-CoV-2/isolation & purification , Seroconversion , Spike Glycoprotein, Coronavirus/immunology
3.
J Cardiothorac Vasc Anesth ; 2020 Oct 08.
Article in English | MEDLINE | ID: covidwho-1292184

ABSTRACT

OBJECTIVE: The authors aimed to explore whether tricuspid annular plane systolic excursion (TAPSE) and right ventricular outflow fractional shortening (RVOT-FS) were associated with long-term prognosis in mechanically ventilated septic patients. DESIGN: A prospective observational study. SETTING: A tertiary hospital intensive care unit (ICU). PARTICIPANTS: One hundred eighty-one septic patients who were on mechanical ventilation. INTERVENTIONS: Echocardiography was performed within 24 hours of ICU admission. MEASUREMENTS AND MAIN RESULTS: Several echocardiographic parameters, including TAPSE and RVOT-FS, as well as prognostic information, were collected. A Cox regression survival analysis showed that TAPSE was independently associated with one-year all-cause mortality (hazard ratio [HR] 0.407, 95% confidence interval [CI]: 0.200-0.827, p = 0.013), but ROVT-FS was not (HR 0.997, 95% CI: 0.970-1.025, p = 0.828). ROC analysis showed that the optimal cutoff value for TAPSE and RVOT-FS to determine one-year mortality was TAPSE <18 mm and RVOT-FS <40%. The one-year mortality in patients with low TAPSE (n = 88) and in patients with both low TAPSE and low RVOT-FS (n = 60) was 45.5% and 48.3%, respectively; p = 0.724. In a multivariate analysis, RVOT-FS did not add significant prognostic information to that provided by TAPSE <18 mm (p = 0.197). CONCLUSIONS: TAPSE was an independent predictor of one-year all-cause mortality in mechanically ventilated septic patients. RVOT-FS was not associated with one-year mortality and added no prognostic value to TAPSE in these patients.

4.
J Proteome Res ; 20(7): 3463-3474, 2021 07 02.
Article in English | MEDLINE | ID: covidwho-1253876

ABSTRACT

The COVID-19 pandemic has become a worldwide health crisis. So far, most studies have focused on the epidemiology and pathogenesis of this infectious disease. Little attention has been given to the disease sequelae in patients recovering from COVID-19, and nothing is known about the mechanisms underlying these sequelae. Herein, we profiled the serum proteome of a cohort of COVID-19 patients in the disease onset and recovery stages. Based on the close integration of our proteomic analysis with clinical data, we propose that COVID-19 is associated with prolonged disorders in cholesterol metabolism and myocardium, even in the recovery stage. We identify potential biomarkers for these disorders. Moreover, severely affected patients presented more serious disturbances in these pathways. Our findings potentially support clinical decision-making to improve the prognosis and treatment of patients.


Subject(s)
COVID-19 , Proteomics , Cholesterol , Humans , Myocardium , Pandemics , Proteome , SARS-CoV-2
5.
Nat Immunol ; 22(7): 829-838, 2021 07.
Article in English | MEDLINE | ID: covidwho-1220263

ABSTRACT

The innate immune response is critical for recognizing and controlling infections through the release of cytokines and chemokines. However, severe pathology during some infections, including SARS-CoV-2, is driven by hyperactive cytokine release, or a cytokine storm. The innate sensors that activate production of proinflammatory cytokines and chemokines during COVID-19 remain poorly characterized. In the present study, we show that both TLR2 and MYD88 expression were associated with COVID-19 disease severity. Mechanistically, TLR2 and Myd88 were required for ß-coronavirus-induced inflammatory responses, and TLR2-dependent signaling induced the production of proinflammatory cytokines during coronavirus infection independent of viral entry. TLR2 sensed the SARS-CoV-2 envelope protein as its ligand. In addition, blocking TLR2 signaling in vivo provided protection against the pathogenesis of SARS-CoV-2 infection. Overall, our study provides a critical understanding of the molecular mechanism of ß-coronavirus sensing and inflammatory cytokine production, which opens new avenues for therapeutic strategies to counteract the ongoing COVID-19 pandemic.


Subject(s)
COVID-19/immunology , Coronavirus Envelope Proteins/metabolism , Cytokine Release Syndrome/immunology , SARS-CoV-2/immunology , Toll-Like Receptor 2/metabolism , Animals , COVID-19/complications , COVID-19/diagnosis , COVID-19/drug therapy , COVID-19/virology , Chlorocebus aethiops , Cytokine Release Syndrome/diagnosis , Cytokines/metabolism , Disease Models, Animal , Female , Gene Expression Profiling , Humans , Immunity, Innate/drug effects , Leukocytes, Mononuclear , Macrophages , Male , Mice , Mice, Knockout , Myeloid Differentiation Factor 88/genetics , Myeloid Differentiation Factor 88/metabolism , Primary Cell Culture , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Severity of Illness Index , Signal Transduction/drug effects , Signal Transduction/genetics , Signal Transduction/immunology , Toll-Like Receptor 2/antagonists & inhibitors , Toll-Like Receptor 2/genetics , Vero Cells
6.
Cell ; 184(1): 149-168.e17, 2021 01 07.
Article in English | MEDLINE | ID: covidwho-1064910

ABSTRACT

COVID-19 is characterized by excessive production of pro-inflammatory cytokines and acute lung damage associated with patient mortality. While multiple inflammatory cytokines are produced by innate immune cells during SARS-CoV-2 infection, we found that only the combination of TNF-α and IFN-γ induced inflammatory cell death characterized by inflammatory cell death, PANoptosis. Mechanistically, TNF-α and IFN-γ co-treatment activated the JAK/STAT1/IRF1 axis, inducing nitric oxide production and driving caspase-8/FADD-mediated PANoptosis. TNF-α and IFN-γ caused a lethal cytokine shock in mice that mirrors the tissue damage and inflammation of COVID-19, and inhibiting PANoptosis protected mice from this pathology and death. Furthermore, treating with neutralizing antibodies against TNF-α and IFN-γ protected mice from mortality during SARS-CoV-2 infection, sepsis, hemophagocytic lymphohistiocytosis, and cytokine shock. Collectively, our findings suggest that blocking the cytokine-mediated inflammatory cell death signaling pathway identified here may benefit patients with COVID-19 or other infectious and autoinflammatory diseases by limiting tissue damage/inflammation.


Subject(s)
COVID-19/immunology , COVID-19/pathology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/pathology , Interferon-gamma/immunology , Tumor Necrosis Factor-alpha/immunology , Animals , Antibodies, Neutralizing/administration & dosage , Cell Death , Disease Models, Animal , Female , Human Umbilical Vein Endothelial Cells , Humans , Inflammation/immunology , Inflammation/pathology , Lymphohistiocytosis, Hemophagocytic/chemically induced , Male , Mice , Mice, Transgenic , THP-1 Cells
7.
Preprint | SciFinder | ID: ppcovidwho-5396

ABSTRACT

A review. New coronavirus (Dec. 19-nCoV) from Dec. 2019, The pneumonia epidemic has gradually developed. With the effective implementation of a series of preventive control and medical treatment measures taken by China, the current upward trend in the country's epidemic has been suppressed to a certain extent. However, there are still many cases of resurgence, overseas imports, and virus resident. Risks: In clin. practice of general surgery in China, laparoscopic minimally invasive surgery currently accounts for more than 50% of the total operation volume Therefore, during and after the outbreak, laparoscopic surgery and related clin. diagnosis and treatment, perioperative management It has withstood a huge test. The Laparoscopy and Endoscopy Surgery Group of the Surgery Branch of the Chinese Medical Association based on the "New Coronavirus Pneumonia Diagnosis and Treatment Program (Trial Seventh Edition)" issued by the General Office of the National Health and Health Commission Viral pneumonia prevention and control plan (Fifth Edition) [2], combined with the relevant characteristics of clin. practice in laparoscopic surgery, invited some domestic experts to discuss and develop this consensus for the current and post-epidemic surgeries to carry out laparoscopic surgery Related clin. work as a reference

8.
Chinese Journal of Dermatovenereology ; 34(5):500-503, 2020.
Article in Chinese | GIM | ID: covidwho-958860

ABSTRACT

The novel coronavirus pneumonia outbreak was seriously and showed a rapid spread of the transmission on December 2019. All parts of the country have been actively raising medical resources and methodically preventing and controlling the epidemic. In this particular situation, the control and follow-up of patients with chronic skin conditions, especially psoriasis patients need constant guidance and treatment. In addition, most patients have impaired skin barrier function, and the improper protection may increase susceptibility to the virus. Due to the need of prevention and control, travel restrictions initiative increased the mental tension, and the anxiety, depression and other psychological reactions from the psoriasis may further produce emotional tension and thus aggravate the disease. Therefore, guidance of uninterrupted effective treatment, establishing a good state of mind, maintaining patients' personal health and treatment, and improving the quality of life are important under the special occasion.

9.
bioRxiv ; 2020 Nov 13.
Article in English | MEDLINE | ID: covidwho-915984

ABSTRACT

The COVID-19 pandemic has caused significant morbidity and mortality. Currently, there is a critical shortage of proven treatment options and an urgent need to understand the pathogenesis of multi-organ failure and lung damage. Cytokine storm is associated with severe inflammation and organ damage during COVID-19. However, a detailed molecular pathway defining this cytokine storm is lacking, and gaining mechanistic understanding of how SARS-CoV-2 elicits a hyperactive inflammatory response is critical to develop effective therapeutics. Of the multiple inflammatory cytokines produced by innate immune cells during SARS-CoV-2 infection, we found that the combined production of TNF-α and IFN-γ specifically induced inflammatory cell death, PANoptosis, characterized by gasdermin-mediated pyroptosis, caspase-8-mediated apoptosis, and MLKL-mediated necroptosis. Deletion of pyroptosis, apoptosis, or necroptosis mediators individually was not sufficient to protect against cell death. However, cells deficient in both RIPK3 and caspase-8 or RIPK3 and FADD were resistant to this cell death. Mechanistically, the JAK/STAT1/IRF1 axis activated by TNF-α and IFN-γ co-treatment induced iNOS for the production of nitric oxide. Pharmacological and genetic deletion of this pathway inhibited pyroptosis, apoptosis, and necroptosis in macrophages. Moreover, inhibition of PANoptosis protected mice from TNF-α and IFN-γ-induced lethal cytokine shock that mirrors the pathological symptoms of COVID-19. In vivo neutralization of both TNF-α and IFN-γ in multiple disease models associated with cytokine storm showed that this treatment provided substantial protection against not only SARS-CoV-2 infection, but also sepsis, hemophagocytic lymphohistiocytosis, and cytokine shock models, demonstrating the broad physiological relevance of this mechanism. Collectively, our findings suggest that blocking the cytokine-mediated inflammatory cell death signaling pathway identified here may benefit patients with COVID-19 or other cytokine storm-driven syndromes by limiting inflammation and tissue damage. The findings also provide a molecular and mechanistic description for the term cytokine storm. Additionally, these results open new avenues for the treatment of other infectious and autoinflammatory diseases and cancers where TNF-α and IFN-γ synergism play key pathological roles.

10.
Cell Discov ; 6(1): 76, 2020 Oct 29.
Article in English | MEDLINE | ID: covidwho-904771

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread globally with more than 33 million patients diagnosed, taking more than a million lives. Abundant mutations were observed but the functional consequences of these mutations are largely unknown. We report the mutation spectrum, replication dynamics, and infectivity of 11 patient-derived viral isolates in diverse cell lines, including the human lung cancer cell line Calu-3. We observed 46 mutations, including 9 different mutations in the spike gene. Importantly, these viral isolates show significant and consistent variations in replication dynamics and infectivity in tested cell lines, up to a 1500-fold difference in viral titers at 24 h after infecting Calu-3 cells. Moreover, we show that the variations in viral titers among viral isolates are positively correlated with blood clotting function but inversely correlated with the amount of red blood cell and hemoglobin in patients. Therefore, we provide direct evidence that naturally occurring mutations in SARS-CoV-2 can substantially change its replication dynamics and infectivity in diverse human cell lines, with clinical implications in vivo.

11.
Signal Transduct Target Ther ; 5(1): 237, 2020 10 13.
Article in English | MEDLINE | ID: covidwho-867546

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an emerging virus that is highly pathogenic and has caused the recent worldwide pandemic officially named coronavirus disease (COVID-19). Currently, considerable efforts have been put into developing effective and safe drugs and vaccines against SARS-CoV-2. Vaccines, such as inactivated vaccines, nucleic acid-based vaccines, and vector vaccines, have already entered clinical trials. In this review, we provide an overview of the experimental and clinical data obtained from recent SARS-CoV-2 vaccines trials, and highlight certain potential safety issues that require consideration when developing vaccines. Furthermore, we summarize several strategies utilized in the development of vaccines against other infectious viruses, such as severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), with the aim of aiding in the design of effective therapeutic approaches against SARS-CoV-2.


Subject(s)
Antibodies, Viral/biosynthesis , Coronavirus Infections/prevention & control , Pandemics/prevention & control , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/prevention & control , Receptors, Virus/genetics , Viral Vaccines/biosynthesis , Angiotensin-Converting Enzyme 2 , Betacoronavirus/drug effects , Betacoronavirus/immunology , Betacoronavirus/pathogenicity , COVID-19 , COVID-19 Vaccines , Clinical Trials as Topic , Coronavirus Infections/immunology , Coronavirus Infections/virology , Gene Expression Regulation/drug effects , Humans , Immunity, Innate/drug effects , Immunization Schedule , Immunogenicity, Vaccine , Middle East Respiratory Syndrome Coronavirus/drug effects , Middle East Respiratory Syndrome Coronavirus/immunology , Middle East Respiratory Syndrome Coronavirus/pathogenicity , Patient Safety , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , Protein Binding , Receptors, Virus/antagonists & inhibitors , Receptors, Virus/metabolism , SARS Virus/drug effects , SARS Virus/immunology , SARS Virus/pathogenicity , SARS-CoV-2 , Severe Acute Respiratory Syndrome/immunology , Severe Acute Respiratory Syndrome/prevention & control , Severe Acute Respiratory Syndrome/virology , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/metabolism , Vaccines, Attenuated , Vaccines, DNA , Vaccines, Subunit , Vaccines, Virus-Like Particle , Viral Vaccines/administration & dosage
12.
Infect Genet Evol ; 82: 104286, 2020 08.
Article in English | MEDLINE | ID: covidwho-826349

ABSTRACT

Bufavirus (BuV) can infect a variety of hosts, including human, bats, rats, dog, swine and shrew species and are suggested related to diarrhea disease. Porcine bufaviruses (PoBuV) were first detected in Hungarian pig farms in 2016. To determine the prevalence and genetic diversity of PoBuV in China, we developed SYBR Green-based real-time PCR assays to detect PoBuV in Guangxi pigs. Real-time PCR detected PoBuV in 30 (29.13%, 30/103) of the samples with diarrhoeal intestinal tissues and rectal swabs. PoBuV-positive intestinal tissues and rectal swabs samples, co-infection with PEDV (15/30, 50.0%), followed by PDCoV (8/30, 26.67%), PoRV (6/30, 20.0%), PRRSV (5/30, 16.67%), and PCV2 (3/30, 10.0%) were observed. Fourteen complete genomes were cloned and sequenced. The results showed that they were 4189 bp in length and combined three open reading frames (ORFs) in the order 5'-NS1-VP1/VP2-3'. Fourteen strains shared 96.5%-99.8% identity among themselves and 92.7%-97.9% with the PoBuV reference sequences. Phylogenetic analysis based on the deduced amino acid sequence of the VP2 gene showed fourteen strains belonging to PoBuV and were grouped into the three branches. These results help to provide new insight into the molecular epidemiology of PoBuV in the world.


Subject(s)
Parvovirinae/genetics , Phylogeny , Swine Diseases/virology , Animals , China/epidemiology , Diarrhea/epidemiology , Diarrhea/veterinary , Diarrhea/virology , Genome, Viral , Genomics , Molecular Epidemiology , Parvovirinae/isolation & purification , Real-Time Polymerase Chain Reaction/methods , Swine , Swine Diseases/epidemiology
13.
J Biol Chem ; 295(41): 14040-14052, 2020 10 09.
Article in English | MEDLINE | ID: covidwho-704089

ABSTRACT

Coronaviruses have caused several zoonotic infections in the past two decades, leading to significant morbidity and mortality globally. Balanced regulation of cell death and inflammatory immune responses is essential to promote protection against coronavirus infection; however, the underlying mechanisms that control these processes remain to be resolved. Here we demonstrate that infection with the murine coronavirus mouse hepatitis virus (MHV) activated the NLRP3 inflammasome and inflammatory cell death in the form of PANoptosis. Deleting NLRP3 inflammasome components or the downstream cell death executioner gasdermin D (GSDMD) led to an initial reduction in cell death followed by a robust increase in the incidence of caspase-8- and receptor-interacting serine/threonine-protein kinase 3 (RIPK3)-mediated inflammatory cell deathafter coronavirus infection. Additionally, loss of GSDMD promoted robust NLRP3 inflammasome activation. Moreover, the amounts of some cytokines released during coronavirus infection were significantly altered in the absence of GSDMD. Altogether, our findings show that inflammatory cell death, PANoptosis, is induced by coronavirus infection and that impaired NLRP3 inflammasome function or pyroptosis can lead to negative consequences for the host. These findings may have important implications for studies of coronavirus-induced disease.


Subject(s)
Caspase 8/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Pyroptosis , Receptor-Interacting Protein Serine-Threonine Kinases/metabolism , Animals , Cells, Cultured , Coronavirus/physiology , Coronavirus Infections/metabolism , Coronavirus Infections/pathology , Coronavirus Infections/veterinary , Cytokines/metabolism , Inflammasomes/metabolism , Intracellular Signaling Peptides and Proteins/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Macrophages/cytology , Macrophages/metabolism , Macrophages/virology , Mice , Mice, Inbred C57BL , Mice, Knockout , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , Necroptosis , Phosphate-Binding Proteins/genetics , Phosphate-Binding Proteins/metabolism
14.
Gastroenterol Rep (Oxf) ; 8(3): 167-174, 2020 Jun.
Article in English | MEDLINE | ID: covidwho-632301

ABSTRACT

Novel coronavirus disease-2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an ongoing public-health pandemic worldwide. Although SARS-CoV-2 has been known to spread primarily through respiratory droplets, recent evidence also supports fecal/oral as an additional route of transmission, raising concerns over gastrointestinal (GI) transmission of the infection. Herein, we, as the front-line Chinese GI surgeons, would like to share our experience and lessons in the combat against COVID-19. It is essential to create science-based, rational, and practical strategies during the outbreak of COVID-19. Here, we provide multi-institutional consensus on minimizing disease transmission while continuing to provide care from all aspects for patients in GI surgery, including outpatient clinics, inpatient units, gastrointestinal endoscopy centers, and adjustments in perioperative care. Our experiences and recommendations are worth sharing and may help to establish specific infection-control and outcome measures.

16.
Virus Res ; 278: 197869, 2020 03.
Article in English | MEDLINE | ID: covidwho-2388

ABSTRACT

Porcine deltacoronavirus (PDCoV) is the etiological agent of acute diarrhoea and vomiting in pigs, threatening the swine industry worldwide. Although several PDCoV studies have been conducted in China, more sequence information is needed to understand the molecular characterization of PDCoV. In this study, the partial ORF1a, spike protein (S) and nucleocapsid protein (N) were sequenced from Shandong Province between 2017 and 2018. The sequencing results for the S protein from 10 PDCoV strains showed 96.7 %-99.7 % nucleotide sequence identity with the China lineage strains, while sharing a lower level of nucleotide sequence identity, ranging from 95.7 to 96.8%, with the Vietnam/Laos/Thailand lineage strains. N protein sequencing analysis showed that these strains showed nucleotide homologies of 97.3%-99.3% with the reference strains. Phylogenetic analyses based on S protein sequences showed that these PDCoV strains were classified into the China lineage. The discontinuous 2 + 3 aa deletions at 400-401 and 758-760 were found in the Nsp2 and Nsp3 coding region in five strains, respectively, with similar deletions having been identified in Vietnam, Thailand, and Laos. Three novel patterns of deletion were observed for the first time in the Nsp2 and Nsp3 regions. Importantly, those findings suggest that PDCoV may have undergone a high degree of variation since PDCoV was first detected in China.


Subject(s)
Coronavirus Infections/veterinary , Deltacoronavirus/classification , Deltacoronavirus/genetics , Genome, Viral , Phylogeny , Animals , China/epidemiology , Coronavirus Infections/epidemiology , Diarrhea/virology , Feces/virology , Gene Deletion , Prevalence , Swine , Swine Diseases/virology , Viral Proteins/genetics
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