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1.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-324208

ABSTRACT

To date, viral RNA detection is almost the only way to confirm SARS-CoV-2infectionin practice.However, variousreasons can cause low sensitivity for RNA detection, and thisposes aserious challenge to disease control. We tested the performance of detecting total antibody(Ab) and IgM levels in serum by the methods of chemiluminescence, enzyme-linked immunosorbent assay (ELISA), and colloidal golddetection. The datashowed that the sensitivity and specificity for detecting total Ab and IgM levels were high by all three methods, and the sensitivity was higher for detecting total Ab than for detecting IgM. Evidence from studieshas shown thatviral RNA testingcombinedwith serological testing could increase the diagnostic sensitivity while maintaining a high specificity. Specific serology testsfor SARS-CoV-2 havegreat value for clinical practice and public health.

2.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-319481

ABSTRACT

Background: A new disease called Coronavirus disease (COVID-19) related to SARS-CoV-2 has brought serious attacks to the world. It causes damage to multiple organ systems of the body include liver. Here we intend to shed light on the clinical features its mechanism related to liver damage which caused by COVID-19. Methods: Clinical records and laboratory results were obtained from 138 patients with laboratory-confirmed COVID-19 who were admitted to Tongji hospital, Wuhan, China from February 8, 2020 to February 18, 2020. Information on clinical features of patients with abnormal liver tests were collected for analysis. Results: Fifty-four (39.1%) and eighty-three (60.1%) patients had abnormal liver enzyme levels on admission and during the course of disease. Hepatocyte type was more common than cholestatic type abnormal. 24(17.4%) patients reached the liver injury standard in the course of disease. Patients with abnormal liver enzyme levels were more likely to be male, had higher levels of inflammation indicators, lower pulse oxygen saturation and lymphocyte count. There is a significantly higher proportion of abnormal liver enzymes levels in the patients which administrated antibiotics during hospitalization, compared with that in the ones without antibiotics therapy (56.6% vs 32.7%). Patients with liver injury was an independent predictor of a poor prognosis (p<0.0001, OR 7.774, 95%CI 2.674-22.599). Conclusions: Liver injury in COVID-19 patients was an independent predictor of a poor prognosis. The COVID-19-related abnormal liver enzymes levels may be considered as the result of secondary liver damage caused mainly by several factors. Hypoxia and disease severity account for the largest proportion.

3.
J Med Virol ; 93(3): 1378-1386, 2021 03.
Article in English | MEDLINE | ID: covidwho-1196511

ABSTRACT

Since December 2019, coronavirus disease (COVID-19) has rapidly swept the world. So far, more than 30 million people have been infected and nearly one million have died. Although the world is still in the stage of COVID-19 pandemic, the treatment of new cases and critically ill patients is the focus of the current work. However, COVID-19 patients lead to pulmonary fibrosis, such a serious threat to the prognosis of complications were also worthy of our attention. First of all, we proposed the possible mechanism of pulmonary fibrosis caused by SARS-CoV-2, based on the published data of COVID-19 ((i) Direct evidence: pulmonary fibrosis was found in autopsy and pulmonary puncture pathology. (ii) Indirect evidence: increased levels of fibrosis-related cytokines[transforming growth factor [TGF]- ß, tumor necrosis factor [TNF]- α, interleukin [IL]-6, etc] in peripheral blood of severe patients.) What is more, we summarized the role of three fibrosis-related signaling pathways (TGF- ß signal pathway, WNT signal pathway and YAP/TAZ signal pathway) in pulmonary fibrosis. Finally, we suggested the therapeutic value of two drugs (pirfenidone and nintedanib) for idiopathic pulmonary fibrosis in COVID-19-induced pulmonary fibrosis.


Subject(s)
COVID-19/complications , Indoles/therapeutic use , Pulmonary Fibrosis/drug therapy , Pulmonary Fibrosis/etiology , Pyridones/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19/metabolism , COVID-19/pathology , Humans , Lung/pathology , Patient Discharge , Pulmonary Fibrosis/metabolism , Pulmonary Fibrosis/pathology , Severity of Illness Index , Signal Transduction
4.
Infect Dis Poverty ; 10(1): 45, 2021 Mar 31.
Article in English | MEDLINE | ID: covidwho-1166939

ABSTRACT

BACKGROUND: The management of discharge COVID-19 patients with recurrent positive SARS-CoV-2 RNA is challenging. However, there are fewer scientific dissertations about the risk of recurrent positive. The aim of this study was to explore the relationship between SARS-COV-2 RNA positive duration (SPD) and the risk of recurrent positive. METHODS: This case-control multi-center study enrolled participants from 8 Chinese hospital including 411 participants (recurrent positive 241). Using unadjusted and multivariate-adjusted logistic regression analyses, generalized additive model with a smooth curve fitting, we evaluated the associations between SPD and risk of recurrent positive. Besides, subgroup analyses were performed to explore the potential interactions. RESULTS: Among recurrent positive patients, there were 121 females (50.2%), median age was 50 years old [interquartile range (IQR): 38-63]. In non-adjusted model and adjusted model, SPD was associated with an increased risk of recurrent positive (fully-adjusted model: OR = 1.05, 95% CI: 1.02-1.08, P = 0.001); the curve fitting was not significant (P = 0.286). Comparing with SPD < 14 days, the risk of recurrent positive in SPD > 28 days was risen substantially (OR = 3.09, 95% CI: 1.44-6.63, P = 0.004). Interaction and stratified analyses showed greater effect estimates of SPD and risk of recurrent positive in the hypertension, low monocyte count and percentage patients (P for interaction = 0.008, 0.002, 0.036, respectively). CONCLUSION: SPD was associated with a higher risk of recurrent positive and especially SPD > 28 day had a two-fold increase in the relative risk of re-positive as compared with SPD < 14 day. What's more, the risk may be higher among those with hypertension and lower monocyte count or percentage.


Subject(s)
COVID-19/virology , RNA, Viral/isolation & purification , SARS-CoV-2/isolation & purification , Adult , COVID-19/epidemiology , COVID-19/pathology , Case-Control Studies , Female , Hospitalization , Humans , Male , Middle Aged , Pharynx/virology , RNA, Viral/genetics , Recurrence , Risk Factors , SARS-CoV-2/genetics , Time Factors , Virus Shedding
5.
J Med Virol ; 93(3): 1378-1386, 2021 03.
Article in English | MEDLINE | ID: covidwho-891893

ABSTRACT

Since December 2019, coronavirus disease (COVID-19) has rapidly swept the world. So far, more than 30 million people have been infected and nearly one million have died. Although the world is still in the stage of COVID-19 pandemic, the treatment of new cases and critically ill patients is the focus of the current work. However, COVID-19 patients lead to pulmonary fibrosis, such a serious threat to the prognosis of complications were also worthy of our attention. First of all, we proposed the possible mechanism of pulmonary fibrosis caused by SARS-CoV-2, based on the published data of COVID-19 ((i) Direct evidence: pulmonary fibrosis was found in autopsy and pulmonary puncture pathology. (ii) Indirect evidence: increased levels of fibrosis-related cytokines[transforming growth factor [TGF]- ß, tumor necrosis factor [TNF]- α, interleukin [IL]-6, etc] in peripheral blood of severe patients.) What is more, we summarized the role of three fibrosis-related signaling pathways (TGF- ß signal pathway, WNT signal pathway and YAP/TAZ signal pathway) in pulmonary fibrosis. Finally, we suggested the therapeutic value of two drugs (pirfenidone and nintedanib) for idiopathic pulmonary fibrosis in COVID-19-induced pulmonary fibrosis.


Subject(s)
COVID-19/complications , Indoles/therapeutic use , Pulmonary Fibrosis/drug therapy , Pulmonary Fibrosis/etiology , Pyridones/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19/metabolism , COVID-19/pathology , Humans , Lung/pathology , Patient Discharge , Pulmonary Fibrosis/metabolism , Pulmonary Fibrosis/pathology , Severity of Illness Index , Signal Transduction
6.
J Med Virol ; 92(6): 556-563, 2020 06.
Article in English | MEDLINE | ID: covidwho-153833

ABSTRACT

In the past few decades, coronaviruses have risen as a global threat to public health. Currently, the outbreak of coronavirus disease-19 (COVID-19) from Wuhan caused a worldwide panic. There are no specific antiviral therapies for COVID-19. However, there are agents that were used during the severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) epidemics. We could learn from SARS and MERS. Lopinavir (LPV) is an effective agent that inhibits the protease activity of coronavirus. In this review, we discuss the literature on the efficacy of LPV in vitro and in vivo, especially in patients with SARS and MERS, so that we might clarify the potential for the use of LPV in patients with COVID-19.


Subject(s)
Antiviral Agents/therapeutic use , Coronavirus Infections/drug therapy , Lopinavir/therapeutic use , Pandemics , Pneumonia, Viral/drug therapy , Ritonavir/therapeutic use , Severe Acute Respiratory Syndrome/drug therapy , Animals , Betacoronavirus/drug effects , Betacoronavirus/enzymology , Betacoronavirus/pathogenicity , COVID-19 , Cell Line , Clinical Trials as Topic , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Coronavirus Infections/virology , Disease Models, Animal , Humans , Mice , Middle East Respiratory Syndrome Coronavirus/drug effects , Middle East Respiratory Syndrome Coronavirus/enzymology , Middle East Respiratory Syndrome Coronavirus/pathogenicity , Pneumonia, Viral/diagnosis , Pneumonia, Viral/epidemiology , Pneumonia, Viral/virology , SARS Virus/drug effects , SARS Virus/enzymology , SARS Virus/pathogenicity , SARS-CoV-2 , Severe Acute Respiratory Syndrome/diagnosis , Severe Acute Respiratory Syndrome/epidemiology , Severe Acute Respiratory Syndrome/virology , Treatment Outcome
8.
Int J Antimicrob Agents ; 55(5): 105954, 2020 May.
Article in English | MEDLINE | ID: covidwho-17680

ABSTRACT

Since December 2019, a viral pneumonia, named coronavirus disease 2019 (COVID-19), from Wuhan, China, has swept the world. Although the case fatality rate is not high, the number of people infected is large and there is still a large number of patients dying. With the collation and publication of more and more clinical data, a large number of data suggest that there are mild or severe cytokine storms in severe patients, which is an important cause of death. Therefore, treatment of the cytokine storm has become an important part of rescuing severe COVID-19 patients. Interleukin-6 (IL-6) plays an important role in cytokine release syndrome. If it is possible to block the signal transduction pathway of IL-6, it is expected to become a new method for the treatment of severe COVID-19 patients. Tocilizumab is an IL-6 receptor (IL-6R) blocker that can effectively block the IL-6 signal transduction pathway and thus is likely to become an effective drug for patients with severe COVID-19.


Subject(s)
Antibodies, Monoclonal, Humanized/therapeutic use , Betacoronavirus , Coronavirus Infections/drug therapy , Cytokine Release Syndrome/etiology , Pneumonia, Viral/drug therapy , Receptors, Interleukin-6/antagonists & inhibitors , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/mortality , Humans , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/mortality , SARS-CoV-2 , Severity of Illness Index
9.
J Med Virol ; 92(7): 726-730, 2020 07.
Article in English | MEDLINE | ID: covidwho-17559

ABSTRACT

This article reviews the correlation between angiotensin-converting enzyme 2 (ACE2) and severe risk factors for coronavirus disease 2019 (COVID-19) and the possible mechanisms. ACE2 is a crucial component of the renin-angiotensin system (RAS). The classical RAS ACE-Ang II-AT1R regulatory axis and the ACE2-Ang 1-7-MasR counter-regulatory axis play an essential role in maintaining homeostasis in humans. ACE2 is widely distributed in the heart, kidneys, lungs, and testes. ACE2 antagonizes the activation of the classical RAS system and protects against organ damage, protecting against hypertension, diabetes, and cardiovascular disease. Similar to SARS-CoV, SARS-CoV-2 also uses the ACE2 receptor to invade human alveolar epithelial cells. Acute respiratory distress syndrome (ARDS) is a clinical high-mortality disease, and ACE2 has a protective effect on this type of acute lung injury. Current research shows that the poor prognosis of patients with COVID-19 is related to factors such as sex (male), age (>60 years), underlying diseases (hypertension, diabetes, and cardiovascular disease), secondary ARDS, and other relevant factors. Because of these protective effects of ACE2 on chronic underlying diseases and ARDS, the development of spike protein-based vaccine and drugs enhancing ACE2 activity may become one of the most promising approaches for the treatment of COVID-19 in the future.


Subject(s)
Betacoronavirus/pathogenicity , Cardiovascular Diseases/genetics , Coronavirus Infections/genetics , Pandemics , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/genetics , Spike Glycoprotein, Coronavirus/genetics , Age Factors , Angiotensin I/therapeutic use , Angiotensin-Converting Enzyme 2 , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus/drug effects , COVID-19 , Cardiovascular Diseases/complications , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/epidemiology , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Gene Expression Regulation , Host-Pathogen Interactions/genetics , Humans , Peptide Fragments/therapeutic use , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Pneumonia, Viral/epidemiology , Prognosis , Receptor, Angiotensin, Type 1/genetics , Receptor, Angiotensin, Type 1/metabolism , Receptors, Virus/genetics , Receptors, Virus/metabolism , SARS-CoV-2 , Sex Factors , Signal Transduction , Spike Glycoprotein, Coronavirus/metabolism
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