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1.
Aging (Albany NY) ; 14(10): 4211-4219, 2022 May 18.
Article in English | MEDLINE | ID: covidwho-1856446

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) is spreading around the world. The COVID-19 vaccines may improve concerns about the pandemic. However, the roles of inactivated vaccines in older patients (aged ≥60 years) with infection of Delta variant were less studied. METHODS: We classified the older patients with infection of Delta variant into three groups based on the vaccination status: no vaccination (group A, n = 113), one dose of vaccination (group B, n = 46), and two doses of vaccination (group C, n = 22). Two inactivated COVID-19 vaccines (BBIBP-CorV or CoronaVac) were evaluated in this study. The demographic data, laboratory parameters, and clinical severity were recorded. RESULTS: A total of 181 older patients with infection of Delta variant were enrolled. 111 (61.3%) patients had one or more co-morbidities. The days of "turn negative" and hospital stay in Group C were lower than those in the other groups (P < 0.05). The incidences of multiple organ dysfunction syndrome (MODS), septic shock, acute respiratory distress syndrome (ARDS), acute kidney injury, and cardiac injury in Group A were higher than those in the other groups (P < 0.05). The MV-free days and ICU-free days during 28 days in Group A were also lower than those in the other groups (P < 0.05). In patients with co-morbidities, vaccinated cases had lower incidences of MODS (P = 0.015), septic shock (P = 0.015), and ARDS (P = 0.008). CONCLUSIONS: The inactivated COVID-19 vaccines were effective in improving the clinical severity of older patients with infection of Delta variant.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Shock, Septic , Aged , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines , China/epidemiology , Humans , Multiple Organ Failure , SARS-CoV-2 , Vaccines, Inactivated
2.
EuropePMC; 2022.
Preprint in English | EuropePMC | ID: ppcovidwho-335758

ABSTRACT

We diagnosed 66 peripheral nerve injuries in 34 patients who survived severe coronavirus disease 2019 (COVID-19). We combine our latest data with published case series re-analyzed here (117 nerve injuries;58 patients) to provide a comprehensive accounting of lesion sites. The most common are ulnar (25.1%), common fibular (15.8%), sciatic (13.1%), median (9.8%), brachial plexus (8.7%) and radial (8.2%) nerves at sites known to be vulnerable to mechanical loading. Protection of peripheral nerves should be prioritized in the care of COVID-19 patients. To this end, we report proof of concept data of a wearable, wireless pressure sensor to provide real time monitoring in the intensive care unit setting.

3.
Sci Rep ; 12(1): 5493, 2022 03 31.
Article in English | MEDLINE | ID: covidwho-1768855

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, China, has led to the rapid development of Coronavirus disease 2019 (COVID-19) pandemic. COVID-19 represents a fatal disease with a great global public health importance. This study aims to develop a three-parameter Weibull mathematical model using continuous functions to represent discrete COVID-19 data. Subsequently, the model was applied to quantitatively analyze the characteristics for the mortality of COVID-19, including the age, sex, the length of symptom time to hospitalization time (SH), hospitalization date to death time (HD) and symptom time to death time time (SD) and others. A three-parameter mathematical model was developed by combining the reported cases in the Data Repository from the Center for Systems Science and Engineering at Johns Hopkins University and applied to estimate and analyze the characteristics for mortality of COVID-19. We found that the scale parameters of males and females were 5.85 and 5.45, respectively. Probability density functions in both males and females were negative skewness. 5% of male patients died under the age of 43.28 (44.37 for females), 50% died under 69.55 (73.25 for females), and 95% died under 86.59 (92.78 for females). The peak age of male death was 67.45 years, while that of female death was 71.10 years. The peak and median values of SH, HD and SD in male death were correspondingly 1.17, 5.18 and 10.30 days, and 4.29, 11.36 and 16.33 days, while those in female death were 1.19, 5.80 and 12.08 days, and 4.60, 12.44 and 17.67 days, respectively. The peak age of probability density in male and female deaths was 69.55 and 73.25 years, while the high point age of their mortality risk was 77.51 and 81.73 years, respectively. The mathematical model can fit and simulate the impact of various factors on IFR. From the simulation results of the model, we can intuitively find the IFR, peak age, average age and other information of each age. In terms of time factors, the mortality rate of the most susceptible population is not the highest, and the distribution of male patients is different from the distribution of females. This means that Self-protection and self-recovery in females against SARS-CoV-2 virus might be better than those of males. Males were more likely to be infected, more likely to be admitted to the ICU and more likely to die of COVID-19. Moreover, the infection fatality ration (IFR) of COVID-19 population was intrinsically linked to the infection age. Public health measures to protect vulnerable sex and age groups might be a simple and effective way to reduce IFR.


Subject(s)
COVID-19 , Aged , Aged, 80 and over , Disease Susceptibility , Female , Humans , Male , Models, Theoretical , Public Health , SARS-CoV-2
4.
Expert Rev Mol Med ; 24: e4, 2022 01 21.
Article in English | MEDLINE | ID: covidwho-1641781

ABSTRACT

Viruses completely rely on the energy and metabolic systems of host cells for life activities. Viral infections usually lead to cytopathic effects and host diseases. To date, there are still no specific clinical vaccines or drugs against most viral infections. Therefore, understanding the molecular and cellular mechanisms of viral infections is of great significance to prevent and treat viral diseases. A variety of viral infections are related to the p38 MAPK signalling pathway, and p38 is an important host factor in virus-infected cells. Here, we introduce the different signalling pathways of p38 activation and then summarise how different viruses induce p38 phosphorylation. Finally, we provide a general summary of the effect of p38 activation on virus replication. Our review provides integrated data on p38 activation and viral infections and describes the potential application of targeting p38 as an antiviral strategy.


Subject(s)
Virus Diseases , p38 Mitogen-Activated Protein Kinases , Humans , MAP Kinase Signaling System , Phosphorylation , Virus Replication , p38 Mitogen-Activated Protein Kinases/genetics , p38 Mitogen-Activated Protein Kinases/metabolism
5.
Int J Environ Res Public Health ; 18(21)2021 10 29.
Article in English | MEDLINE | ID: covidwho-1512289

ABSTRACT

Overqualification is prevalent in times of economic downturn, and research has increasingly focused on its outcomes. This study aimed to explore the psychological burden caused by perceived overqualification (POQ) and its impact on creativity among high-tech enterprise employees. Drawing from effort-reward imbalance theory, we examined the effect of POQ on emotional exhaustion, along with the mediating role of emotional exhaustion in the POQ-creativity relationship and the moderating role of pay for performance (PFP) in strengthening the link between POQ and emotional exhaustion. Using cross-sectional data from a sample of 359 employees in China, we found that (1) POQ was positively related to emotional exhaustion; (2) emotional exhaustion was negatively related to creativity; (3) PFP moderated the effect of POQ on emotional exhaustion as well as the indirect effect of POQ on creativity via emotional exhaustion. These findings have both theoretical and practical implications.


Subject(s)
Emotions , Reimbursement, Incentive , Creativity , Cross-Sectional Studies , Reward
6.
Int J Biol Sci ; 17(9): 2348-2355, 2021.
Article in English | MEDLINE | ID: covidwho-1285527

ABSTRACT

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has led to more than 150 million infections and about 3.1 million deaths up to date. Currently, drugs screened are urgently aiming to block the infection of SARS-CoV-2. Here, we explored the interaction networks of kinase and COVID-19 crosstalk, and identified phosphoinositide 3-kinase (PI3K)/AKT pathway as the most important kinase signal pathway involving COVID-19. Further, we found a PI3K/AKT signal pathway inhibitor capivasertib restricted the entry of SARS-CoV-2 into cells under non-cytotoxic concentrations. Lastly, the signal axis PI3K/AKT/FYVE finger-containing phosphoinositide kinase (PIKfyve)/PtdIns(3,5)P2 was revealed to play a key role during the cellular entry of viruses including SARS-CoV-2, possibly providing potential antiviral targets. Altogether, our study suggests that the PI3K/AKT kinase inhibitor drugs may be a promising anti-SARS-CoV-2 strategy for clinical application, especially for managing cancer patients with COVID-19 in the pandemic era.


Subject(s)
COVID-19/drug therapy , Proto-Oncogene Proteins c-akt/antagonists & inhibitors , Pyrimidines/therapeutic use , Pyrroles/therapeutic use , SARS-CoV-2/drug effects , Virus Internalization/drug effects , Animals , COVID-19/enzymology , Chlorocebus aethiops , Computer Simulation , Humans , Neoplasms/enzymology , Neoplasms/mortality , Proto-Oncogene Proteins c-akt/metabolism , Pyrimidines/pharmacology , Pyrroles/pharmacology , Receptor Cross-Talk , Vero Cells
7.
J Med Virol ; 93(9): 5635-5637, 2021 09.
Article in English | MEDLINE | ID: covidwho-1208550

ABSTRACT

An outbreak of a novel coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) had emerged in 2019 and rapidly posed a global epidemic. Here, we report the breadth of concomitant virological features of a family cluster with COVID-19. The period of virus shedding is significantly different between upper respiratory and feces samples. Even the SARS-CoV-2 virus titers were undetectable in feces, it could be positive again soon and likely related to fluctuated inflammation levels (interleukin-6, etc.) and lowered immune responses (CD4 + T lymphocyte, etc.). Our findings expand the novel understanding of the breadth of concomitant virological features during a non-severe family cluster of COVID-19.


Subject(s)
COVID-19/physiopathology , Feces/virology , SARS-CoV-2 , Virus Shedding , Adolescent , Adult , COVID-19/virology , China , Disease Outbreaks , Family , Female , Humans , Male , Middle Aged
9.
Theranostics ; 10(26): 12223-12240, 2020.
Article in English | MEDLINE | ID: covidwho-934619

ABSTRACT

Rationale: Many viral infections are known to activate the p38 mitogen-activated protein kinase (MAPK) signaling pathway. However, the role of p38 activation in viral infection and the underlying mechanism remain unclear. The role of virus-hijacked p38 MAPK activation in viral infection was investigated in this study. Methods: The correlation of hepatitis C virus (HCV) infection and p38 activation was studied in patient tissues and primary human hepatocytes (PHHs) by immunohistochemistry and western blotting. Coimmunoprecipitation, GST pulldown and confocal microscopy were used to investigate the interaction of p38α and the HCV core protein. In vitro kinase assays and mass spectrometry were used to analyze the phosphorylation of the HCV core protein. Plaque assays, quantitative real time PCR (qRT-PCR), western blotting, siRNA and CRISPR/Cas9 were used to determine the effect of p38 activation on viral replication. Results: HCV infection was associated with p38 activation in clinical samples. HCV infection increased p38 phosphorylation by triggering the interaction of p38α and TGF-ß activated kinase 1 (MAP3K7) binding protein 1 (TAB1). TAB1-mediated p38α activation facilitated HCV replication, and pharmaceutical inhibition of p38α activation by SB203580 suppressed HCV infection at the viral assembly step. Activated p38α interacted with the N-terminal region of the HCV core protein and subsequently phosphorylated the HCV core protein, which promoted HCV core protein oligomerization, an essential step for viral assembly. As expected, SB203580 or the HCV core protein N-terminal peptide (CN-peptide) disrupted the p38α-HCV core protein interaction, efficiently impaired HCV assembly and impeded normal HCV replication in both cultured cells and primary human hepatocytes. Similarly, severe fever with thrombocytopenia syndrome virus (SFTSV), herpes simplex virus type 1 (HSV-1) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection also activated p38 MAPK. Most importantly, pharmacological blockage of p38 activation by SB203580 effectively inhibited SFTSV, HSV-1 and SARS-CoV-2. Conclusion: Our study shows that virus-hijacked p38 activation is a key event for viral replication and that pharmacological blockage of p38 activation is an antiviral strategy.


Subject(s)
COVID-19/metabolism , Hepacivirus/metabolism , Hepatitis C/metabolism , Mitogen-Activated Protein Kinase 14/metabolism , SARS-CoV-2/metabolism , Spike Glycoprotein, Coronavirus/metabolism , A549 Cells , Adaptor Proteins, Signal Transducing/metabolism , Animals , COVID-19/virology , Chlorocebus aethiops , Enzyme Activation , HEK293 Cells , Hepatitis C/pathology , Hepatitis C/virology , Hepatocytes/metabolism , Humans , Imidazoles/pharmacology , MAP Kinase Kinase Kinases/metabolism , MAP Kinase Signaling System/drug effects , Mitogen-Activated Protein Kinase 14/antagonists & inhibitors , Phosphorylation , Pyridines/pharmacology , Vero Cells , Viral Core Proteins/metabolism , Virus Replication/drug effects
10.
Nature ; 583(7815): 282-285, 2020 07.
Article in English | MEDLINE | ID: covidwho-17844

ABSTRACT

The ongoing outbreak of viral pneumonia in China and across the world is associated with a new coronavirus, SARS-CoV-21. This outbreak has been tentatively associated with a seafood market in Wuhan, China, where the sale of wild animals may be the source of zoonotic infection2. Although bats are probable reservoir hosts for SARS-CoV-2, the identity of any intermediate host that may have facilitated transfer to humans is unknown. Here we report the identification of SARS-CoV-2-related coronaviruses in Malayan pangolins (Manis javanica) seized in anti-smuggling operations in southern China. Metagenomic sequencing identified pangolin-associated coronaviruses that belong to two sub-lineages of SARS-CoV-2-related coronaviruses, including one that exhibits strong similarity in the receptor-binding domain to SARS-CoV-2. The discovery of multiple lineages of pangolin coronavirus and their similarity to SARS-CoV-2 suggests that pangolins should be considered as possible hosts in the emergence of new coronaviruses and should be removed from wet markets to prevent zoonotic transmission.


Subject(s)
Betacoronavirus/genetics , Betacoronavirus/isolation & purification , Eutheria/virology , Evolution, Molecular , Genome, Viral/genetics , Sequence Homology, Nucleic Acid , Amino Acid Sequence , Animals , Betacoronavirus/chemistry , Betacoronavirus/classification , COVID-19 , China/epidemiology , Chiroptera/virology , Coronavirus Infections/epidemiology , Coronavirus Infections/transmission , Coronavirus Infections/virology , Disease Reservoirs/virology , Genomics , Humans , Malaysia , Pandemics , Phylogeny , Pneumonia, Viral/epidemiology , Pneumonia, Viral/transmission , Pneumonia, Viral/virology , Recombination, Genetic , SARS-CoV-2 , Sequence Alignment , Spike Glycoprotein, Coronavirus/chemistry , Spike Glycoprotein, Coronavirus/genetics , Zoonoses/virology
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