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1.
Frontiers in public health ; 10, 2022.
Article in English | EuropePMC | ID: covidwho-1939836

ABSTRACT

Purpose This research focused primarily on the impact of the SARS-CoV-2 Vaccine (VeroCell) on Chinese physical education (PE) students' health and physical activity (PA) performance. Methods This study used quantitative methods and phenomenological procedures to collect and analyze data. Survey techniques were the main method used for collecting data from Chinese university students, using a self-designed questionnaire with a Cronbach's alpha α value of 0.76. To ensure the quality of the study, confirmatory factor analyses (CFA) were conducted, and the internal consistency reliability of the instrument was measured (alpha coefficient = 0.82). The determined sample size was 490 and around 90% as the minimum sample size was determined with the help of a sample size calculator. The author using factor loadings with h2 and an independent-sample t-test analyzed the responses of the remaining valid participants (n = 443 with a response rate of 90.40). Results Most participants (around 94%) did not experience any adverse reactions that impacted their daily life activities, health, or performance during physical activity. However, about 30–40% of students felt lethargy, weakness, muscle pain, or swelling. Regarding the impact of the vaccine on daily life, there was no difference in the responses between participants who had only received one shot of the coronavirus disease 2019 (COVID-19) vaccine and those who had received two shots (p > 0.05 in most cases). Conclusion The study concluded that the COVID-19 vaccine had no significant effect on PE students' daily activities, health, and PA performance. The results of this study could be used by policymakers to encourage people to get vaccinated and eradicate the isolation caused by COVID-19, which leads many people to develop various non-communicable diseases (NCDs).

2.
J Virol ; 96(5): e0208621, 2022 03 09.
Article in English | MEDLINE | ID: covidwho-1736026

ABSTRACT

Coronavirus infections induce the expression of multiple proinflammatory cytokines and chemokines. We have previously shown that in cells infected with gammacoronavirus infectious bronchitis virus (IBV), interleukin 6 (IL-6), and IL-8 were drastically upregulated, and the MAP kinase p38 and the integrated stress response pathways were implicated in this process. In this study, we report that coronavirus infection activates a negative regulatory loop that restricts the upregulation of a number of proinflammatory genes. As revealed by the initial transcriptomic and subsequent validation analyses, the anti-inflammatory adenine-uridine (AU)-rich element (ARE)-binding protein, zinc finger protein 36 (ZFP36), and its related family members were upregulated in cells infected with IBV and three other coronaviruses, alphacoronaviruses porcine epidemic diarrhea virus (PEDV), human coronavirus 229E (HCoV-229E), and betacoronavirus HCoV-OC43, respectively. Characterization of the functional roles of ZFP36 during IBV infection demonstrated that ZFP36 promoted the degradation of transcripts coding for IL-6, IL-8, dual-specificity phosphatase 1 (DUSP1), prostaglandin-endoperoxide synthase 2 (PTGS2) and TNF-α-induced protein 3 (TNFAIP3), through binding to AREs in these transcripts. Consistently, knockdown and inhibition of JNK and p38 kinase activities reduced the expression of ZFP36, as well as the expression of IL-6 and IL-8. On the contrary, overexpression of mitogen-activated protein kinase kinase 3 (MKK3) and MAPKAP kinase-2 (MK2), the upstream and downstream kinases of p38, respectively, increased the expression of ZFP36 and decreased the expression of IL-8. Taken together, this study reveals an important regulatory role of the MKK3-p38-MK2-ZFP36 axis in coronavirus infection-induced proinflammatory response. IMPORTANCE Excessive and uncontrolled induction and release of proinflammatory cytokines and chemokines, the so-called cytokine release syndrome (CRS), would cause life-threatening complications and multiple organ failure in severe coronavirus infections, including severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and COVID-19. This study reveals that coronavirus infection also induces the expression of ZFP36, an anti-inflammatory ARE-binding protein, promoting the degradation of ARE-containing transcripts coding for IL-6 and IL-8 as well as a number of other proteins related to inflammatory response. Furthermore, the p38 MAP kinase, its upstream kinase MKK3 and downstream kinase MK2 were shown to play a regulatory role in upregulation of ZFP36 during coronavirus infection cycles. This MKK3-p38-MK2-ZFP36 axis would constitute a potential therapeutic target for severe coronavirus infections.


Subject(s)
Coronavirus Infections/metabolism , Interleukin-6/metabolism , Interleukin-8/metabolism , Tristetraprolin/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism , Adenine/metabolism , Animals , Cell Line , Chlorocebus aethiops , Coronavirus Infections/genetics , Gene Expression Regulation , Humans , Infectious bronchitis virus/metabolism , Infectious bronchitis virus/pathogenicity , Interleukin-6/genetics , Interleukin-8/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Phosphorylation , Transcriptional Activation , Up-Regulation , Uridine/metabolism , Vero Cells
3.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-311344

ABSTRACT

Background: The outbreak of the 2019 novel coronavirus since December, 2019, has now causing nearly 75 thousand confirmed cases in China (until paper preparing). This epidemic has posed significant threats to international health and the economy. Zhejiang province, which once had the 2nd most accumulative cases among all provinces, has now dropped to top No.5 (until paper preparing). It had a high discharge rates (43.86%) from hospital and the lowest death rate among all top 5 epidemic provinces, this drew our attention to the epidemiological, clinical characteristics and local government engagement of this region.MethodsIn this study, we included all confirmed cases of COVID-19 pneumonia in Zhejiang province from Jan 21 to Feb 11, 2020. All data come from cases issued by Zhejiang provincial health commission.ResultsUntil Feb 11, 2020, 1143 cases were confirmed in Zhejiang province. We analysed the cases growth information in Zhejiang province and age, gender, severe cases percent, the source of the patients, the time of disease onset to confirm and the clinical symptoms of the patients. We also compared the clinical symptoms of elders and the young.ConclusionsThe patients in Zhejiang province had no age and gender preference, and the average time of disease onset to confirm was 5.9 days. The clinical symptoms were mainly fever, cough and weakness, similarly with before reported. The difference between elders and younger are not significant. Until paper preparing, Zhejiang province has very high discharge rate and low death rate, low cases increase rate in China.

4.
Int J Mol Sci ; 22(11)2021 May 26.
Article in English | MEDLINE | ID: covidwho-1244042

ABSTRACT

Infection induces the production of proinflammatory cytokines and chemokines such as interleukin-8 (IL-8) and IL-6. Although they facilitate local antiviral immunity, their excessive release leads to life-threatening cytokine release syndrome, exemplified by the severe cases of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In this study, we investigated the roles of the integrated stress response (ISR) and activator protein-1 (AP-1) family proteins in regulating coronavirus-induced IL-8 and IL-6 upregulation. The mRNA expression of IL-8 and IL-6 was significantly induced in cells infected with infectious bronchitis virus (IBV), a gammacoronavirus, and porcine epidemic diarrhea virus, an alphacoronavirus. Overexpression of a constitutively active phosphomimetic mutant of eukaryotic translation initiation factor 2α (eIF2α), chemical inhibition of its dephosphorylation, or overexpression of its upstream double-stranded RNA-dependent protein kinase (PKR) significantly enhanced IL-8 mRNA expression in IBV-infected cells. Overexpression of the AP-1 protein cJUN or its upstream kinase also increased the IBV-induced IL-8 mRNA expression, which was synergistically enhanced by overexpression of cFOS. Taken together, this study demonstrated the important regulatory roles of ISR and AP-1 proteins in IL-8 production during coronavirus infection, highlighting the complex interactions between cellular stress pathways and the innate immune response.


Subject(s)
Coronavirus Infections/metabolism , Endoplasmic Reticulum Stress/genetics , Eukaryotic Initiation Factor-2/metabolism , Interleukin-8/metabolism , Unfolded Protein Response/genetics , Alphacoronavirus/metabolism , Alphacoronavirus/pathogenicity , Animals , Cell Line , Chlorocebus aethiops , Coronavirus Infections/genetics , Gammacoronavirus/metabolism , Gammacoronavirus/pathogenicity , Gene Expression Regulation , Humans , Immunity, Innate , Infectious bronchitis virus/metabolism , Infectious bronchitis virus/pathogenicity , Interleukin-8/genetics , Phosphorylation , Porcine epidemic diarrhea virus/metabolism , Porcine epidemic diarrhea virus/pathogenicity , Proto-Oncogene Proteins c-fos/genetics , Proto-Oncogene Proteins c-fos/metabolism , Proto-Oncogene Proteins c-jun/genetics , Proto-Oncogene Proteins c-jun/metabolism , Signal Transduction/genetics , Transcription Factor AP-1/genetics , Transcription Factor AP-1/metabolism , Up-Regulation , Vero Cells , eIF-2 Kinase/genetics , eIF-2 Kinase/metabolism
5.
Int J Gen Med ; 14: 1167-1172, 2021.
Article in English | MEDLINE | ID: covidwho-1175485

ABSTRACT

OBJECTIVE: This study was designed to explore the impact of different scoring settings of disease severity on the accuracy of screening by NRS2002. METHODS: Patients with severe COVID-19 who were admitted to our hospital from January 26, 2020, to March 16, 2020, were enrolled in this study. The basic data, the scores of the NRS2002 score sheet, and the serum prealbumin (PAB) level when these patients were admitted were collected, and the reflection of NRS2002 scores under different disease severity score settings to abnormal patients was analyzed. RESULTS: 1. When the severity of the disease was set to 0 points, four of the six hospitalized patients with PAB levels below the lower normal limit were not screened out; 2. When the severity was set to 1 point, two patients with COVID-19 who developed to a severe stage during the treatment process were screened out, but three of the six hospitalized patients with PAB levels below the lower normal limit at admission were not screened out; 3. When the severity of the disease of a patient with severe COVID-19 and fever scored 2 points, and that of a patient without fever scored 1 point, two patients with COVID-19 who developed to the severe stage during the treatment process were screened out, and six patients who were hospitalized with PAB levels below the lower normal limit at admission were also screened out. CONCLUSION: When the severe degree of patients with COVID-19 and fever is rated as 2 points, and that of the patients without fever is rated as 1 point, it can more accurately reflect the severity degree of patients with undernourishment.

6.
J Virol ; 2020 Nov 25.
Article in English | MEDLINE | ID: covidwho-947807

ABSTRACT

Coronaviruses have evolved a variety of strategies to optimize cellular microenvironment for efficient replication. In this study, we report the induction of AP-1 transcription factors by coronavirus infection based on genome-wide analyses of differentially expressed genes in cells infected with avian coronavirus infectious bronchitis virus (IBV). Most members of the AP-1 transcription factors were subsequently found to be upregulated during the course of IBV and porcine epidemic diarrhea virus (PEDV) infection of cultured cells as well as in IBV-infected chicken embryos. Further characterization of the induction kinetics and functional roles of cFOS in IBV replication demonstrated that upregulation of cFOS at early to intermediate phases of IBV replication cycles suppresses IBV-induced apoptosis and promotes viral replication. Blockage of nuclear translocation of cFOS by peptide inhibitor NLSP suppressed IBV replication and apoptosis, ruling out the involvement of the cytoplasmic functions of cFOS in the replication of IBV. Furthermore, knockdown of ERK1/2 and inhibition of JNK and p38 kinase activities reduced cFOS upregulation and IBV replication. This study reveals an important function of cFOS in the regulation of coronavirus-induced apoptosis, facilitating viral replication.IMPORTANCE The ongoing pandemic of coronavirus disease 2019 (COVID-19), caused by a newly emerged zoonotic coronavirus (SARS-CoV-2), highlights the importance of coronaviruses as human and animal pathogens and our knowledge gaps in understanding the cellular mechanisms, especially mechanisms shared among human and animal coronaviruses, exploited by coronaviruses for optimal replication and enhanced pathogenicity. This study reveals that upregulation of cFOS, along with other AP-1 transcription factors, as a cell-survival strategy is such a mechanism utilized by coronaviruses during their replication cycles. Through induction and regulation of apoptosis of the infected cells at early to intermediate phases of the replication cycles, subtle but appreciable differences in coronavirus replication efficiency were observed when the expression levels of cFOS were manipulated in the infected cells. As the AP-1 transcription factors are multi-functional, further studies of their regulatory roles in proinflammatory responses may provide new insights into the pathogenesis and virus-host interactions during coronavirus infection.

8.
Cell Mol Life Sci ; 78(2): 531-544, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-708549

ABSTRACT

Currently, a novel coronavirus (SARS-CoV-2, also called 2019-nCoV) has triggered pandemic Coronavirus Disease 2019 (COVID-19), an acute infectious respiratory disease that first became epidemic in Wuhan (China) and is now spreading worldwide. Although 2019-nCoV and SARS-CoV are very similar viruses genomically and structurally, the huge number of severe cases and deaths now being caused by 2019-nCoV infections has understandably prompted intense research on the receptor used by it to enter human cells. Angiotensin converting enzyme 2 (ACE2), a functional receptor for SARS-CoV, now appears likely to mediate 2019-nCoV entry into human cells. In this review, we describe the roles performed by ACE2 as an enzymatic catalyst and as a receptor for this novel coronavirus. We also summarize the latest research pertaining to the changes noted in ACE2 expression after viral binding, and the relationships relating to virus transmission and population susceptibility to it. Lastly, we speculate on the pathogenesis of COVID-19 and provide a useful reference for drug development against this aggressive virus.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/metabolism , COVID-19/virology , SARS-CoV-2/physiology , Animals , Humans , Pandemics , SARS-CoV-2/metabolism , Virus Internalization
9.
Front. Microbiol. ; (10)20200124.
Article in English | WHO COVID, ELSEVIER | ID: covidwho-326186

ABSTRACT

Coronavirus (CoV) envelope (E) protein is a small structural protein critical for virion morphogenesis and release. The recently characterized E protein ion channel activity (EIC) has also been implicated in modulating viral pathogenesis. In this study, we used infectious bronchitis coronavirus (IBV) as a model to study EIC. Two recombinant IBVs (rIBVs) harboring EIC-inactivating mutations – rT16A and rA26F – were serially passaged, and several compensatory mutations were identified in the transmembrane domain (TMD). Two rIBVs harboring these putative EIC-reverting mutations – rT16A/A26V and rA26F/F14N – were recovered. Compared with the parental rIBV-p65 control, all four EIC mutants exhibited comparable levels of intracellular RNA synthesis, structural protein production, and virion assembly. Our results showed that the IBV EIC contributed to the induction of ER stress response, as up-regulation of ER stress-related genes was markedly reduced in cells infected with the EIC-defective mutants. EIC-defective mutants also formed smaller plaques, released significantly less infectious virions into the culture supernatant, and had lower levels of viral fitness in cell culture. Significantly, all these defective phenotypes were restored in cells infected with the putative EIC revertants. EIC mutations were also implicated in regulating IBV-induced apoptosis, induction of pro-inflammatory cytokines, and viral pathogenicity in vivo. Taken together, this study highlights the importance of CoV EIC in modulating virion release and various aspects of CoV – host interaction.

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