Roles of p53-Mediated Host–Virus Interaction in Coronavirus Infection

Wang, Xue; Liu, Yi; Li, Kaiyuan; Hao, Zhihui

doi:10.3390/ijms24076371

Cited by 9 publications

(2 citation statements)

References 115 publications

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“…The other 11 variants on chromosome 6, instead, mapped in the PERP gene locus and some of them were already annotated as eQTLs of this gene. Although no functions related to COVID-19 have been reported for the PERP gene, so far, it encodes a protein that is a p53 apoptosis effector, and, recently, Wang and colleagues reviewed the possible roles of p53 in mediating host-virus interactions in infections caused by Coronaviruses 42 .…”

Section: Discussionmentioning

confidence: 99%

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

Minnai,

Biscarini,

Esposito

et al. 2024

Sci Rep

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The clinical manifestations of SARS-CoV-2 infection vary widely among patients, from asymptomatic to life-threatening. Host genetics is one of the factors that contributes to this variability as previously reported by the COVID-19 Host Genetics Initiative (HGI), which identified sixteen loci associated with COVID-19 severity. Herein, we investigated the genetic determinants of COVID-19 mortality, by performing a case-only genome-wide survival analysis, 60 days after infection, of 3904 COVID-19 patients from the GEN-COVID and other European series (EGAS00001005304 study of the COVID-19 HGI). Using imputed genotype data, we carried out a survival analysis using the Cox model adjusted for age, age2, sex, series, time of infection, and the first ten principal components. We observed a genome-wide significant (P-value < 5.0 × 10−8) association of the rs117011822 variant, on chromosome 11, of rs7208524 on chromosome 17, approaching the genome-wide threshold (P-value = 5.19 × 10−8). A total of 113 variants were associated with survival at P-value < 1.0 × 10−5 and most of them regulated the expression of genes involved in immune response (e.g., CD300 and KLR genes), or in lung repair and function (e.g., FGF19 and CDH13). Overall, our results suggest that germline variants may modulate COVID-19 risk of death, possibly through the regulation of gene expression in immune response and lung function pathways.

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Section: Discussionmentioning

confidence: 99%

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

Minnai,

Biscarini,

Esposito

et al. 2024

Sci Rep

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“…It can also be a target for RNA viruses; for example, p53 is mislocalized to the cytoplasm by the NS2 protein during hepatitis C virus (HCV) infection [149]. However, only limited information is available on the relationship between SARS-CoV-2 and p53 (reviewed in [150]). It has been shown that the viral protease Nsp5 can act as a repressor of the p53 signalling pathway and that p53 can restrict SARS-CoV-2 production [151].…”

Section: Cell Cycle Regulation By Sars-cov-2mentioning

confidence: 99%

SARS-CoV-2 and the DNA damage response

Grand

2023

Journal of General Virology

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The recent coronavirus disease 2019 (COVID-19) pandemic was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is characterized by respiratory distress, multiorgan dysfunction and, in some cases, death. The virus is also responsible for post-COVID-19 condition (commonly referred to as ‘long COVID’). SARS-CoV-2 is a single-stranded, positive-sense RNA virus with a genome of approximately 30 kb, which encodes 26 proteins. It has been reported to affect multiple pathways in infected cells, resulting, in many cases, in the induction of a ‘cytokine storm’ and cellular senescence. Perhaps because it is an RNA virus, replicating largely in the cytoplasm, the effect of SARS-Cov-2 on genome stability and DNA damage responses (DDRs) has received relatively little attention. However, it is now becoming clear that the virus causes damage to cellular DNA, as shown by the presence of micronuclei, DNA repair foci and increased comet tails in infected cells. This review considers recent evidence indicating how SARS-CoV-2 causes genome instability, deregulates the cell cycle and targets specific components of DDR pathways. The significance of the virus’s ability to cause cellular senescence is also considered, as are the implications of genome instability for patients suffering from long COVID.

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Losartan and enalapril maleate differently influence SARS-CoV-2-infected vero cells

Majolo,

Gonçalves,

Souza

et al. 2024

Sci Rep

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Background: The COVID-19 pandemic has posed significant challenges to global healthcare systems, particularly impacting individuals with pre-existing conditions like hypertension. This study sought to assess the impact of the antihypertensive medications, losartan and enalapril maleate on SARS-CoV-2 infected cells. Vero E6 cells were infected and treated in vitro, evaluating cell viability via the MTT colorimetric assay. Additionally, the study measured relative levels of viral RNA and selected gene messenger RNAs using reverse transcriptase followed by quantitative real-time polymerase chain reaction. Results: The findings revealed that losartan substantially reduced nucleocapsid RNA levels of SARS-CoV-2 to nearly undetectable levels, while enalapril maleate did not demonstrate a significant effect. In response to viral infection, the expression of il-18 , p53 , p21 , and p62 increased compared to uninfected-untreated cells. Notably, il-6 expression was upregulated by both infection and treatments. A comparison between infected cells treated with losartan or enalapril maleate highlighted the presence of distinct profiles in the expression of il-6 , p53 , p21 , and p62 . Conclusions: The data from our study suggest that these medications could interfere with certain effects triggered by SARS-CoV-2 infection in Vero E6 cells. However, their influence appears to vary both quantitatively and qualitatively in the modulation of metabolic and signal transduction pathways. Supplementary Information The online version contains supplementary material available at 10.1038/s41598-024-76657-7.

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Roles of p53-Mediated Host–Virus Interaction in Coronavirus Infection

Cited by 9 publications

References 115 publications

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

SARS-CoV-2 and the DNA damage response

Losartan and enalapril maleate differently influence SARS-CoV-2-infected vero cells

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