Virus-host interaction networks as new antiviral drug targets for IAV and SARS-CoV-2

Chen, Na; Zhang, Baoge; Deng, Lulu; Liang, Bing; Ping, Jihui

doi:10.1080/22221751.2022.2071175

Cited by 23 publications

(18 citation statements)

References 81 publications

(111 reference statements)

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“…The modulation of host factors involved in regulating viral replication and/or injury or tissue recovery has been demonstrated to be a potential strategy against viral diseases, including influenza ( 13 , 14 ). Whereas, CRP has been considered a potential therapeutic target for inflammatory diseases, including infections, since CRP bound to a multivalent ligand can efficiently initiate the assembly of a C3 convertase through the classical pathway and thus decorate the surface of the ligand with opsonic complement fragments ( 6 , 15 , 16 ).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of C-reactive protein or human C-reactive protein transgenic treatment aggravates influenza A infection in mice

Zhang

Gao²,

Li³

et al. 2022

Front. Immunol.

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C-reactive protein (CRP) has been shown to be a potential candidate target in the immunotherapy of severe influenza A infection. However, it is unclear on the pathogenesis associated with CRP in influenza infections. Here, we used influenza A H1N1 CA04 to infect human CRP transgenic mice (KI), CRP knockout mice (KO), and wild-type mice (WT), respectively, and compared the viral pathogenicity and associated immune response in those mice. The results showed that CA04 infection resulted in 100%, 80%, and 60% death in KO, KI, and WT mice, respectively. Compared to WT mice, CA04 infection resulted in higher TCID50 in lungs on day 3 after infection but lowered HI antibody titers in sera of survivors on day 21 after infection in KI mice. ELISA assay showed that IFN-γ concentration was significantly increased in sera of WT, KI, or KO mice on day 7 after infection, and IL-17 was remarkably increased in sera of WT mice but decreased in sera of KI mice while no significant change in sera of KO mice on day 3 or 7 after infection. Quantitative RT-PCR showed that the relative expression levels of immune checkpoint CTLA-4, LAIR-1, GITR, BTLA, TIM-3, or PD-1 mRNA in the lung presented decreased levels on day 3 or 7 after infection in KI or KO mice. The correlation analysis showed that mRNA expression levels of the 6 molecules positively correlated with viral TICD50 in WT mice but negatively correlated with viral TCID50 in KI or KO mice. However, only LAIR-1 presented a significant correlation in each lung tissue of WT, KI, or KO mice with CA07 infection statistically. IHC results showed that LAIR-1 positive cells could be found in WT, KO, or KI mice lung tissues with CA04 infection, and the positive cells were mainly distributed in an inflammatory dense area. Our results suggested that deficiency of CRP or human CRP transgenic treatment aggravates influenza A virus infection in mice. CRP is a double sword in immune regulation of influenza infection in which IL-17 and immune checkpoint may be involved.

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Section: Discussionmentioning

confidence: 99%

Deficiency of C-reactive protein or human C-reactive protein transgenic treatment aggravates influenza A infection in mice

Zhang

Gao²,

Li³

et al. 2022

Front. Immunol.

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“…In recent years, more and more researchers have focused on the host cell pathway and virus–host interaction [ 94 , 95 , 96 ]. Tp53 is a crucial tumor suppressor gene in host cells.…”

Section: P53 Is a Potential Target For Anti-coronavirus Drugsmentioning

confidence: 99%

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

Wang

Liu

et al. 2023

IJMS

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The emergence of the SARS-CoV-2 coronavirus has garnered global attention due to its highly pathogenic nature and the resulting health crisis and economic burden. Although drugs such as Remdesivir have been considered a potential cure by targeting the virus on its RNA polymerase, the high mutation rate and unique 3’ to 5’ exonuclease with proofreading function make it challenging to develop effective anti-coronavirus drugs. As a result, there is an increasing focus on host–virus interactions because coronaviruses trigger stress responses, cell cycle changes, apoptosis, autophagy, and the dysregulation of immune function and inflammation in host cells. The p53 tumor suppressor molecule is a critical regulator of cell signaling pathways, cellular stress responses, DNA repair, and apoptosis. However, viruses can activate or inhibit p53 during viral infections to enhance viral replication and spread. Given its pivotal role in cell physiology, p53 represents a potential target for anti-coronavirus drugs. This review aims to summarize the relationship between p53 and coronaviruses from various perspectives, to shed light on potential targets for antiviral drug development and vaccine design.

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“…This has caused heavy human and economic losses worldwide (3).In addition, the beginning of the flu season can seriously affect human health. As a common respiratory pathogen, the flu causes seasonal epidemics and severe sporadic epidemics worldwide (4). The combination of the prevalence of the influenza virus during the influenza season and the current pandemic poses additional challenges and greater threats to public health.…”

Section: Introductionmentioning

confidence: 99%

The use of bioinformatics methods to identify the effects of SARS-CoV-2 and influenza viruses on the regulation of gene expression in patients

Sun

Li²,

Zhao³

et al. 2023

Front. Immunol.

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BackgroundSARS-CoV-2 infection is a respiratory infectious disease similar to influenza virus infection. Numerous studies have reported similarities and differences in the clinical manifestations, laboratory tests, and mortality between these two infections. However, the genetic effects of coronavirus and influenza viruses on the host that lead to these characteristics have rarely been reported.MethodsCOVID-19 (GSE157103) and influenza (GSE111368, GSE101702) datasets were downloaded from the Gene Expression Ominbus (GEO) database. Differential gene, gene set enrichment, protein-protein interaction (PPI) network, gene regulatory network, and immune cell infiltration analyses were performed to identify the critical impact of COVID-19 and influenza viruses on the regulation of host gene expression.ResultsThe number of differentially expressed genes in the COVID-19 patients was significantly higher than in the influenza patients. 22 common differentially expressed genes (DEGs) were identified between the COVID-19 and influenza datasets. The effects of the viruses on the regulation of host gene expression were determined using gene set enrichment and PPI network analyses. Five HUB genes were finally identified: IFI27, OASL, RSAD2, IFI6, and IFI44L.ConclusionWe identified five HUB genes between COVID-19 and influenza virus infection, which might be helpful in the diagnosis and treatment of COVID-19 and influenza. This knowledge may also guide future mechanistic studies that aim to identify pathogen-specific interventions.

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Virus-host interaction networks as new antiviral drug targets for IAV and SARS-CoV-2

Cited by 23 publications

References 81 publications

Deficiency of C-reactive protein or human C-reactive protein transgenic treatment aggravates influenza A infection in mice

Deficiency of C-reactive protein or human C-reactive protein transgenic treatment aggravates influenza A infection in mice

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

The use of bioinformatics methods to identify the effects of SARS-CoV-2 and influenza viruses on the regulation of gene expression in patients

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