Potential of H1N1 influenza A virus as an air borne pathogen to induce infectivity in pancreas: a mouse model study

Sadeghi, Kaveh; Salimi, Vahid; Rezaei, Fatemeh; Jalilian, Farid Azizi; Ghavami, Nastaran; Azad, Talat Mokhtari

doi:10.1007/s40201-020-00468-x

Cited by 9 publications

(8 citation statements)

References 24 publications

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“…The hypothesised role of viral infections in the initiation of IA and the progression to T1D is supported by a large body of epidemiological and animal model-based evidence [ 43 , 44 ]. Multiple viruses have been associated with IA/T1D to date, including enterovirus (EV) [ 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 ], rotavirus [ 55 , 56 , 57 , 58 , 59 , 60 , 61 ], cytomegalovirus [ 62 , 63 , 64 , 65 , 66 , 67 , 68 ], Epstein-Barr virus [ 63 , 69 , 70 ], parechovirus [ 71 , 72 , 73 ], influenza [ 74 , 75 , 76 ], parvovirus [ 77 , 78 ], mumps [ 79 , 80 , 81 ], rubella [ 80 , 81 , 82 , 83 , 84 , 85 ] and human endogenous retrovirus [ 86 , ...…”

Section: Environmental Triggersmentioning

confidence: 99%

Viruses and Type 1 Diabetes: From Enteroviruses to the Virome

et al. 2021

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For over a century, viruses have left a long trail of evidence implicating them as frequent suspects in the development of type 1 diabetes. Through vigorous interrogation of viral infections in individuals with islet autoimmunity and type 1 diabetes using serological and molecular virus detection methods, as well as mechanistic studies of virus-infected human pancreatic β-cells, the prime suspects have been narrowed down to predominantly human enteroviruses. Here, we provide a comprehensive overview of evidence supporting the hypothesised role of enteroviruses in the development of islet autoimmunity and type 1 diabetes. We also discuss concerns over the historical focus and investigation bias toward enteroviruses and summarise current unbiased efforts aimed at characterising the complete population of viruses (the “virome”) contributing early in life to the development of islet autoimmunity and type 1 diabetes. Finally, we review the range of vaccine and antiviral drug candidates currently being evaluated in clinical trials for the prevention and potential treatment of type 1 diabetes.

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Section: Environmental Triggersmentioning

confidence: 99%

Viruses and Type 1 Diabetes: From Enteroviruses to the Virome

et al. 2021

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“…The colony-stimulating granulocyte factor (G-CSF) can alter the function of Tcells and induces Th2 immune response (Franzke et al 2003) . There is also some evidence of a link between elevated G-CSF expression level and the induction of the cellular immune response in H1N1 infected individuals (Sadeghi et al 2020) .…”

Section: We Identified a Strong Association Between Covid-19 Infectiomentioning

confidence: 99%

The transcriptomic profiling of COVID-19 compared to SARS, MERS, Ebola, and H1N1

Alsamman

Zayed

2020

Preprint

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COVID-19 pandemic is a global crisis that threatens our way of life. As of April 29, 2020, COVID-19 has claimed more than 200,000 lives, with a global mortality rate of~7% and recovery rate of~30%. Understanding the interaction of cellular targets to the SARS-CoV2 infection is crucial for therapeutic development. Therefore, the aim of this study was to perform a comparative analysis of transcriptomic signatures of infection of COVID-19 compared to different respiratory viruses (Ebola, H1N1, MERS-CoV, and SARS-CoV), to determine unique anti-COVID1-19 gene signature. We identified for the first time molecular pathways for Heparin-binding, RAGE, miRNA, and PLA2 inhibitors, to be associated with SARS-CoV2 infection. The NRCAM and SAA2 that are involved in severe inflammatory response, and FGF1 and FOXO1genes, which are associated with immune regulation, were found to be associated with a cellular gene response to COVID-19 infection. Moreover, several cytokines, most significantly the IL-8, IL-6, demonstrated key associations with COVID-19 infection. Interestingly, the only response gene that was shared between the five viral infections was SERPINB1. The PPI study sheds light on genes with high interaction activity that COVID-19 shares with other viral infections. The findings showed that the genetic pathways associated with Rheumatoid arthritis, AGE-RAGE signaling system, Malaria, Hepatitis B, and Influenza A were of high significance. We found that the virogenomic transcriptome of infection, gene modulation of host antiviral responses, and GO terms of both COVID-19 and Ebola are more similar compared to SARS, H1N1, and MERS. This work compares the virogenomic signatures of highly pathogenic viruses and provides valid targets for potential therapy against COVID-19.

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“…Colony-stimulating granulocyte factor ( G-CSF) can alter the function of T-cells and induces the Th2 immune response [ 24 ]. There is also some evidence of a link between an elevated G-CSF expression level and the induction of the cellular immune response in H1N1 infected individuals [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

The transcriptomic profiling of SARS-CoV-2 compared to SARS, MERS, EBOV, and H1N1

Alsamman

Zayed

2020

PLoS ONE

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The SARS-CoV-2 (COVID-19) pandemic is a global crisis that threatens our way of life. As of November 18, 2020, SARS-CoV-2 has claimed more than 1,342,709 lives, with a global mortality rate of ~2.4% and a recovery rate of ~69.6%. Understanding the interaction of cellular targets with the SARS-CoV-2 infection is crucial for therapeutic development. Therefore, the aim of this study was to perform a comparative analysis of transcriptomic signatures of infection of SARS-CoV-2 compared to other respiratory viruses (EBOV, H1N1, MERS-CoV, and SARS-CoV), to determine a unique anti-SARS-CoV-2 gene signature. We identified for the first time that molecular pathways for heparin-binding, RAGE, miRNA, and PLA2 inhibitors were associated with SARS-CoV-2 infection. The NRCAM and SAA2 genes, which are involved in severe inflammatory responses, and the FGF1 and FOXO1 genes, which are associated with immune regulation, were found to be associated with the cellular gene response to SARS-CoV-2 infection. Moreover, several cytokines, most significantly IL-8 and IL-6, demonstrated key associations with SARS-CoV-2 infection. Interestingly, the only response gene that was shared among the five viral infections was SERPINB1. The protein-protein interaction (PPI) analysis shed light on genes with high interaction activity that SARS-CoV-2 shares with other viral infections. The findings showed that the genetic pathways associated with rheumatoid arthritis, the AGE-RAGE signaling system, malaria, hepatitis B, and influenza A were of high significance. We found that the virogenomic transcriptome of infection, gene modulation of host antiviral responses, and GO terms of SARS-CoV-2 and EBOV were more similar than to SARS, H1N1, and MERS. This work compares the virogenomic signatures of highly pathogenic viruses and provides valid targets for potential therapy against SARS-CoV-2.

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Potential of H1N1 influenza A virus as an air borne pathogen to induce infectivity in pancreas: a mouse model study

Cited by 9 publications

References 24 publications

Viruses and Type 1 Diabetes: From Enteroviruses to the Virome

Viruses and Type 1 Diabetes: From Enteroviruses to the Virome

The transcriptomic profiling of COVID-19 compared to SARS, MERS, Ebola, and H1N1

The transcriptomic profiling of SARS-CoV-2 compared to SARS, MERS, EBOV, and H1N1

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