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COVID-19 research v0.348 MIR155 Rebecca Foulger commented on gene: MIR155: Evidence Summary from Illumina curation team (Alison Coffey and Julie Taylor): MIR155 (also referred to as BIC) is an endogenous noncoding RNA involved in regulation of the immune response, in particular T-cell differentiation, and in regulation of innate immunity (PMID: 32233818; 217121651;1746328969;20852130). This miRNA has been associated with various virus infections (PMID: 32233818;28139244;23686237;26072128). miR-155-5p expression has been shown to be induced in mice infected with influenza A virus (PMID: 32308197 - in this study, lung injury by ARDS was attenuated by deletion of miR-155, making this miRNA a potential therapeutic target in the context of COVID-19). Through single cell and bulk RNA profiling of SARS-CoV-2 and SARS-CoV infections in three human cell lines (H1299, Caco-2 and Calu-3 cells), Emanuel et al. (2020) (bioRxiv preprint doi: https://doi.org/10.1101/2020.05.05.079194) demonstrated strong expression of the immunity and inflammation-associated microRNA miRNA-155 upon viral infection with both viruses. Both viruses triggered a 16-fold upregulation of one form of miR-155 and a 3-fold upregulation of another.

A role for MIR155 in viral susceptibility for a range of viruses and the immune response has also been demonstrated in a series of mouse models:

PMID 23601686: In Mir155 -/- mice, Dudda et al. (2013) observed severely reduced accumulation of Cd8-positive T cells during acute and chronic viral infections with impaired control of viral replication. Lack of Mir155 led to an accumulation of Socs1 resulting in defective cytokine signaling through Stat5. Dudda et al. also concluded that MIR155 and its target, SOCS1, are key regulators of CD8-positive T cells.

PMID 23275599: Lind et al. (2013) found that mice lacking Mir155 had impaired Cd8 positive T-cell responses to infections with lymphocytic choriomeningitis virus and the intracellular bacteria Listeria monocytogenes and concluded that MIR155 is required for acute CD8-positive T-cell responses and proposed that targeting MIR155 may be useful in modulating immune responses.

PMID 24516198: Bhela et al. (2014) – 75 to 80% of MIR155 null mice infected ocularly with herpes simplex virus (HSV)-1 developed herpes simplex encephalitis with elevated viral titers in brain, but not in cornea. Immunohistochemical and flow cytometric analyses in Mir155-null mice showed diminished Cd8-positive T-cell numbers, functionality, and homing capacity. Adoptive transfer of HSV-1-immune Cd8-positive T cells to Mir155-null mice 24 hours after infection provided protection from HSE. The authors concluded that MIR155 deficiency results in enhanced susceptibility of the nervous system to HSV-1 infection.
COVID-19 research v0.243 SOCS1 Sarah Leigh edited their review of gene: SOCS1: Changed publications: 12588885, 12588885, 18172216, https://doi.org/10.1101/499988
COVID-19 research v0.243 SOCS1 Sarah Leigh changed review comment from: PMID 12588885: In coxsackievirus-infected mice cardiac myocyte-specific transgenic expression of SOCS1 inhibited virus-induced signaling of JAK and STAT resulting in increased viral replication, cardiomyopathy, and mortality compared to controls. Inhibition of SOCS in cardiac myocytes increased myocyte resistance to the acute cardiac injury of enteroviral infection. It was suggested that inhibition of SOCS could augment the host-cell antiviral system and might prevent viral-mediated end-organ damage during the early stages of infection.
Sources: Literature; to: PMID 12588885: In coxsackievirus-infected mice cardiac myocyte-specific transgenic expression of SOCS1 inhibited virus-induced signaling of JAK and STAT resulting in increased viral replication, cardiomyopathy, and mortality compared to controls. Inhibition of SOCS in cardiac myocytes increased myocyte resistance to the acute cardiac injury of enteroviral infection. It was suggested that inhibition of SOCS could augment the host-cell antiviral system and might prevent viral-mediated end-organ damage during the early stages of infection.
https://doi.org/10.1101/499988 reports: Genome-wide association study to identify loci that are associated with PID, and found evidence for the colocalization of—and interplay between—novel high-penetrance monogenic variants and common variants (at the PTPN2 and SOCS1 loci).

Sources: Literature
COVID-19 research v0.243 SOCS1 Sarah Leigh gene: SOCS1 was added
gene: SOCS1 was added to COVID-19 research. Sources: Literature
Mode of inheritance for gene: SOCS1 was set to Unknown
Publications for gene: SOCS1 were set to 12588885; 12588885; 18172216
Phenotypes for gene: SOCS1 were set to primary immunodeficiency
Review for gene: SOCS1 was set to AMBER
Added comment: PMID 12588885: In coxsackievirus-infected mice cardiac myocyte-specific transgenic expression of SOCS1 inhibited virus-induced signaling of JAK and STAT resulting in increased viral replication, cardiomyopathy, and mortality compared to controls. Inhibition of SOCS in cardiac myocytes increased myocyte resistance to the acute cardiac injury of enteroviral infection. It was suggested that inhibition of SOCS could augment the host-cell antiviral system and might prevent viral-mediated end-organ damage during the early stages of infection.
Sources: Literature
COVID-19 research v0.242 PTPN2 Sarah Leigh gene: PTPN2 was added
gene: PTPN2 was added to COVID-19 research. Sources: Literature
Mode of inheritance for gene: PTPN2 was set to Unknown
Publications for gene: PTPN2 were set to 19825843; https://doi.org/10.1101/499988
Phenotypes for gene: PTPN2 were set to primary immunodeficiency
Review for gene: PTPN2 was set to RED
Added comment: https://doi.org/10.1101/499988 reports: genome-wide association study to identify loci that are associated with PID, and found evidence for the colocalization of—and interplay between—novel high-penetrance monogenic variants and common variants (at the PTPN2 and SOCS1 loci).
Sources: Literature