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Source: COVID-19 News - OAS Genes - Heart Failure  Oct 31, 2022  1 year, 1 month, 3 days, 23 hours, 16 minutes ago

COVID-19 News: Scientist From China Find That OAS Genes Play A Key Role In SARS-CoV-2 Induced Heart Failure

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COVID-19 News: Scientist From China Find That OAS Genes Play A Key Role In SARS-CoV-2 Induced Heart Failure
Source: COVID-19 News - OAS Genes - Heart Failure  Oct 31, 2022  1 year, 1 month, 3 days, 23 hours, 16 minutes ago
COVID-19 News: Researchers from Shanxi Medical University – China have found that the OAS genes plays a key role in COVID-19 induced heart failure.

According to the study team, SARS-CoV-2 infections can damage the heart and lead to heart failure (HF) and even cardiac death. The 2',5'-oligoadenylate synthetase (OAS) gene family encode interferon (IFN)-induced antiviral proteins which is associated with the antiviral immune responses of COVID-19 and also play a role in COVID-19 induced heart failures
To date according to latest COVID-19 News, the ongoing COVID-19 pandemic has infected more than 635 million people globally according to reported data and also caused more than 6.59 million COVID-19 deaths. (Actual figures could be as high as 5 to 6-fold!). Excess deaths in the last three years have also been increasing with many being attributed due to heart failures.
It is already known that COVID-19 can also damage multiple organs especially the heart, causing myocardial injury and heart failure (HF).
In fact, heart failure is the fourth most frequent complication of COVID-19, and is also the final outcome of most cardiovascular diseases.
Worryingly, the mortality rate of heart failure is extremely high.
Hence it is necessary to investigate the regulatory mechanisms of heart failure (HF) in COVID‐19 in order to better control the worse cardiac consequences of this infectious disease.
The OAS gene has long been suspected of playing a role in COVID-19 associated cardiac issues and even in other organ failures and disease progression seen in COVID-19.
The OAS gene family in the human genome includes OAS1, OAS2, OAS3, and OASL. As an important immune regulator, OAS gene family participates in antiviral biological process and innate immune.
It has been found that upon virus infection, OAS genes catalyze ATP into 2',5'-linked oligomers of adenosine in the presence of double-stranded (ds) RNA. These oligomers then activate RNaseL.
The OAS proteins act as a sensor of dsRNA and block viral replication by activating RNaseL. In this process, NOD-like proteins can interact with the OAS family to enhance the activity of RNase L.
Interestingly, the degraded RNA activates retinoic acid-inducible gene-I (RIG-1). RIG-1 amplify production of IFN-α/β and activate NF-κB to produce inflammatory factors, leading to cell apoptosis. In addition, the JAK-STAT pathway an d IFN regulatory factor (IRF) family are involved in the regulation of this process.
It is however unknown whether the OAS gene family actually plays a beneficial or harmful role in SARS-CoV-2-infected cardiomyocytes and COVID-19-induced cardiac injury and failure, because activations of antiviral genes do not necessarily produce a beneficial effect on the viral diseases such as COVID-19.
The study team already initially speculated prior to the study that OAS gene family is an effective mediator for COVID-19 to worsen the cardiac function and cause heart failure.
Past studies have found that untimely or overreacted antiviral responses may cause imbalance of the immune system, leading to inflammatory response or cytokine storm.
It has been found that SARS-CoV-2 infects the respiratory cells and other cells including the cardiomyocytes, causes host cell apoptotic death by inducing inflammation and even cytokine storm, thus may worsen the cardiac function and cause heart failure (HF), one of the most common outcomes of COVID-19.
Utilizing extensive bioinformatic analyses and experimental validation, the study team found that the expressions of OAS genes were significantly upregulated in both the SARS-CoV-2-infected cardiomyocytes and in the failing hearts of COVID-19-free cases.
The study findings support our speculation and suggest that OAS gene family promotes the development of heart failures (HF) in COVID-19. Targeting OAS genes may be a potential therapeutic approach in treating COVID-19 associated heart failure (HF).
For the study, the expression levels and biological functions of OAS gene family in SARS-CoV-2 infected cardiomyocytes dataset (GSE150392) and HF dataset (GSE120852) were determined by comprehensive bioinformatic analysis and experimental validation. The associated microRNAs (miRNAs) were explored from Targetscan and GSE104150 databases. The potential OAS gene family-regulatory chemicals or ingredients were predicted using Comparative Toxicogenomics Database (CTD) and SymMap database.
The study findings showed that the OAS genes were highly expressed in both SARS-CoV-2 infected cardiomyocytes and in the failing hearts. The differentially expression genes (DEGs) in the two datasets were enriched in cardiovascular disease and COVID-19 related pathways, respectively. The miRNAs-target analysis indicated that 9 miRNAs could increase the expression of OAS genes. A variety of chemicals or ingredients were predicted regulating the expression of OAS gene family especially estradiol.
The study findings concluded that the OAS gene family is an important mediator of heart failure (HF) in COVID-19 and may serve as a potential therapeutic target for cardiac injury and HF in COVID-19.
The study findings were published in on a preprint server and are currently being peer reviewed for publication in the Journal of Translational Medicine (BMC).
The key highlight of the study was the discovery of an important role of OAS gene family in the process of COVID-19 induced heart failure. Heart failure is one of the major adverse consequences of COVID-19.
The study findings that OAS genes were highly expressed in both SARS-CoV-2-infected cardiomyocytes and human HF tissues provides a reason to believe that some similar signaling molecules may mediate the developments of COVID-19 and HF. Or in other words, there may be some similar or common molecular mechanisms in the two diseases, and OAS genes may be the common genetic factors.
Based on the present bioinformatics analysis and previous reports, OAS genes are highly expressed in SARS-CoV-2 infected cardiomyocytes and COVID-19 patients, and the present qPCR experiments further verified the high expressions of OAS genes in the myocardium of COVID-19-free HF cases.
Past studies have also reported that OAS cluster variants are associated with greater risk of severe COVID-19, and OAS gene family plays an important role in the innate antiviral mechanisms linking to SARS-CoV-2 infection.
The study findings may be associated with the immune dysregulation and cytokine storm leading to heart failure (HF) in COVID-19 patients.
It has been found that during the cytokine storm, a large number of inflammatory factors are produced, such as TNF-α, IL1, IL-6, and IFN-γ, leading to severe inflammation, multi-organ failure and even death. Several previous studies have reported that cytokine storm can occur in COVID-19 patients, and the level of pro-inflammatory factors is positively correlated with disease severity.
Hence, this may be a crucial reason for developing heart failure (HF) in COVID-19 cases.
In order to corelate OAS gene family with COVID-19 associated HF, it is worthy to mention the important roles of IFN and IFN-stimulated genes (ISGs) in the endogenous anti-virus processes.
The OAS gene family is closely related to the induction of IFN. In COVID-19 patients, SARS-CoV-2 strongly triggers the expressions of many ISGs and activates immune cells. ISGs have immunopathogenic potentials, including overexpression of inflammatory genes.
Interestingly, in some COVID-19 cases, the level of IFN-I is low at the early stage, leading to excessive viral proliferation; when the IFN-I reaches a high level at the advanced stage, it may be too late to be rescued. Massive viral replication and early immune escape result in hyperactivation of pro-inflammatory responses.
Also, in severe COVID-19 cases, IFN-I response arouses an excessive inflammatory response by promoting TNF/IL-1β-driven inflammation leading to cytokine storm.
Being critical members of innate immunity, the OAS genes play important roles in immune responses and even the cytokine storm, this may one reason why COVID19 can cause heart failures (HF).
A past study also found a highly preserved transcriptional profile of IFN-I dependent genes for COVID-19 complementary diagnosis, and OAS genes were included in the profile.
All these data suggest the important role of OAS gene family in COVID-19.
Another past study reported that SARSCoV-2 invasion can damage the heart via the following mechanisms:
- ) inflammatory cells infiltrate into the myocardium;
-) pro-inflammatory cytokines cause cardiomyocyte death;
-) viruses damage the endothelial cells coupled with micro-thrombosis;
-) hypoxia caused by respiratory failure indirectly contributes to HF.
Among these mechanisms, OAS genes may take roles at least in some of them, for example, the immune responses.
The study team concluded that OAS genes are highly expressed in SARS-CoV-2 infected cardiomyocytes, tissues of COVID-19 patients, and COVID-19-free human failing hearts. OAS gene family strongly links COVID-19 with heart failure (HF). Also, OAS genes can interact with the invaded SARS-CoV-2 and activates the OAS/RNaseL antiviral system to degrade the virus. The degraded small RNA molecules activate NF-kB inflammation-related pathways, produce inflammatory factors or even cytokine storms, lead to cell death, and ultimately cause heart failure (HF).
For the latest COVID-19 News, keep on logging to Thailand Medical News.
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