It appears in the American Journal of Physiology-Lung Cellular and Molecular Physiology.
Coronaviruses (COVs) are single-stranded RNA viruses that experts consider to be mild first. They come with viruses that cause colds.
However, the researchers stopped treating these viruses as benign after outbreaks of severe acute respiratory coronavirus (SARS-CoV) in 2002, Middle East Respiratory Syndrome (MERS-CoV) in 2012 and the existing PANdemic of COVID-19, for which severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) is responsible.
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Neither SARS nor MERS had the highest infectiousness of the new coronavirus, but neither was dangerous, resulting in 774 and 866 deaths, respectively. Although there are similarities in their RNA sequences, they differ significantly in their infection methods.
Currently, no vaccine is available for SARS-CoV-2. Research has focused on understanding the pathogenicity of the virus and, most importantly, restoring and improving patient immunity. Researchers are now contemplating cutting-edge approaches, such as the use of human microARNs (miARN).
MIRNAs are essential players in the body’s immune defense against viruses. These are short, non-coding RNA, which are expressed by their complementary mating with RNA express messengers in the cell.
By retaining and cutting viral RNA, miARN react to the cell reaction to create an antiviral effect. However, viruses also have the ability to maneuver the host’s miARN networks according to their own rules.
When microRNs are inhibited or unequal, the virus may more freely reflect immune responses and increase the severity of the disease.
In the existing study, the researchers looked for why these viruses are so different from commonly innocent bloodless viruses.
They hypothesized that the virus that causes COVID-19 has binding sites for some miARNs that are other miARN binding sites in the coronaviruses that cause the cold.
The most pathogenic SARS-CoV-2 virus can particularly serve as a miARN sponge, cutting moving miARN grades to make it a more harmful human coronavirus.
By analyzing existing literature and using computer-assisted bioinformatics techniques, the team evaluated possible miARN interactions with the SARS-CoV-2 genome and sought imaginable miARN targets for 896 human miAN sequences in seven other coronavirus genomes.
Genomes included those of the 3 pathogenic coronaviruses – SARS-CoV-2, MERS-CoV and SARS-CoV – and 4 non-pathogenic coronaviruses.
Research revealed that the number of target sites for micro-RNSRs is higher in pathogenic viruses than in non-pathogens.
In addition, microRNs targeted through pathogenic coronaviruses were different from those targeted through non-pathogenic coronaviruses.
Specifically, the researchers discovered a set of 28 miARNs that are unique to SARS-CoV-2, as well as sets of 21 and 24 other miARNs that are unique to SARS-CoV and MERS-CoV, respectively.
Further research from the 28 miARN for COVID-19 revealed that the maximum of these MIRNs are particularly expressed in bronchial epithelial cells. Researchers studied their deregulation in human lung diseases such as tuberculosis, cystic fibrosis, chronic obstructive pulmonary disease (COPD) and lung cancer.
As an immune defense mechanism, these miRNs are programmed to induce cells to commit suicide if they are mutated, inflamed or stressed.
In addition, nine of those microRNAs that SRAS-CoV-2 “sponge” prospectively can succeed in viral loads. “Therefore, the COVID-19 virus, through its possible relief from the host miARN set, can announce the survival of inflamed cells and therefore the continuation of their replication cycle,” the authors explain.
The authors then detailed how the virus replicated an inflamed cell, the molecular pathways involved, and the cellular responses to it.
The researchers’ findings “encourage speculation that pathogenic human coronaviruses, adding the COVID-19 virus, use host miARN to fine-tune cellular processes to facilitate the production of viral proteins.”
One limitation of the study is that the team took into account individual differences in people’s myARN profiles, but susceptibility to infection varies from user to user. For example, the severity of the disease and mortality rates were higher in the elderly.
A recent study suggests that in older patients, COVID-19 virulence may be caused by a decrease in the amount of miARN, indicating that they play a role in the severity of the disease. “Understanding these types of differences in patients is to create personalized antiviral therapies,” the test authors say.
The effects of this study provided a new prospective strategy for coVID-19 remedy. Synthetic miARNs can help repair key levels of miARN, helping them fight COVID-19.
The researchers acknowledge that their “hypothesis will require validations, with the evaluation of those miARN grades in inflamed tissues and ending with the recovery of the host miARN balance with miARN analogues”.
“In addition,” they add, “full of how viruses take credit for the endoplastic pathway and [the response of the disseminated protein] can also lead to new healing strategies.”
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