Is the COVID-19 virus pathogenic because it depletes specifi
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Why is the COVID-19 virus deadly, while many other coronaviruses are fairly innocuous and just cause colds?

A team of University of Alabama at Birmingham and Polish researchers propose an answer -- the COVID-19 virus acts as a microRNA "sponge." This action modulates host microRNA levels in ways that aid viral replication and stymies the host immune response.

The miRNAs are only about 0.01 percent of total human cell and tissue RNA, while replicating viral RNA of a virus like the COVID-19 virus may reach 50 percent of the total cellular RNA. So, the researchers say, if the COVID-19 virus has binding sites for specific miRNAs -- and these sites are different from the binding sites for miRNAs found on coronaviruses that cause colds -- the more pathogenic COVID-19 virus may selectively sponge up certain miRNAs to dysregulate the cell in ways that make it a dangerous human coronavirus.

In the present study, the researchers used computer-aided bioinformatic analysis to find potential miRNA target sites for 896 mature human miRNA sequences on seven different coronavirus genomes. These genomes included the three pathogenic coronaviruses -- the SARS, MERS and COVID-19 viruses -- and four non-pathogenic coronaviruses.

The researchers found that the number of target sites was elevated in the pathogenic viruses compared to the non-pathogenic strains. Furthermore, they found that pathogenic human coronaviruses attracted sets of miRNAs that differ from the non-pathogenic human coronaviruses. In particular, a set of 28 miRNAs were unique for the COVID-19 virus; the SARS and MERS viruses had their own unique sets of 21 and 24 miRNAs, respectively.

Focusing on the 28 unique miRNAs for the COVID-19 virus, the researchers found that the majority of these miRNAs are well expressed in bronchial epithelial cells, and their dysregulation has been reported in human lung pathologies that include lung cancers, chronic obstructive pulmonary disease, cystic fibrosis and tuberculosis.

"Hence, the COVID-19 virus -- by its potential reduction of the host's miRNA pool -- may promote infected cell survival and thus continuity of its replication cycle," the researchers said.

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