SARS-CoV-2 causes disease but some other coronaviruses don't, new study finds possible reason
A group of researchers at the University of Alabama in Birmingham claim that they have found a possible reason why the novel coronavirus is pathogenic while some of its relatives only cause the common cold or many don’t cause disease in humans at all.
SARS-CoV-2, the causative agent of the COVID-19, is a type of coronavirus that enters the body through the nose, mouth or eyes and causes infection of the respiratory tract. This is not the first coronavirus that causes disease in humans. There are at least four different types of common cold-causing coronaviruses, SARS-CoV, MERS-CoV and several other non-pathogenic (those that do not cause disease) coronaviruses.
Now, a group of researchers at the University of Alabama in Birmingham claim that they have found a possible reason why the novel coronavirus is pathogenic while some of its relatives only cause the common cold or many don’t cause disease in humans at all.
The findings of the study are published in American Journal of Physiology - Lung Cellular and Molecular Physiology and suggest that SARS-CoV-2 acts as an miRNA sponge and weakens the host immune system, which allows viral replication and spread of infection in the body.
MiRNAs and viral sponges
MiRNAs (microRNAs) are short stretches of RNAs (ribonucleic acid). These help in the production of various proteins and help in fine-tuning cellular metabolism and the response of a cell to adverse challenges like stress or viral entry. It constitutes only 0.01 percent of the total RNA in a cell. However, during a viral infection, viral RNA constitutes about 50 percent of the total RNA in a cell. Viruses are intracellular parasites. They enter the host cells and replicate their RNA inside the cells before assembling new copies of itself and releasing them into the body to affect more cells.
The concept of viral sponges has previously been noted in Epstein Barr virus, hepatitis C and herpes virus. Viruses sponge up miRNAs by binding to them at various sites. A viral sponge can stop the miRNA of the cell from functioning. This makes the host cell unable to express certain proteins that can otherwise help it to fight the virus and eliminate it.
The latest study
In the latest study, the researchers used computer analysis and bioinformatics to find out the interaction between the 896 miRNAs in humans and the seven coronaviruses - four non-pathogenic coronaviruses along with the most pathogenic ones: SARS-CoV, MERS-CoV and SARS-CoV-2.
It was found that all three pathogenic strains had many more miRNA binding sites than the non-pathogenic strains. SARS-CoV-2 had a set of 28 unique miRNA binding sites and SARS and MERS virus had unique sets of 21 and 24 miRNA binding sites, respectively.
The miRNAs that SARS-CoV-2 effects are mainly expressed in the epithelial cells of the bronchi — tubes that send air into the lungs — and are mostly associated with lung conditions like lung cancer, tuberculosis and cystic fibrosis.
“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,” said the authors of the study in a news release.
It was further shown that about 9 of the 28 miRNAs sponged by the COVID-19 causing virus have a role in viral replication and stopping the production of host cell proteins among other things that this virus needs to perpetuate in the body.
The researchers say that these findings will need further validation, including checking the levels of the target miRNAs in host cells and tissues, and they may help develop novel therapeutic strategies involving the balancing of these miRNAs.
The study may help establish why some people are more prone to severe COVID-19. It has previously been suggested that older people have lesser miRNAs, which may be contributing to the severity of the disease.
Also, it may help understand how this virus can exist both in animals and humans. Bats have already been shown to have certain miRNAs that give it tolerance to SARS-CoV-2.
For more, read our article on The difference between coronavirus and COVID-19.
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