Researchers at HSE University have discovered microRNA molecules that may suppress the replication of human coronavirus, including SARS-CoV-2. The virus has been shown to use miRNA hsa-miR-21-3p to inhibit growth in the first stages of infection by delaying the active immune response. Research results published in journal PeerJ..
later Virus Once inside the cell, it begins to actively interact with various intracellular molecules. One such molecular class is the microRna (miRNA). This is a small RNA whose main function is to regulate gene expression. When a virus invades, miRNAs begin to bind to specific parts of their genomic RNA, leading to the destruction of the viral RNA. Such an attack could completely stop virus replication. However, if the miRNA is not very “aggressive,” such interactions slow down replication rather than destroying the virus. This scenario is beneficial to the virus as it helps to avoid the rapid immune response inside the cell. In addition, some viruses intentionally accumulate host miRNA binding sites. This is their advantage. Viruses with more binding sites survive, reproduce better, and lead to evolutionary dominance.
HSE Biology and Biotechnology researchers Stepan Nersisyan and Alexander Tonevitsky, and first-year students Narek Engibaryan, Aleksandra Gorbonos, Ksenia Kirdey, and Alexey Makhonin have detected bindable cellular miRNAs. Coronavirus genome.
There are seven types of human coronavirus in all. Four of them (HCoV-OC43, HCoV-NL63, HCoV-HKU1, and HCoV-229E) spread and cause colds, but the viruses MERS-CoV, SARS-CoV, SARS-CoV-2 are dangerous atypical. It can cause pneumonia. Researchers have discovered four families of human miRNAs that have been found to bind to all viruses under consideration.
This image shows the miRNA binding sites hsa-miR-21-3p and hsa-miR-421. These are 6 of the 7 human coronaviruses interacting with each other.
To investigate how the virus interacts with detected miRNAs, we analyzed available data on lung miRNA sequences in SARS-CoV-infected mice. They found that the infection increased the expression of previously detected miRNA hsa-miR-21-3p by a factor of 8.
“MiRNA hsa-miR-21-3p has great potential to bind to all human coronaviruses, but after infection with SARS-CoV, the concentration of this miRNA in the lungs increases significantly. Assuming this is the mechanism of the immune response, it is not clear why the virus does not eliminate binding sites for cellular miRNAs during the course of mutation. Conversely, the virus “accumulates” them in the genome during evolution. I understand this. In this way, the virus is thought to use this miRNA to slow replication and delay the active immune response in the early stages of infection, “said Stepan Nersisyan.
The next step in the team’s research is the experimental verification of their findings. Researchers are also planning to investigate the potential efficacy of the discovered miRNA-targeting viruses. In particular, they plan to determine if their artificial introduction or elimination can prevent virus replication.
Stepan Nersisyan et al, Potential role of cellular miRNAs in coronavirus-host interactions, PeerJ (2020). DOI: 10.7717 / peerj.9994
Provided by the Higher School of Economics, National Research University
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