We all know viruses cause deadly diseases on their cycle of invading hosts, with most of them eventually killing their host. We have always dealt with deadly viral diseases starting from smallpox to Spanish flu and the recent COVID-19 pandemic. Whatever the disease, it is always fascinating how a tiny organism makes uses of its host to produce its own copies. But a new study gives us more clarity on this aspect. Scientists have found that viruses can steal signals from genes to produce their own genomes. The findings, published in Journal Cell, is a collaborative study of virologists from Glasgow and New York.
The research was oriented towards the single-stranded Negative sense RNA viruses [(-) ss RNA viruses, according to Baltimore classification], which include a wide array of viruses that infect humans, animals, and plants. They also include deadly viruses that cause influenza and Lassa fever. Researchers say that these viruses were capable of stealing genetic codes from their hosts to produce previously undetected proteins. Going by the name UFO (Upstream Frankenstein Open reading frame), these proteins are mere products of host and viral sequences. Experts say that these novel proteins can be the target for future vaccine purposes.
While viruses cannot build their own proteins so they depend on their host to build their proteins. One such process by which they acquire portions us a process called cap snatching in which they cut a portion of host RNA and extend it to their genome to initiate viral mRNA synthesis. The research shoe that viruses make hybrids of host mRNAs with their own genes and also can produce signals from host-derived codons by start snatching. In this way, they found that the virus is able to initiate translation from previously not known proteins from the same hybrid host sequence. But there is speculation of this hybrid gene on its visibility on the host’s immune system and their modification of virulency. They further reveal that the genes are expressed by influenza and other viruses.
Currently, the team only studies this effect on the influenza viruses, and therefore, we can see that there can be a number of other viruses that can show the same previously not known protein for their replication. The team next is to focus on the unsuspected genes on the role of replication and to see whether they used to eradicate the disease. As these discoveries are new, we need to pour in a lot of research work to exploit the benefits of these to combat diseases.
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