Old infectious particles that left viral DNA in our genes serve as defensive mechanisms shielding cells from some viruses. This is demonstrated in the study issued in the academic journal Science.
How cells are protected from a range of viruses
According to the study, endogenous viral elements (ERVs), pieces of old viral DNA, give defense against current submicroscopic infectious agents that arise externally by guarding them against accessing living cells that harbours an infectious agent. They are abundant in the genomes of jawed vertebrates, and they comprise up to 5–8% of the genome of humans (lower estimates of ~1%). Though this work used cells grown in a favorable artificial environment, it demonstrates that ERVs have the ability to stop the growth and reproduction of viruses that is probably also present in humans.
When an ERV affects a cell, its ribonucleic acid is turned into deoxyribonucleic acid and included in the host’s genes. The cell then produces other viruses following the gene’s instructing. The virus makes use of molecular machines that carry out complex, multistep reactions in transcription initiation and elongation to multiply. The ability for DNA to transmit from parent to child and ultimately get ingrained in the host genes is provided by ERVs that affect germ cells.
Generally, this category of viruses affects cellular units that are not transmitted from parents to children. For RNA viruses to come into a cell, viral envelope proteins, mostly glycoproteins, must bind to cellular receptors, just as a key entering a lock. Researchers searched the genes for possible glycoprotein-coding areas that might retain receptor-binding activities using computational and statistical analysis of genomes.
Then, further experiments were carried out to see if any of them was showing activity, that is, creating enveloped gene items in certain cell types.
After discovering glycoproteins, the researchers concentrated on SUPYN, a protein that in humans is encoded by the ERVH48-1 gene, revealed in the placentas and in the first stages of growth of the human embryo. Researchers then carried out studies using cells that resembled human placentas since viruses frequently affect this organ. The RD114/simian type D virus was introduced to the cells. SUPYN-negative human cell types may be more sensitive to infections. As a result, the cells lost their defense against the RD114 virus when SUPYN was removed from them in the course of the experiment; following its return, the cells regained it.
The study illustrates how a protein “switches off” cell surface receptors that make it possible for enveloped RNA viruses occurring in several nonhuman species to affect cells and cause viral entrance. The finding is crucial because it might uncover a source of naturally occurring proteins-protectors that can be exploited to create drugs without having conditions arising from an abnormal immune response to a functioning body part.
