The solution to permanently beat infections such as the cold, caused by the rhinovirus, could be found within our own cells according to a new study conducted by researchers at the University of California in San Francisco.
According to experiments conducted by researchers on human cell cultures and mice, temporarily disabling a particular protein can prevent many species of enteroviruses, including rhinoviruses, from replicating within the cells. All enteroviruses seem to need this particular protein to replicate.
To understand what proteins were vital for enteroviruses, researchers first generated a culture with human cells and had them infected by rhinovirus RV-C15, which causes asthma in children, and EV-C68, which causes acute flaccid myelitis. They then used genetic editing to randomly disable individual genes in each of the cells and found that a single gene produces an enzyme called SETD3 that was clearly essential to the success of the infection.
To prove it, they created a new culture of human cells without SETD3 and tried to infect them with various enteroviruses, including two varieties of coxsackievirus, a virus that can cause myocarditis. None of these viruses could replicate in cells that no longer produced the enzyme SETD3.
Performing the same experiment but in vivo on mice, the latter, completely missing SETD3, grew up to adulthood in good health and were also fertile. The same researchers also discovered that enteroviruses do not seem to make any particular use of the enzyme SETD3; more than anything else they move around this protein that, in yet unknown ways, is almost necessary for their replication.
This latest discovery gives researchers hope that they can develop a drug with an antiviral activity similar to that of the absence of SETD3 without disturbing the latter in the cells.
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