Washington University logoSince ages, viruses that lead to diseases in animals are known to overpower the security system. However researchers from Washington University School of Medicine now reveal the discovery of a security system in host cells courtesy of viruses. This, they believe should help them investigate in depth the likelihood of getting the system in the picture against a number of diseases. This includes sudden acute respiratory syndrome (SARS), West Nile virus, dengue and yellow fever.

According to the scientists involved, these findings may unravel nearly a 35-year old mystery. It included National Institutes of Health researcher Bernard Moss, MD, PhD, who observed poxviruses to dress specific spots in each part of genetic material on DNA transcribed with chemical ‘caps’. This is RNA and helps recreate viruses that may be required to lead the host cell into believing that viral proteins can be formed from this RNA. Moss suggested that the caps were a manner for the cells to differentiate between their RNA and an invader’s.

The researcher further pointed that the caps could be acting like a false labelling badge for the virus’ RNA. This could apparently enable it to beat the host cell security systems prepared to attack any RNA that may not have caps. Scientists have since learned that certain viruses may have a plan of action for robbing RNA caps from host cells so as to place them on their own RNA. A range of disease-causing viruses may need to fabricate their own caps counting poxviruses, flaviviruses, rhabdoviruses, coronaviruses and reoviruses.

The scientists additionally suggest that one of the chemical caps supplemented to RNA may aid in stabilizing it, this averting break down of the RNA. A mystery however was the need for an additional cap close to the start of each RNA strand in the 2’ position. The new paper put forth by senior author Michael S. Diamond, MD, PhD, is said to unravel this puzzle while also nodding in agreement to Moss’ speculation. For the investigation, the researchers employed a mutant form of the West Nile virus. It was tailored by Pei-Yong Shi, PhD.

While having the ability to fasten the cap to keep RNA stable, the mutant strain may not have the capacity to add the 2’ cap. Diamond found that when this mutant virus infected mice, it could not lead to a disease. Following this, the scientists had the mice lacking receptors for interferons injected with the mutant virus. Reportedly, these proteins play an integral part in defensive reactions to viruses that attack within the cell. With the mutant virus sickening the mice, the intrinsic immunity this reveals blocks the mutant viruses in normal mice. The 2’ cap is also suggested to aid normal viruses from dodging this area of the immune system.

A gene IFIT2, the researchers recognized to have been activated by interferons. Probably having subtle antiviral effects against the West Nile virus, it appears to have the potential association to interpret RNA into proteins. On turning IFIT2 levels up in cell culture, Diamond then described it to the mutant West Nile virus which the virus was found to hardly duplicate. Similar results were found with tests of a mutant poxvirus and a mutant coronavirus when it couldn’t fasten the 2′ cap. IFIT1 was found to beat a linked gene in mice, to allow the mutant virus avoid intrinsic immunity. This may have resulted in an infection upon injection to the brain.

These findings have been published in Nature.