14 DAY TRIAL // Microbiologists at the University of California in Irvine (UCI) say they've recently developed a new method of fighting off viral infections. The approach is based on novel data about how RNA viruses infect and hijack cells in the host organisms, and use them to multiply.
Gaining more insight into how this happens provides researchers around the world with potential targets for new drugs and therapies. Interestingly, the treatments that could result from this investigation would be universal, capable of addressing a wide array of viral illnesses.
The work is very important because this category of pathogens leads to the development of conditions that are both dangerous, and capable of infecting large numbers of people. Some of the diseases caused by RNA viruses include the common cold, hepatitis, encephalitis and meningitis.
In order to produce the genetic material needed to multiply, these pathogens hijack a very important DNA repair activity inside the host cells, experts from UCI and the Leiden University, in the Netherlands, explain.
Details of the research effort were published in the August 20 early online issue of the esteemed journal Proceedings of the National Academy of Sciences (PNAS). The leader of the international team was Bert Semler, a microbiology and molecular genetics professor at UCI.
The research focused on a special group of RNA viruses, called picornaviruses. The team found that these pathogens are able to hijack the protein TDP2, an enzyme that is used for repairing cellular DNA.
“These findings are significant because all known picornaviruses harbor the target for this DNA repair enzyme, despite the fact that their genetic material is made up of RNA rather than DNA,” Semler says.
“Thus, identifying drugs or small molecules that interfere with the interaction between the virus and TDP2 could result in a broad-spectrum treatment for picornaviruses,” adds the team leader, who also holds an appointment as the director of the UCI Center for Virus Research.
With the new data, researchers could develop a drug that does not target the virus itself – therefore avoiding the challenge of antiviral drug resistance – but rather the host cell mechanisms the pathogen needs to multiply.
It remains to be seen how such a chemical would act, and what its effects would be on the human body. However, scientists are optimistic that this new avenue of research will eventually materialize in new therapies against RNA viruses.