The Hepatitis virus scare is too much to handle, Hepatitis C alone infects more than 170 million people worldwide. The main danger is to the liver which leads to both acute and chronic liver diseases.
The protective mechanism that denies any anti viral therapy to be produced against it the refusal to reproduce in test tubes for more than a few hours or days. This has been a major problem and therefore scientists have not been able to find an efficient virus production and infection system.
AdvertisementThe reason for cheer in FSU is that Assistant Professor Hengli Tang and doctoral student/co-author Heather B. Nelson have discovered the molecular mechanism that inhibits HCV replication in vitro after its host cells become crowded and stopped dividing. This is a revolutionary study and will pave a way for further research in the direction of development of anti-viral therapies for HCV as well as for related RNA viruses such as West Nile and influenza.
The test that they have developed can quickly and easily monitor HCV replication in the laboratory. So scientists can easily monitor the nuances of the virus and study it closely.
The Feb. 8 edition of the Journal of Virology has the privilege to host the groundbreaking study that could change the way we look at hepatitis now.
Put in to words by the researcher himself Dr. Tang said, "Our findings could prove critical to research on HCV's complex virus-host cell interactions and lead to better, targeted treatments. Currently, any nucleotide starvation therapies, used primarily to treat cancer, can inhibit replication by depriving viral agents of their molecular building blocks. However, those therapies may impact healthy cells, as well, causing undesired side effects. That's not all. Our new cell line also allows us to rapidly identify and isolate drug-resistant HCV mutants in vitro and to screen for anti-viral drug candidates. This will help researchers, better study the mechanism of drug resistance, a big problem with this virus and others such as HIV (human immunodeficiency virus) that mutate quickly."
As a grand finale to this discovery he added ,"I find it particularly rewarding to play a part in research that may actually help somebody soon."