Stanford’s Jeffrey Glenn , MD, PhD, and colleagues, in a just-published study, have discovered a promising class of compounds that could help defeat the hepatitis C virus, or HCV, while reducing the side effects that all too often accompany current treatments.
Designing a new antiviral agent is tough, because a virus thrives by commandeering a host cell’s own essential functions. . . . By itself, a virus is little more than a speck of gene-encoding nucleic acid. Unlike bacteria, which multiply by dividing, a virus reproduces by breaking into cells and diverting their manufacturing machinery to produce copies of itself, which eventually depart the ravaged cell to find and exploit fresh ones.
The compounds Glenn and his associates identified act by impairing a virus-initiated process that is essential to its own replication but never occurs in normal, healthy cells. So, in principle, such compounds might nail HCV, yet cause little or no damage to human cells.
Hepatitis C affects about 150 million people worldwide and, in the United States, is the number-one cause of liver cancer and liver-transplantion, according to Glenn. Yet, he adds, many of those who are infected don’t even know it.
An estimated . . . 75 percent of those with hepatitis C are not aware of their infections. This lack of awareness extends to health-care providers and policymakers. As a result, policymakers fail to allocate adequate resources to address it. The CDC’s division of HIV, STD, TB and viral hepatitis has an annual budget of about $1 billion. Only 2 percent is allocated to viral hepatitis.
It will be a good year or two before his team’s preclinical experiments yield to actual clinical trials in human beings and, certainly, a couple of more years beyond that under the best of circumstances before any drug based on the discovery can gain FDA approval. Hurry the day.