Viral escape hatch could be treatment target for hepatitis E
The technique that the hepatitis E virus — an emerging liver virus historically found in developing countries but now on the rise in Europe — uses to spread could present a weak spot scientists can exploit to treat the disease, according to a new study.
Princeton University-led researchers report in the Proceedings of the National Academy of Sciences that when the hepatitis E virus infects a cell, it makes proteins that poke holes in the cell's membrane to allow newly made virus particles to escape and spread. Known as viroporins, these proteins create channels that allow the inflow and outflow of charged particles called ions that disrupt the infected cell's physiology and lead it to release the infectious particles.
Yet the very proteins the virus uses to escape a host cell and spread infection could in fact provide an avenue for developing antivirals that target hepatitis E, the researchers said. They suggest that curtailing the virus' ability to produce viroporins may prevent the pathogen from being able to burst forth from infected cells to attack other cells. Drugs that target viroporin production have already been developed for other viruses that employ the proteins to aid infection, including hepatitis C virus, HIV-1 and influenza A.
Researchers at Princeton and Rutgers universities have found that the hepatitis E virus — an emerging liver virus historically found in developing countries but now on the rise in Europe — uses a technique to spread infection that scientists could in fact exploit to treat the disease. The researchers found that, when in an infected cell (above), the hepatitis E virus pokes holes in a host cell's membrane by producing a protein known as viroporin (green dots). The holes act as ion channels that eventually cause the infected cell to burst, releasing new hepatitis E viruses that can infect more cells. The researchers suggest that curtailing the virus' ability to produce viroporins may prevent it from being able to attack other cells. (Image courtesy of Alexander Ploss, Department of Molecular Biology)
"These proteins cause changes in the cell membrane that allow the newly made hepatitis E virus particles to spread," said senior author Alexander Ploss, a Princeton assistant professor of molecular biology. "If we can prevent the release of viral particles, we could slow the spread of infection and give the immune system time to clear the virus from the body."