Scientists at the University of California, San Francisco and the UCSF-affiliated San Francisco General Medical Center have developed a model to study at the cellular level how viruses like HIV and Hepatitis B and C evade and co-opt the defense strategies of the cells they invade to cause chronic infections.
In a study reported in the Proceedings of the National Academy of Sciences, a group led by Allan Lau, and Michael Yeung, scientists in the Department Of Pediatrics at UCSF, has shown that a virus can establish a persistent infection if it can overcome cell suicide, an important host defense. And they have shown that once the virus establishes a lasting presence in the host's cells, physiological changes begin. The cells grow more slowly and the virus becomes less infectious over time -- evidence of co-evolution for the virus and its host.
The discovery could lead to methods to find new antiviral agents, to boost the effectiveness of antiviral drugs - and possibly to end Hepatitis C and other persistent viral infections.
Most viral infections begin with a virulent phase straight out of science fiction: The virus invades and kills cells, the immune system mounts a response to keep it from invading further and the infected person suffers misery as a result. Some viruses later change their tactics from invader to dominator. The virus takes over part of the cell's machinery and dwells there, becoming a persistent infection. Persistent viral infections can continue for life and wreak slow havoc, as HIV does to the immune system and Hepatitis B and C do to the liver.
Now Lau, Yeung and their colleagues have taken a virulent, cell-killing virus and converted it to a persistently infective virus. They turned off the host cell's last-ditch defense mechanism, which normally attempts to stop the viral invasion by a process of programmed destruction called apoptosis -- cell suicide.