Here is karmaswimswarmi (who is an MD/Phd molecular biologist)...

Here is karmaswimswarmi (who is an MD/Phd molecular biologist) reply to the AAV-8 paper that has appeared on the original link.

"John Gilmore: Thanks for posting and providing those links. The recent paper doesn’t pose a problem for Benitec at all, and has been rather irresponsibly misconstrued by bloggers at (another forum SS, not HC), clearly nonscientists and nonphysicians. The Nature paper is a deliberation on AAV8 in mouse vs. human hepatocytes in a xenograft model. It has implications for studies in mice, but not in people or nonhuman primates. Comments about relative lack of efficacy have been taken quite out of context by bloggers. Benitec’s rAAV8 vector HAS already been given to humans and found to transduce hepatocytes with resounding efficacy. What has not yet been given to humans, and will be this month, is that vector with shRNA encoding strands installed, an “armed” AAV, if you will. But that the vector transduces human hepatocytes effectively is now quite established. Also, Benitec gave TT-034 (the rAAV8 plus 3 antiHCV shRNA’s) to cynomolgus monkeys (extreme similarity to human livers) and proved very high levels of production of shRNAs there. It may be more than you wanted to know, but the most elemental problem for Benitec is this: no one knows what the true preferred cellular sanctuary is for HCV in humans. It’s called “hepatitis,” yes, but it loves replicating in lymphocytes and macrophages. I put my biggest concern to the company: if the agent transduces only hepatocytes, how is it going to get rid of an infection in many non-iiver compartments? HCV only infects about 1 of every 10-15 hepatocytes, but abounds in lymphoid tissue. The answers are complex and sophisticated, but I scientifically believe it will work. It would honestly take a 10,000-word disquisition on why, but the data suggests that all those other compartments are in equilibrium with liver. Deplete the liver pool of virus, and all other cell types follow."