Non-cytotoxic control of HBV

So what? What difference does it make how the CTL are clearing virus, so long as they do clear it? Here are some reasons to care:
This way a few CTL can affect many target cells. There are some 1011 hepatocytes, and hepatitis viruses can infect a lot of them, very fast. There are different estimates for how long it takes for a CTL to deliver a lethal hit when it’s being cytotoxic, but let’s say something like 30 - 60 minutes per cell. That’s a long, long time for CTL to kill off all the infected cells. If all they have to do is release interferon, they can probably pick off many cells at once and move on. This is a faster way to control viruses, and it doesn’t take as many CTL. Guidotti et al transferred 5 x 106 HBV-specific CTL into the transgenic mice; within 24 hours, all of the virus had been shut down (remember. these are transgenic mice expressing “virus” in every liver cell).
Again: There are some 1011 hepatocytes, and hepatitis viruses can infect a lot of them, very fast. If CTL have to kill all the virus-infected cells, what’s left of the liver to do it’s usual liverly duties? If the infection can be shut down without killing the cells, you’ve saved your liver. Those 5 x 106 CTL shut down the virus without killing more than 10% of the liver cells.
Potentially, any inflammation in the liver can lead to protection. If you have HBV, and you’re infected by lymphocytic choriomeningitis, (well, first you’d likely be a mouse), the inflammation induced by the LCMV might shut down the HBV, as a handy side effect. This cross-protection from other viruses has actually been seen both in mice8 and — maybe — in humans as well.9
So the finding that CTL are capable of shutting down virus replication without having to kill the infected cells, fit very nicely with the new technology showing that CTL commonly have these mechanisms availabl