Sharon Lewin
speaker
233 appearances
3 recordings
1 series
first heard Oct 2007
last heard Feb 2020
Sharon Lewin’s voice in public audio — every appearance, attributed to the second.
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And those signals for the chemokines that we're looking at, C C L nineteen and C C L twenty one is what they're called.
They drag T cells into lymph nodes.
So we began thinking, well maybe it was these chemokines that were sort of conditioning resting cells to become infected.
That's right.
So T cells are constantly travelling around the body.
Each T cell has a unique receptor for a particular foreign
antigen or foreign protein and it's each T cell's designed to get rid of anything that we might contact, infections or other foreign antigens.
But in order to get the best response to the T cell needs to be in a lymph node.
So these chemokines give the signal to those T cells to come into the lymph node.
So we did a s pretty simple experiment.
We just took resting T cells or resting purified C D four T cells from blood donors.
And we incubated those T cells with these chemokines and then tried to infect the cells.
And what we found was we could establish latency in the test tube.
We got infection, we got integration, and then the cell just sat there, it didn't start pumping out virus.
Yeah, that's exactly right.
So in fact in an unactivated resting cell, HIV will enter
will start trying to replicate, but it can't get into the nucleus, it can't get into the DNA.
But we've shown that if we tickle them up with these chemokines, we get very good high levels of HIV integration.
There's a whole lot of things we want to do now.
We want to understand how those chemokines change the cells, so which would allow efficient entry and integration.
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