Debunking myths on genetics and DNA

Saturday, August 27, 2011

Tell me a joke, please!

I'm scheduled to give a 1-hr talk on Tuesday. I'm very nervous: I've never given a talk that long. Typically conferences give you a 10-20 minute slot, so you zip through a dozen slides, try to be convincing enough to make people happy while hand-waving enough to skip the dirty details.

But heck, one whole hour?
I suppose that means I'm growing up.

So, I'm told the way to start is to break the ice with a joke. Except I'm terrible at jokes. Nobody ever laughs when I tell one. Maybe it's my accent. Do I need a particular "joke-voice" I'm not aware of?

Or maybe it's the topic. HIV is not a funny subject to discuss.

In a talk that long, aimed at a general audience, I will have to start introducing the pandemic. Last June marked the 30th anniversary of the discovery of the AIDS disease. According to UNAIDS, at the end of 2010, there were over 34 million people leaving with HIV/AIDS worldwide. There are 2.6 million new infections per year, and 1.8 million deaths per year.

Those are some stunning numbers.

What's even more stunning--no, wait, let me use another word. Appalling. Two thirds of all infected people live in Sub-Saharan Africa. While in the western world the average life expectancy (how many years we "hope" to live) has steadily grown in the past 5 decades, and it's well beyond 60, in countries like Botswana people aren't expected to live past their 35th birthday. There are parts of Africa where villages have been wiped off of an entire generation and kids are raised by their grandparents. In these countries, teenagers have a 50% chance of contracting AIDS in their lifetime.

Why is this virus so deadly?

For one thing, HIV attacks the immune system. It's like striking under the belt: in order to reproduce itself, the virus uses the very same cells that are supposed to defend us from it.

But the virus's most effective weapon is its genetic variability. The way our immune system works, it takes a few days for our sentinels to recognize the "attacker" and put together a big enough platoon of soldiers to deploy a counterattack. Typically, a macrophage will recognize a viral particle, destroy it, then bring the "debris" to a T-cell. The T-cell carries the pathogen to the thymus in order to start a process called T-cell activation: once the pathogen is presented, T-cells able to recognize it and destroy it are mass-produced and sent off on a clean-up mission.

Problem: by the time the platoon leaves its quarters, the enemy has changed.


They are called T-cell escapes: mutations that appear in the viral genome and disguise the virus. The proteins on its surface change shape. They fold in a different way, and suddenly the T-cell is no longer able to grab the virus. The darn little thing slips away unharmed.

That's the challenge that HIV has posed for the past thirty years. Vaccines are typically made of a deactivated strain that, injected inside the body, elicits the proper immune response. But when you have a virus this variable what are you going to use as a strain? This enemy has a million different faces, and as soon as the immune system finds a weapon against it, the virus comes up with a new disguise to escape it.

Wait, not all hope is lost. We can beat the monster with its own weapons. How? Well, I've got to leave something for my talk, right? So read next post or come to the talk. And if you do come, please tell the jokes for me. Or give me a crush course.

Edit: the talk went well. Nobody laughed, but I didn't attempt telling jokes. So that was good, I really didn't want people laughing when I was NOT telling jokes. Nobody fell asleep either, which, for a 1pm talk was quite an achievement. Yay.

Photo: seagull. Canon 40D, focal length 17mm, exposure time 1/500. Tonemapped for pretty background.


  1. You may be terrible at jokes but you are good enough at "captatio benevolentiae" from the audience! Shall I come to the talk?!...


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