Populations of viruses are just like populations of humans in one particularly important way: they are diverse. Diversity amongst humans gives us biological benefits - if we were all carbon copies of each other, we would all have not only the exact same strengths, but also the exact same weaknesses. If we were all carbon copies, if one of us had a predisposition to anxiety, all of us would. If one of us had a gene polymorphism, or a small difference in our DNA that can change the functioning of our proteins, that made us more susceptible to one particular virus, we all would. In the former case, we might end up with a very cautious, but also boing, version of humanity. And in the latter case, that one virus could wipe all of us out in one fell swoop.
Viruses need diversity for the same reason. In the dance of evolution against their hosts, small differences between individual virus particles can give some of those individual viruses an edge - permitting them to sneak past certain immune cells, or infect new types of cells, for example.
This is applicable to all viruses, as far as I know - from influenza to SARS to HIV. But in today's post, I'm going to focus in on research done by my colleagues in Amsterdam that highlights one of the ways that diversity amongst individual virus particles is important - for the virus, that is. Today's post is a story of HIV.
When a person is infected with HIV, and goes untreated, their human body becomes its own little microcosm of evolution for the virus. Within that one person, many different strains of HIV-1 will arise, and each of those strains will be better at accomplishing different actions that are important for the survival of the virus. Some will be really good at infecting particular types of cells, for instance, while others will specialize in finding a new human host - to expand the microcosm to a duality. And in the case of HIV, these viruses that specialize in transmitting to new susceptible hosts have a special name: transmitted/founder viruses.
Transmitted/founder viruses are so named because they transmit effectively to a new susceptible host to found a new infection there - a new microcosm with resources ripe for the virus to capitalize on. In this paper that I want to talk to you about today, my colleagues in Amsterdam describe a newly identified ability of transmitted/founder HIV-1 viruses that probably helps facilitate their transmitter function.
A few years back, my supervisor showed that specific human cells that reside at the surface of human skin and genital tissue are actually able to protect against HIV infection. When these cells, called Langerhans cells, come into contact with HIV, the virus is routed to the recycling system of the cell, and broken down into its harmless subcomponents. Thus, Langerhans cells act as a physical barrier against incoming HIV.
In this follow-up paper, some new light has been shed on why this system isn't perfect -and why we still get HIV. It isn't entirely clear why at this point, but these transmitted/founder viruses are actually able to evade this recycling of the virus, in a way that other strains of HIV can't. Instead of getting broken down inside the Langerhans cells, transmitted/founder HIV viruses can replicate inside them, and from there likely go on to spread through the rest of the human body.
At the moment, we still aren't totally sure why transmitted/founder viruses have this particular ability. We don’t know the exact mechanism. But, I think this example is very illustrative of the impressive differences that can exist within one type of virus. These viruses that can and cannot replicate in Langerhans cells are all HIV. They're all a microbial invader that we often think of as being one unified, defined threat. But actually, every virus is an army, or a population, composed of individuals with different strengths and weaknesses. In that sense, they are indeed a lot like us.
Until next week, be like a virus and celebrate diversity!
~Alex