Link to go viral 11/04/15 – HIV spreads like internet malware and should be treated earlier

HIV spreads like internet malware and should be treated earlier – UCL News – Published on: 2 Apr 2015

The reason we call nasty computer programmes ‘viruses’ is because their behaviour mimics the real thing – spread between individuals, make more copies of yourself and repeat. So it’s kind of glorious that we can flip this around and learn about the viruses that make us sick by studying their digital analogues.

Here a team from London, Oxford and Changsha (in China) looked at the role of ‘hybrid spreading’ – a phenomenon shared by HIV infection and computer malware such as the Conficker worm. These viruses both spread over long-distances (bloodstream / the internet) and between close contacts (between cells / between computers on a local network). And both are also extremely difficult to get rid of once the infection is fully established because local ‘pockets’ of virus can be difficult to eliminate1.

The computer model the research team have developed suggests that to combat HIV infection in people, we need treatments that work effectively against both means of spread, and we need to treat earlier than we currently do. The team’s model may also provide a way of testing whether drugs are effective at stopping cell-to-cell spread; a measurement that is otherwise difficult to study.

  1. Retroviruses such as HIV may also be impossible to completely eliminate, as these guys can hang out in cell DNA, where such drug treatments can’t reach them.

LET’S GET RETRO! – 2 – In their fight against ‘feline HIV’, cats are betrayed by a virus in their DNA

In Part 1 of this series, I wrote a primer on what retroviruses are and how human DNA is riddled with these personal parasites. But it’s not all about you. While HIV may be the most notable human retrovirus circulating today, so help me internet, I’m going to talk about retroviruses that infect cats. Not only does their story have an extra fascinating twist, but I need to justify all these lolcat photos. If you haven’t read Part 1: Peculiarly Personal Parasites, you can find it here.

You have my attention… – (image:

You see cats, like dogs, mice, men (and more!) have their very own brands of these personal parasites. One such retrovirus is Feline Leukemia Virus (FeLV), and like many of its counterparts elsewhere in the zoo, it has a nasty habit of infecting the white blood cells of the immune system. This vicious double punch not only produces new viruses but thwarts the very defenders trying to repel them.

FeLV is spread between cats by mutual grooming or fighting and is passed in saliva and other bodily fluids. Around 2–3% of cats (in the USA, at least) are infected with the virus and you can learn more about the disease itself over at the Cornell University FeLV webpage.

As if it wasn’t already bad for the kitties, the genomes of retroviruses like FeLV readily mutate during infection. While a change in the genome is a potential evolutionary path for the virus to tread, all of the changes present in the swarm of infecting microbes is a fur-tile landscape. If a path is good for the virus1 it is easily taken, like walking downhill. But if it damages the virus’ prospects of making new viruses, the swarm will avoid the hill rather than climb it. Some paths, like the envelope protein ‘key’ on the outside of the virus no longer providing entry into cells, are an evolutionary Everest. These same evolutionary phenomena are also true of HIV infection in humans, but a shadowy sherpa in the DNA of cats – an endogenous retrovirus – allows FeLV to scale to sinister new heights and is bad news for Bagpuss. Whilst the endogenous virus is otherwise dormant, its envelope protein gene is not. The cat’s own body churns out free spare keys that allow FeLV to infect cells even when its own mutated key no longer fits the locks.

There’s a lot of landscape to explore. It’s not all a pretty sight – (image:

This might not seem like worse news for Garfield than already being sick, but it’s actually a short sprint to being stuck up the feline AIDS tree. Usually, retroviruses do not enter cells that have already been infected – the virus envelope protein acting like a ‘SOLD’ sign that shows this patch of host is occupied. But nasty variants of FeLV, known as FeLV-T, carry changes in their own envelope proteins that allow them to ignore these signs and repeatedly infect the same cell. The result is a rapidly growing pile of dead immune cells, unravelling the cat immune system like a ball of string. And while these changes in the FeLV-T envelope protein also make it a terrible key to enter cells, the virus can take this evolutionary path because the cat’s bloodstream is full of working spares.

It seems these spare pieces of virus, charmingly and yet kind of disturbingly named FeLIX (oh scientists and their naming things), can only be found in the blood of domestic cats. Blood from related cat species and other mammals doesn’t contain any FeLIX or proteins that act like it (link not free, sorry!). It’s not clear right now whether the endogenous retroviruses in other cats are completely dormant, or whether our pet moggies picked up the FeLIX-producing retroviruses after they split from other cat lineages. And while it seems like bad news for our friendly furballs, so long as their chance of catching FeLV is low, the FeLIX endogenous retrovirus timebomb isn’t one to keep them up at night. Or during the daytime. Lazy felines.

OK kitties, no more posting about cat viruses for now – (image:

Reference articles:

Anderson et al., 2000. Identification of a Cellular Cofactor Required for Infection by Feline Leukemia Virus (link)

Sakaguchi et al., 2015. A soluble envelope protein of endogenous retrovirus (FeLIX) present in serum of domestic cats mediates infection of a pathogenic variant of feline leukemia virus (link)

Image credits:

Images 1 & 3 from (link and link)

Image 2 from (link)

  1. Making it spread better or escape the immune system, for example.