A cut away picture of HIV, a retrovirus. Credit: John Wildgoose, Wellcome Images
I’m afraid to tell you that you’re riddled with viruses; in almost every cell of your body. Sorry to be the one to break it to you. You have your parents to blame. Though not because of anything they did wrong, in fact, without these viruses, you wouldn’t even be here reading this spam.
As with all good stories worth reading, this one starts with sex.
(Though sadly not in the sweaty, exhaustive then have a cigarette kinda way. Sorry about that. I’m sure you could find other blogs for that kind of thing…?)
Something like 50 million years ago, your ancestor, and mine, probably looked something like a rat. Anyhow, this little fella, while shuffling around the undergrowth looking for bugs, was fortunate enough contract a virus; a virus of a type similar to HIV, a retrovirus.
Viruses don’t carry any machinery within themselves to be able to replicate on their own, like bacteria and us, for example. They get around this by invading their host organism and hijacking its cellular machinery for its own purpose – making copies of itself. This means they can only replicate in another organism, we call this an ‘obligate parasite’.
A retrovirus is a type of virus that uses DNAs sister molecule, RNA, as its genome. It uses an enzyme called ‘reverse transcriptase’ – which it brings with it when it infects its host - to translate its RNA into DNA and then incorporate this DNA directly in to its hosts genome. A bit like adding an extra paragraph in the middle of a text (or blog post… :D). This DNA is then translated into proteins by the host in the normal way.
Normally this infection either goes un-noticed, makes you a bit ill, kills you or whatever, basically it only affects you, and possibly any others you somehow manage to infect. Anyway, back to our little rat-like friend. S/he was one of the first of our ancestors that contracted this virus, but the interesting bit is, it infected its germ lines, that is to say, the sperm and egg cells. This means that, by mating, it would pass on the viral DNA to the next generation, fully intact. So we can assume that, for our ancestor, this must have been a fairly mild disease and its offspring subsequently survived long enough to mate and pass it on again, and again, and again and...
Something like this is happening to Koala bear populations right now in Australia.
Throughout the millions of years of our ancestry other similar viruses achieved the same trick.
We call these endogenous retroviruses (ERVs), or specifically to us, Human Endogenous Retroviruses (HERVs) and we can track their pattern of infection over time by looking for them in other species, for example, by analysing the DNA of chimps for the exact sequence present in humans. At least 5 of the same ERVs have been identified in chimps as humans. 3 of them were also found in old world monkeys.
A whopping 5-8% of our genome, at least, comes from such viral elements. I’ll just say that again 5-8% of us, what makes us US, came from viruses. Did you know that‽
The exact figure is a little in dispute, some think it’s as high as 50%.
For a long time HERVs have been implicated in two types of human disease; cancer and autoimmunity. In certain lymphomas and breast cancers high levels of RNA for a HERV, known as HERV-K, have been isolated and some reverse transcriptase activity has been found, but it is still far from clear if these are the cause or the result of the HERV causing cancer itself.
HERV-K is also one of the “youngest” HERVs we know of and exists in our DNA in an “open reading frame”, which means it is possible for the virus to be fully made afresh; in fact it has been shown to produce intact virus particles, which has led some to suggest it could even replicate by re-infection. But, before you run screaming through the streets, this has not been observed, and is only speculation.
So, that’s all the bad, so what good have they done us?
Well, HERV DNA in the genome has become used by the body as regulators and promoters of various genes, both human and viral in origin, playing a very important (if dull to write about…) bureaucratic role in our genome. So we have that much to thank them for.
The placentas of primates, humans included, have been shown to produce viral particles, now, this might sound bad, but the reason turns out to be good. Two HERV proteins, syncitin-1 and syncitin-2 have been shown to do this, and are expressed by the foetal side of the placenta, fusing cells together and creating a barrier between mother and child called the syncytium. This barrier allows oxygen and other nutrients from the mother to pass across and stops cells from parent or child entering each other’s blood stream, where they could be recognised as being “foreign” and cause an immune reaction or other complication.
In short, there’s still lots of work to be done on HERVs, and they appear to play an important and, until recently, overlooked role in our, and other species, evolution, but are an exciting area of research at the moment, both in evolution and disease.
As with all good stories worth reading, this one starts with sex.
(Though sadly not in the sweaty, exhaustive then have a cigarette kinda way. Sorry about that. I’m sure you could find other blogs for that kind of thing…?)
Something like 50 million years ago, your ancestor, and mine, probably looked something like a rat. Anyhow, this little fella, while shuffling around the undergrowth looking for bugs, was fortunate enough contract a virus; a virus of a type similar to HIV, a retrovirus.
Viruses don’t carry any machinery within themselves to be able to replicate on their own, like bacteria and us, for example. They get around this by invading their host organism and hijacking its cellular machinery for its own purpose – making copies of itself. This means they can only replicate in another organism, we call this an ‘obligate parasite’.
A retrovirus is a type of virus that uses DNAs sister molecule, RNA, as its genome. It uses an enzyme called ‘reverse transcriptase’ – which it brings with it when it infects its host - to translate its RNA into DNA and then incorporate this DNA directly in to its hosts genome. A bit like adding an extra paragraph in the middle of a text (or blog post… :D). This DNA is then translated into proteins by the host in the normal way.
Normally this infection either goes un-noticed, makes you a bit ill, kills you or whatever, basically it only affects you, and possibly any others you somehow manage to infect. Anyway, back to our little rat-like friend. S/he was one of the first of our ancestors that contracted this virus, but the interesting bit is, it infected its germ lines, that is to say, the sperm and egg cells. This means that, by mating, it would pass on the viral DNA to the next generation, fully intact. So we can assume that, for our ancestor, this must have been a fairly mild disease and its offspring subsequently survived long enough to mate and pass it on again, and again, and again and...
Something like this is happening to Koala bear populations right now in Australia.
Throughout the millions of years of our ancestry other similar viruses achieved the same trick.
We call these endogenous retroviruses (ERVs), or specifically to us, Human Endogenous Retroviruses (HERVs) and we can track their pattern of infection over time by looking for them in other species, for example, by analysing the DNA of chimps for the exact sequence present in humans. At least 5 of the same ERVs have been identified in chimps as humans. 3 of them were also found in old world monkeys.
A whopping 5-8% of our genome, at least, comes from such viral elements. I’ll just say that again 5-8% of us, what makes us US, came from viruses. Did you know that‽
The exact figure is a little in dispute, some think it’s as high as 50%.
For a long time HERVs have been implicated in two types of human disease; cancer and autoimmunity. In certain lymphomas and breast cancers high levels of RNA for a HERV, known as HERV-K, have been isolated and some reverse transcriptase activity has been found, but it is still far from clear if these are the cause or the result of the HERV causing cancer itself.
HERV-K is also one of the “youngest” HERVs we know of and exists in our DNA in an “open reading frame”, which means it is possible for the virus to be fully made afresh; in fact it has been shown to produce intact virus particles, which has led some to suggest it could even replicate by re-infection. But, before you run screaming through the streets, this has not been observed, and is only speculation.
So, that’s all the bad, so what good have they done us?
Well, HERV DNA in the genome has become used by the body as regulators and promoters of various genes, both human and viral in origin, playing a very important (if dull to write about…) bureaucratic role in our genome. So we have that much to thank them for.
The placentas of primates, humans included, have been shown to produce viral particles, now, this might sound bad, but the reason turns out to be good. Two HERV proteins, syncitin-1 and syncitin-2 have been shown to do this, and are expressed by the foetal side of the placenta, fusing cells together and creating a barrier between mother and child called the syncytium. This barrier allows oxygen and other nutrients from the mother to pass across and stops cells from parent or child entering each other’s blood stream, where they could be recognised as being “foreign” and cause an immune reaction or other complication.
In short, there’s still lots of work to be done on HERVs, and they appear to play an important and, until recently, overlooked role in our, and other species, evolution, but are an exciting area of research at the moment, both in evolution and disease.
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