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You come see me
Posted on 03/15/2003 11:40:21 PM PST by Mother Abigail
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That's not really true.
The best thing we all can do --
as a culture and
individuals --
is keep our immune system
strong by avoiding
doing drugs for fun,
chronic exhaustion and foods
full of chemicals.
If we stay healthy,
it might not matter what bugs
now and then pop up.
Prcognition?
Dèjá Vu!
Gene-swapping Ebola is a slippery target
Scientists have genetically sequenced Ebola viruses from gorillas and chimpanzees for the first time and found the virus to be more varied than previously thought.
Unexpectedly, they have also discovered that different strains of the virus can swap genes - a find that could make producing a vaccine much more difficult.
The Ebola virus causes fever and haemorrhage and kills up to 90% of people who catch it. It has spread cross Africa since 1976, infecting humans and apes sporadically and also hiding in bats.
An outbreak currently underway in the Democratic Republic of the Congo is so far thought to have infected 76 people. Ebola has also killed thousands of apes and has caused the lowland gorilla to be classed as endangered.
The genetic code for human versions of the viruses taken from humans has been sequenced before.
But, as sick animals are so difficult to find in the wild, and dead ones decompose quickly, until now no one has sequenced the virus from an ape.
Distributed virus
Eric Leroy and colleagues at the International Centre for Medical Research in Franceville, Gabon, managed to retrieve all or part of the Ebola virus from the remains of six gorillas and one chimpanzee. The viral genes were found to be similar to each other and to viruses from human victims in the same region.
But when all the sequences were analysed and compared, they clustered in two groups that, according to a model of how fast such viruses evolve, diverged from each other in 1976.
Furthermore, when all available samples - from both humans and apes - were analysed together, those collected after 1996 were found to be more similar to each other than to those collected (from humans alone) before 1996.
Leroy believes this shows that the virus is already distributed across central Africa and something else must be responsible for the current wave of outbreaks.
Leroy says the genetic differences “add to evidence for the pre-existing distribution of the virus.”
Rare recombination
The results may not resolve the rivalry between competing theories about how Ebola spreads. Peter Walsh of the Max Planck Institute for Anthropology in Leipzig, Germany, does not believe the virus is already distributed, and says different forms of it may simply be spreading together. “We have too few samples to know,” he says.
But both experts agree that the real surprise is that recent samples from humans show some genes from one cluster and some from another.
Such recombination is rare in RNA viruses and has never been seen before in filoviruses such as Ebola.
This recombination also means that a much wider range of genetic variants may emerge, making it harder to create an effective vaccine, says Walsh.
http://www.newscientist.com/article/dn12750-geneswapping-ebola-is-a-slippery-target.html
This is very bad news.
MA
Gene splicing Ebola? They've got to be bat-$hit crazy!
Thank you for the post, and the ping MA.
Joe,
It is the virus that is swapping genes.
The two strains appear to be mixing genes among primate populations.
This recombinant behavior (Dr. Niman please pick up the white courtesy phone) is a worst case scenario.
We need a stable genome to target.
When the target is constantly shifting many bad things can happen. including variations that require less contact for infection.
MA
I think your favorite Dr. is about to be back in the news again.
However, to his credit he has been predicting this for a long time.
MA
Em oh oh en spells...
5.56mm
Love the cheery news on a day like today...thanks.
One is happy to serve...
Doug,
What concerns me most is that we might begin to see an infection pattern with Ebola that is now well documented in Marburg outbreaks.
1. We know that human infection with Ebola comes about through the intermediary of infected great ape carcasses.
2. The viral transmission to primates occurs in the dry season, a period when food resources become increasingly scarce. The great apes then come into competition with bat species for fruit supplies when foraging and can be infected notably by blood or by placental fluid that escapes when bats give birth. (See my post #57 from 2004)
3. The mode of contamination by Marburg virus appears to be different, however. It does not appear to need any intermediary to be pathogenic for humans, as foreseen from the data on Marburg epidemic outbreaks.
In one outbreak, which raged in the north-east of DRC in 2000, most people infected worked in a goldmine, which turned out to be the refuge for a large colony of Egyptian rousettes. During the second epidemic, in Angola, the first victims were children who had gathered fruit from trees where a large population of this species of fruit bat roosted.
4. R. aegyptiacus - Carries both antibodies and viral RNA fragments - strongly suggesting that this bat species is a non-symptom developing carrier of the Marburg virus - (i.e.) the natural reservoir.
If Ebola were to recombine in a way that gave it any of the infection abilities of its cousin Marburg - well.....
Not as far fetched as once it seemed.
MA
Aw, Mom! It's no more difficult than finding a vaccine for the common cold...
Thank you for the ping, MA.
This post’s interesting (the thread’s quite interesting too).
Well, what is *most fascinating* to me, is to see “Mother Abigail” (whoever that is...) responding in post #67, to a 3-1/2 year old comment, post #57, saying (a good 3.5 years later) — “This is very bad news.”
Now, that is the most fascinating part of this whole thread... LOL!
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