Posted on 08/20/2002 7:20:41 AM PDT by blam
Genetic susceptibility to West Nile virus
22:00 19 August 02
NewScientist.com news service
A genetic mutation might explain why only one fifth of people infected with West Nile virus go on to develop symptoms - and why only one fifth of these people develop a severe, often fatal, brain inflammation, say French researchers.
West Nile virus, named after the area in Uganda where it was first detected, is mosquito-borne. It belongs to the family of flaviviruses, which includes dengue and yellow fever. And it is currently sweeping across the US, with the first recorded infection on the west coast reported on Monday.
A team at the Institut Pasteur in Paris, France, studied mice infected with the virus. All those that died rapidly had a mutation in a gene that encodes enzymes called oligoadenylate synthetases. These enzymes are involved destroying viral material in infected cells.
"We found a direct correlation between the mice who died and those with a mutated version of the gene that encodes oligoadenylate synthetase enzymes," says Jean-Louis Guenet, who led the research at the Institut Pasteur in Paris, France.
Although there is no evidence of a similar genetic mutation in humans, the gene is common to all vertebrates and the human version is very similar to that found in mice, Guenet says. "Researchers should now hunt for the mutated gene in humans. Perhaps it will lead to better understanding of how we can detect those most at risk from flavivruses and find ways to protect them," he told New Scientist.
Future epidemics
West Nile is widely distributed through Africa, the Middle East and parts of Asia. It can spread rapidly over vast areas, largely because about 40 species of mosquito can transmit the virus, and about 70 species of birds can harbour it.
The virus first struck the US in 1999 in New York. On Monday it was reported to have spread to the western states of Colorado and Wyoming. Eleven deaths and 251 cases have been recorded in the US so far this year, and the Centers for Disease Control and Prevention predicts another 1,000 infections and 100 deaths will occur in the next week.
Given the low background immunity to the virus in the US, future epidemics are likely, says Charles Samuel of the University of California, Santa Barbara, US.
"Understanding the genetic determinants that affect West Nile virus susceptibility and resistance is of utmost importance," he says. That knowledge will give researchers clues to exactly how the virus causes illness in people - and clues on how to treat it, he says.
There is currently no treatment or vaccine for West Nile virus. But a hybrid vaccine that incorporates genes from the virus into a safe form of the dengue virus is undergoing trials in monkeys.
Journal reference: Proceedings of the National Academy of Sciences (DOI:10.1073/pnas172195399)
If you live in rural America, tuff luck. Cant drain the swamp because the Corps of environmental engineers bulldozed the levy down so to flood the once very productive farmland abd establish a establish a swamp to preserve some critters. Put on lots of spray, or forget the outdoors completely and become a prisoner in your home.
West Nile is here to stay. This is a product of the "Sustainable development" concept of the UN that is gradually being implemented, without binding treaty, or the ratification and approval by the American People. Our way of life is no longer an approved method of living according to the UN. So we are expendable. We have to stop the environmental Nazis NOW!
Geez...I knew that. I don't know why I kept typing 'CYCLE.' (I'm gonna blame it on old age...)
Well, there goes that idea!! (Sorry about the lady) I've already been bitten twice this morning, that's why I'm concerned.
SNP and protein information for OAS1 (2',5'-oligoadenylate synthetase 1
CCR5 Mutation Found Most Commonly in Nordic Populations
The deltaccr5 mutation conferring protection against HIV-1 in Caucasian populations has a single and recent origin in Northeastern Europe.
Dating the origin of the CCR5-Delta32 AIDS-resistance allele by the coalescence of haplotypes...we estimate the origin of the CCR5-Delta32-containing ancestral haplotype to be approximately 700 years ago, with an estimated range of 275-1,875 years. The geographic cline of CCR5-Delta32 frequencies and its recent emergence are consistent with a historic strong selective event (e.g. , an epidemic of a pathogen that, like HIV-1, utilizes CCR5), driving its frequency upward in ancestral Caucasian populations. What was about ~700 years ago and after the 'Age of the Vikings' had distributed this mutation? Black Death probably was pestis
The vikings 'viked' from ~800-1100ad and spread this mutation all around Europe, especially the northern parts and along river basins. Once they achieved respectability and became part of the nobility themselves they tended to marry other Viking descent Normans. Ultimately many of the noble families of Europe, particularly the northern european nobilities, were descended from Norman stock.
When the plague came along, something about this mutation (either homozygously, or heterozygously) may have rendered them more able to withstand the plague. Contemporary writers at the time of the first plague outbreak noted that it was much more common for peasants to lose whole families than the nobility. There wasn't a great deal of difference at that time between the cleanliness of the nobles and that of the peasants, they were all fairly 'gross'. Their descendants would have carried this mutation as well. This is why this particular mutation is found in a north/south gradient and also along estuaries where the native population hasn't had a great deal of 'shifting about' during the past 1000 years or so.
This mutation has the effect in that HIV uses the CCR5 receptor (among others) to pick the lock and let itself in the immune system cells to do its nasty takeover work. If there is no receptor, there can be no lockpicking. This is one reason HIV is so much more 'virulent' in Africa. They were never 'viked' and thus never got this particular mutation. (Course, i'm not sure the populations being 'viked' considered this a plus at the time...) There are other receptors being studied for mutations with anti-HIV effects as well. The discovery of this particular mutation has brought about a whole new class of anti-HIV therapeutic drugs. If not having the receptor at all isn't a bad thing, then blocking it with a drug probably won't be bad either and might stop the rapid replication of the virus.
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