Goal: To map all of flu's genes

Goal: To map all of flu's genes
Project hopes to find vulnerable spots to aid scientists in crafting better vaccines and drugs for the future
www.newsday.com...


BY DELTHIA RICKS
STAFF WRITER

November 24, 2004

Just as the Human Genome Project pinpointed all of the genes that make up a person, scientists now are embarking on a flu-virus equivalent to identify the genetic makeup of one of the world's most infectious microbes.

Scientists at the National Institutes of Allergy and Infectious Diseases, who will lead the effort, say the hope is to find better ways of fighting the flu by plumbing the gene sequences that make up influenza viruses. The search is on for genes stored in eight single strands of RNA, compared with up to 25,000 genes stored in the DNA of the billions of cells that make up an adult human. Technical assistance is expected from a range of collaborators, including scientists at the New York State Department of Health.

The project comes as public health officials have faced influenza crises two years running: A nationwide outbreak last year and a vaccine shortage this year............

One of the major goals of the flu sequencing project is to understand how the virus jumps species. This is accomplished via recombination as detailed at

www.recombinomics.com...

The species jumping of course leads to pandemic strains, which is just around the corner.

Originally posted by niman
One of the major goals of the flu sequencing project is to understand how the virus jumps species.

The species jumping of course leads to pandemic strains, which is just around the corner.

Thanks niman.

...Have you any information regarding the role of mis-folded proteins in recombination?

...Current virulent strains appear to have evolved from a disease called fibromuscular dysplasia entering domestic turkeys in the USA in 1980. ...the disease spread to quail in Japan by 1996, and the pathology has been found in avian reovirus as well as SARS and H5N1 avian flu.

Briefly, a protein called "a-smooth muscle actin" mis-folds and proliferates in fibroblast stem cells, which causes fibroblasts to mutate into myofibroblasts and then accumulate to cause fibrosis.

Schmidt, Lemke and Essler pointed out around 1986 that "proteinaceous capsids" were using viruses as vehicles of transmission... so it looks like we're dealing with a lot more here than cross-species jumping.

Any more information or comments?



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