The word Genome has been in the news a lot lately. United Devices is now running a program similar to Folding involved in mapping out Human Genomes.
The following showed up in my inbox.

From an ARCAMAX newsletter;

Dog Genome Findings May Benefit Human Health
Source: Medinews.com

Scientists studying the genetic background of dogs, which has revealed more than 150 inherited canine disorders resembling specific human diseases, say their work will provide information that can be used to improve human health.

The study, published in the May 21, 2004, issue of Science, has revealed distinct DNA blueprints for each of the 85 varieties of purebreds analyzed. The researchers expect that understanding these genetic relationships will help them uncover the genes responsible for the physical features and behaviors unique to each breed as well as the diseases to which they are commonly susceptible, such as cancer, deafness, blindness, heart disease, and hip dysplasia.

"This study helps us understand the genetic relationship between breeds, a finding that will facilitate our efforts to map disease genes and genes for what are known as complex traits, which result from the interaction of multiple genes," said Dr. Elaine Ostrander, of the Fred Hutchinson Cancer Research Center (Seattle, WA, USA; www.fhcrc.org), who is head of the dog genome project there.

Since any traits associated with a given breed must result from a shared set of genetic determinants, these genes stand out much more obviously than they would in a population of unrelated, or genetically dissimilar, animals. Since most breeds were developed within the last 300 years, the researchers expect that each distinctive trait has arisen from a small number of genes. These features make it easier to identify a gene or genes responsible for a specific trait.

There are more than 400 breeds of dog, and each is an isolated breeding population, remarked Dr. Ostrander. What that means is that each dog breed is like a little Iceland, an isolated population that allows us to simplify a complicated genetic problem.

To analyze the similarities and differences among purebred dogs, researchers contracted breed clubs and collected DNA samples from five animals from each of 85 breeds. They then genotyped the DNA, using microsatellite analysis. They found that the DNA sequences of microsatellites from dogs within a breed were much more similar than those among breeds.

They were able to sort the breeds into four groups of genetically similar varieties. One group represents an ancient group of animals with Asian and African origins that includes breeds such as the Alaskan Malamute and Siberian Husky, and shows the closest relationship to the wolf. A second group contains Mastiff-like breeds that share common physical characteristics. A third group includes Shetland and Belgian sheepdogs and Collies. The fourth group includes animals with hunting-associated behaviors.

The researchers are now using the information from their analysis to study specific canine diseases. In addition to cancer, they are studying the genetics of blindness and soon will begin a study on the genetics of obsessive-compulsive disease.

"We could not have done the work without the involvement of pet owners, breeders, and community leaders who support the work were doing to improve both canine and human health. This is just the way science is supposed to be done," said Dr. Ostrander.

It appears that progress is being made in the fight.
Those of us who have taken more of an active interest in what it is our machines are doing when running F@H, then some of the things mentioned in this article will be familiar. Those who just run the program, the items mentioned in this article are just some of the things your machine checks for when you fold.

Unlike some other Distributed Computing Programs, the results we turn in to Stanford are shared throughout the scientific community, so that discoveries such as this can be be uncovered. Many papers can be had by the simple process of signing up for an account. Other sites housing complex work might require a fee or paid membership to help offset the cost of running the www version of material one is seeking.

[Edit: 30 Apr, 2006 - Article no longer appears to be on that site]
From: http://www.realcities.com/mld/krwashington/news/nation/10407757.htm

The war against cancer focuses on a key gene By Robert S. Boyd Knight Ridder Newspapers WASHINGTON - In the long, frustrating battle against cancer, one gene has emerged as a key, both to the cause of the disease and to its prevention. This master gene watches out for cells whose DNA has been corrupted by tobacco smoke, ultraviolet light, toxic chemicals or other carcinogens. If it detects a damaged cell, it triggers a process that blocks that cell from reproducing and possibly giving birth to a malignant tumor. But if the gene itself is defective, it can't do its job. Cancer is often the result. The gene's official name is "p53," but some scientists call it the "guardian of the genome," the sum of all 25,000 or so genes in the human body. "You can call p53 the guardian because it's the common denominator in virtually all human tumors," said Bert Vogelstein, a leading cancer expert at the Johns Hopkins Medical Institutions in Baltimore. "It's almost impossible to develop cancer in most organs unless p53 is inactivated." Researchers are looking for drugs that can restore damaged p53, so it can get back to its job of defending us against cancer.

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Source: Harvard Medical School
Date: 2004-12-27

Discovery Of First Demethylase Molecule, A Long-sought Gene Regulator

BOSTON, MA -- Researchers have discovered an enzyme that plays an important role in controlling which genes will be turned on or off at any given time in a cell. The novel protein helps orchestrate the patterns of gene activity that determine normal cell function. Their disruption can lead to cancer.

The elusive enzyme, whose presence in cells was suspected but not proven for decades, came to light in the laboratory of Yang Shi, HMS professor of pathology, and is described in a study published in the Dec. 16 online edition of Cell and appearing in the Dec. 29 print edition.

"This discovery will have a huge impact on the field of gene regulation," said Fred Winston, an HMS professor of genetics who was not involved with the work. "Shi and his colleagues discovered something that many people didn't believe existed."

The enzyme, a histone demethylase, removes methyl groups appended to histone proteins that bind DNA and help regulate gene activity. "Previously, people thought that histone methylation was stable and irreversible," said Shi. "The fact that we've identified a demethylase suggests a more dynamic process of gene regulation via methylation of histones. The idea of yin and yang is universal in biology; our results show that histone methylation is no different."

In the cell, yarnlike strands of DNA wrap around protein scaffolds built of histones. The histones organize DNA into a packed structure that can fit into the nucleus, and the packing determines whether the genes are available to be read or not. Acetyl, methyl, or other chemical tags appended to the histones determine how the histones and DNA interact to form a chromatin structure that either promotes gene activity or represses it.

Some histone tags, particularly acetyl groups, are known to be easily added and removed, helping genes to flick on and off when needed. But the addition of methyl groups was considered a one-way process that could only be reversed by the destruction of histones and their replacement with new ones. Part of the reason scientist believed this was that no one had isolated a demethylase, despite an active search.

The Shi lab was not among those in the hunt, but they stumbled onto the demethylase while probing the function of a new gene repressor protein. Postdoctoral fellow Yujiang Shi had exhausted the likely possibilities for how the mystery protein worked to suppress gene activity, so one day he tried an unlikely experiment. He had the purified protein in a test tube and decided to feed it methylated histones. His finding, that the enzyme could efficiently chew off the methyl group, leaving behind intact, unmodified histone left the postdoc Shi shaking with excitement. "Forty years ago some scientists speculated that histone demethylases existed," he said. "At first, I thought it was impossible that this protein was it." After reproducing the results using several different biochemical techniques, he began to feel comfortable that they had found the first demethylase.

Their enzyme didn't remove just any methyl group from histone. Instead, it removed a very specific methyl found on lysine 4 (K4) of histone 3 (H3). H3K4 methylation is associated with active transcription, so its removal would be consistent with the gene repression function they had identified.

Now that the first demethylase has been recognized, researchers will certainly find more. "This cannot be the only demethylase," said Shi.

Genes turning on at the wrong time or in the wrong place is a hallmark of cancer cells. In some tumors, high levels of methylation of H3K4 seem to play a role in activating genes that drive abnormal cell growth. The discovery of this H3K4 demethylase suggests a way to counterbalance this progrowth signal in some tumors. And if previous experience with histone deacetylases is any guide, the demethylases could one day be targets for cancer therapeutics.

"These findings will impact every walk of biology," said David Allis of Rockefeller University, a leader in studying the regulation and biological roles of histone tags. "Histone modifications are highly dynamic on-off switches that the cell throws a lot. These modifications affect everything DNA does, and getting the enzyme means you've got one upstream point of regulation. This will open up a wealth of new experiments."

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Gene determines risk of HIV/AIDS
Source: World Entertainment News Network

Scientists suggest people with more copies of a certain gene are less likely to become infected with the HIV virus or to develop AIDS. The US National Institutes of Health team say their finding could lead to a screening test to determine someone's susceptibility to HIV/Aids.

The gene the researchers studied is one which helps the body to fight the HIV virus. The research was published online by the journal Science. The gene encodes CCL3L1, a protein which blocks HIV which also interacts with CCR5 - a receptor protein that HIV uses as a doorway to enter and infect immune system blood cells.

The scientists analysed blood samples from more than 4,300 HIV-positive and -negative African-Americans, Europeans and Hispanic-Americans to determine the average number of copies of the CCL3L1 gene in each group. It was found that there was significant variation. (CM/WNWCCB/ZG)

(c) 2004 World Entertainment News Network

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Compound From Rare Plant Shows Promise In Treating Breast Cancer


CHARLOTTESVILLE, Va., Feb. 1, 2005 -- They started with a bare room and an idea. Now, after five years of painstaking, sophisticated tests, scientists at the University of Virginia Health System have discovered that a compound, derived from a rare South American plant, stops the growth of human breast cancer cells in laboratory cultures.


U. Va. Health System scientists Deborah Lannigan and Jeffrey Smith hope that, after further testing, their discovery could translate into a successful drug for the treatment of breast cancer. The disease is the second leading cancer killer of women in the U.S., according to the American Cancer Society, with an estimated 40,410 deaths.

The compound, called SL0101, comes from the plant Forsteronia refracta, a nondescript member of the dogbane family found in the Amazonian rain forest. The compound works like a key in a molecular lock. It inhibits the action of a cancer-linked protein called RSK, which the researchers discovered is important for controlling the growth of breast cancer cells. Interestingly, SL0101 does not alter the growth of normal breast cells. The discovery is detailed in the Feb. 1, 2005 issue of the journal Cancer Research and can be found online at: www.cancerres.aacrjournals.org.

"By preventing RSK from working, we completely stopped the growth of breast cancer cells but did not affect the growth of normal breast cells," said Lannigan, an Assistant Professor of Microbiology at the U. Va. Cancer Center. She compares this discovery to the development of the drug Gleevec for the treatment of chronic myeloid leukemia. Like Gleevec, SL0101 is a signal transduction inhibitor that interferes with the pathways that signal the growth of tumors. "Gleevec is an exciting discovery and we're hoping to have similar success with SL0101," Lannigan said.

For now, Lannigan and Smith have begun testing the compound in animal models. "The next step is to see if SL0101 will prevent the growth of human tumor cells in mice," said Smith, a Research Assistant Professor of Pathology at the U.Va. Cancer Center. "We will modify the structure of SL0101, if necessary, to eventually find a compound that can be carried through to human clinical trials. That's the goal. But human trials will likely be years down the road." The discovery of this potential anti-cancer compound at a U.Va. lab, Lannigan said, also highlights the important role of academic research in drug development.

The researchers collaborated on this discovery with a U.Va. Professor of Chemistry, Dr. Sidney Hecht, who maintains a large number of exotic plants collected by the National Cancer Institute in the 1960's for research purposes. It took years of work to identify and characterize SL0101 as a specific RSK inhibitor. "Finding out that RSK is a good drug target for breast cancer is very exciting," Smith said.

Cancer patients themselves can also take credit for this discovery. A group of volunteers from "Patients and Friends of the U.Va. Cancer Center" provided funds at a crucial stage of the research.
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This story has been adapted from a news release issued by University Of Virginia Health System.
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From: Science Daily
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Source: Pacific Northwest National Laboratory
Date: 2005-02-06
{This story has been adapted from a news release issued by Pacific Northwest National Laboratory.}

Fleshing Out The Genome

SEATTLE – Genomics, the study of all the genetic sequences in living organisms, has leaned heavily on the blueprint metaphor. A large part of the blueprint, unfortunately, has been unintelligible, with no good way to distinguish a bathroom from a boardroom, to link genomic features to cell function.

A national consortium of scientists led by BIATECH, a Seattle-area non-profit research center, and Pacific Northwest National Laboratory, a Department of Energy research institution in Richland, Wash., now suggests a way to put this house in order. They offer a powerful new method that integrates experimental and computational analyses to ascribe function to genes that had been termed "hypothetical" – sequences that appear in the genome but whose biological purposes were previously unknown.

The method not only portends a way to fill in the blanks in any organism's genome but also to compare the genomes of different organisms and their evolutionary relation to one another.

The new tools and approaches offer the most-comprehensive-to-date "functional annotation," a way of assigning the mystery sequences biological function and ranking them based on their similarity to genes known to encode proteins. Proteins are the workhorses of the cell, playing a role in everything from energy transport and metabolism to cellular communication.

This new ability to rank hypothetical sequences according to their likelihood to encode proteins "will be vital for any further experimentation and, eventually, for predicting biological function," said Eugene Kolker, president and director of BIATECH, an affiliate scientist at PNNL and lead author of a study in the Feb. 8 Proceedings of the National Academy of Sciences that applies the new annotation method to a strain of the metal-detoxifying bacterium Shewanella oneidensis.

"In a lot of cases," said James K. Fredrickson, a co-author and PNNL chief scientist, "it was not known from the gene sequence if a protein was even expressed. Now that we have high confidence that many of these hypothetical genes are expressing proteins, we can look for what role these proteins play."

Before this study, nearly 40 percent of the genetic sequences in Shewanella oneidensis—of key interest to DOE for its potential in nuclear and heavy metal waste remediation—were considered as hypothetical. This work identified 538 of these genes that expressed functional proteins and messenger RNA, accounting for a third of the hypothetical genes. They enlisted analytic software to scour public databases and applied expression data to improve gene annotation, identifying similarities to known proteins for 97 percent of these hypothetical proteins. All told, computational and experimental evidence provided functional information for 256 more genes, or 48 percent, but they could confidently assign exact biochemical functions for only 16 proteins, or 3 percent. Finally, they introduced a seven-category system for annotating genomic proteins, ranked according to a functional assignment's precision and confidence.

Kolker said that "a big part of this was the proteomics" – a systematic screening and identification of proteins, in this case those which were expressed in the microbe when subjected to stress. The proteomic analyses were done by four teams led by Kolker; Carol S. Giometti, Argonne National Laboratory; John R. Yates III, The Scripps Research Institute; and Richard D. Smith, W.R. Wiley Environmental Molecular Sciences Laboratory, based at PNNL. BIATECH's analysis of this data included dealing with more than 2 million files.

Fredrickson coordinates a consortium known as the Shewanella Federation. In addition to BIATECH, PNNL and ANL, the Federation also includes teams led by study co-authors James M. Tiedje, Michigan State University; Kenneth H. Nealson, University of Southern California; and Monica Riley, Marine Biology Laboratory. The Federation is supported by the Genomics: GTL Program of the DOE's Offices of Biological and Environmental Research and Advanced Scientific Computer Research. Other collaborators included the National Center for Biotechnology Information of the National Library of Medicine, National Institutes of Health, Oak Ridge National Laboratory and the Wadsworth Center.

BIATECH is an independent nonprofit biomedical research center located in Bothell, Wash. Its mission is to discover and model the molecular mechanisms of biological processes using cutting edge high-throughput technologies and computational analyses that will both improve human health and the environment. Its research focuses on applying integrative interdisciplinary approaches to the study of model microorganisms, and advancing our knowledge of their cellular behavior.

PNNL (http://www.pnl.gov ) is a DOE Office of Science laboratory that solves complex problems in energy, national security, the environment and life sciences by advancing the understanding of physics, chemistry, biology and computation. PNNL employs 3,900, has a $650 million annual budget and has been managed by Ohio-based Battelle since the lab's inception in 1965.

Editor's Note: The original news release can be found here.

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Source: Mayo Clinic
Date: 2005-02-05
{This story has been adapted from a news release issued by Mayo Clinic.}

Mayo Clinic Researchers Create 'Obedient Virus'; First Step To Use Measles Virus Against Cancer

ROCHESTER, Minn. -- An international team of Mayo Clinic-led researchers is first to devise a system that consistently converts the measles virus into a therapeutic killer that hunts down and destroys cancer cells -- and cancer cells only. Their research findings appear as an advanced electronic article of Nature Biotechnology.

The researchers harnessed the viral trait for attacking and commandeering cells, and then redirected the virus to attack diseased, rather than healthy cells. The work was done on laboratory animals implanted with two kinds of human cancer cells -- ovarian cancer and lymphoma -- and is probably still years away from use as a human therapy. But the concept has at last been proved in mice with human cancer tumors -- and that's an essential step toward using this approach to expand and improve human treatments for a variety of cancers.

The "Obedient Virus"

"When I saw the data, I was completely stunned. It's the sort of thing that, having worked on targeting viruses for about 15 years, I just couldn't believe that we'd finally got what we'd been hunting all that time," says Stephen Russell, M.D., Ph.D., lead researcher and director of Mayo Clinic's Molecular Medicine Program.

"It's very clean, very clear targeting. Our results show that we've efficiently ablated (destroyed) the ability of the measles virus to interact with its two natural receptors. And they also show that we can take our pick as to what new receptor we target and send the virus after it."

How They Did It

Using bioengineering techniques, the team reprogrammed the measles virus to seek a cancer cell to bind to instead of its natural binding partner. Then they invented a "molecular tag" that they attached to structures on the outside of the cancer-seeking measles virus. This tag is the key innovation of their work and central to the success of the team's investigation. It enables researchers to grow retargeted measles virus on special "universal substrate cells" -- while at the same time conserving the viral component for targeting and destroying tumors. Mass production of a retargeted virus was not possible before this specific innovation of the molecular tag -- and research in this area was at an impasse. Not any more.

"The virus goes where it's meant to go, and it destroys the tumors in a targeted way," says Dr. Russell.

Background Biology

Natural viruses are cellular parasites. To reproduce more viruses, they need to bind to a partner on their target cell, fuse membranes to enter the target cell and then take over the cellular machinery. When they succeed in doing this, an infection occurs. Viruses are so good at taking over cells that researchers have long dreamed of exploiting the specific attraction viruses have to certain cells and using it as a homing device to seek and enter cancer cells.

The measles virus became the focus of this vision several years ago when the surprising finding was made that the measles strain used internationally for vaccinations has natural anticancer activity.

"But we had a concern that the measles virus may be a little too promiscuous in its ability to infect both cancer cells and non-cancer cells, so we wanted to develop a method whereby we could retarget the virus to infect cancer cells only," says Dr. Russell. "And we succeeded."

Collaboration and Support

In addition to Dr. Russell, the Mayo Clinic research team includes Takafumi Nakamura, Ph.D.; Kah-Whye Peng, Ph.D.; Mary Harvey, Suzanne Greiner and Charles James. From the University of Ottawa, Ian A.J. Lorimer, Ph.D, contributed his expertise. The work was funded by The Mayo Clinic Foundation, the Harold W. Siebens Foundation, and the National Cancer Institute.

To obtain the latest news releases from Mayo Clinic, go to http://www.mayoclinic.org/news. MayoClinic.com is available as a resource for your health stories.

Editor's Note: The original news release can be found here.
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Study Shows Timing Is Everything In Coaxing Stem Cells Into Becoming Other Cells
Source: NewsRx.com

Researchers at the University of Wisconsin-Madison have whipped up an exciting, but intricate, new recipe that could someday treat spinal cord injuries or provide a cure for amyotrophic lateral sclerosis, better known as Lou Gehrig disease.

Step one:

• Take human embryonic stem cells, (the microscopic dots that have brought condemnation from the pope, opposition from the president and people generally opposed to abortion).;
• Add pinches of chemicals;
• Add dashes of other biological ingredients implicated in brain growth at just the right moment;
• and voila: brain cells called motor neurons that control every body movement.

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Source: American Society For Microbiology _____________________ Print this page

Date: 2005-04-22



Newly Identified Protein May Inhibit Hepatitis Virus

A newly identified family of proteins may inhibit replication of the Hepatitis B (HBV) and C (HCV) viruses say researchers from California. Their findings appear in the March 2005 issue of the Journal of Virology.


Hepatitis B (HBV) and C (HCV) are viruses that infect the liver, and in some cases can cause liver failure requiring a transplant for survival. The protein interferon, produced by animal cells when they are invaded by viruses, is released into the bloodstream or intercellular fluid to induce healthy cells to manufacture an enzyme that counters the infection. One class of interferons (alpha) is used to treat chronic infection with HBV and HCV. There is a vaccine available to prevent the spread of HBV but not HCV.


In the study, a new class of interferons, interferon lambda, was tested for its ability to inhibit HBV and HCV replication. Results showed 90% inhibition of HBV after twenty-four hours and 90-99% inhibition in HCV five days posttreatment.


“We have demonstrated here that replication of HBV and HCV is sensitive to the antiviral activities of interferon lambda,” say the researchers. “These results suggest the possibility that interferon lambda may be therapeutically useful in the treatment of chronic HBV or HCV infection.”


(M.D. Robek, B.S. Boyd, F.V. Chisari. 2005. Lambda interferon inhibits hepatitis B and C virus replication. Journal of Virology, 79. 6: 3851-3854.)

Editor's Note: The original news release can be found here.

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This story has been adapted from a news release issued by American Society For Microbiology.

Smallpox could be sent in mail

By Steve Mitchell, Medical Correspondent
Source: United Press International

WASHINGTON, (United Press International via COMTEX) -- The anthrax letter attacks in 2001 are not the first time an infectious agent has been spread through the mail. A recent article in a scientific journal describes two outbreaks of smallpox in 1901 that were attributed to infected letters, and bioweapon experts said it is possible terrorists could spread the deadly disease in this manner today.

Charles Ambrose, the author's article and a microbiologist at the University of Kentucky School of Medicine in Lexington, noted that one of the outbreaks was attributed to infected letters sent from the United States to England -- a trans-Atlantic trip that at the time had to be made by boat. This suggests the virus may be able to survive extended periods in transit and raises the possibility of terrorists sending an infected letter into the United States from abroad.

Ambrose's article appears in the May issue of the journal Emerging Infectious Diseases.

Officials at the Centers for Disease Control and Prevention in Atlanta said it was unlikely smallpox could be transmitted through infected letters, but other bioweapon experts thought it could be done -- if samples of the deadly virus could be obtained in the first place.

"It would be really, really, really difficult" to infect people by sending the smallpox virus through the mail, CDC spokesman Von Roebuck told United Press International.

Bill Kournikakis, of Canada's Chemical Biological Defense Section in Medicine Hat, Alberta, disagreed with that assessment.

"If smallpox were available, then it would be possible to transmit it through the mail," he told UPI.

Kournikakis headed a study that showed anthrax could be transmitted through the mail several months prior to the 2001 attacks.

"Smallpox was well known for its virulence, contagiousness and stability (and) was able to survive for almost a year at room temperature in exudates or crusts from smallpox patients," he said. "It would most likely survive the postal system as well."

Smallpox kills about a third of those infected by the virus. Symptoms include fever, aches and the characteristic pox or raised bumps all over the body that form scabs and can leave disfiguring scars.

William C. Patrick, former chief of the product development for the U.S. Army's biological warfare laboratories at Fort Detrick, Md., told UPI he thought it was possible smallpox could be distributed via mailed items.

"Smallpox could be sent through the mail and cause problems," said Patrick, who has served as a consultant to the FBI and the CIA.

Patrick noted although smallpox is not as stable as anthrax, "it's more infectious." Only about three to five individual virus particles are needed to cause a smallpox infection, compared to 8,000-10,000 spores of anthrax.

The bioterror experts consulted for this article said they consider the real barrier to an attack is obtaining the virus, not the mail system. The only known stocks of smallpox in the world reside at CDC headquarters in Atlanta and a lab in Russia. However, some bioweapons experts think North Korea and Iran also possess smallpox and there are concerns Russia may have leaked samples of the deadly pathogen to various countries.

Ambrose noted in his article there may be a second, unconventional source of smallpox in Russia in the Sakha Republic region in northeast Siberia -- one of the coldest inhabited regions on Earth. In 1991, bioweapons experts went searching for smallpox victims who had become frozen and mummified under the ice in the 19th Century.

The concern was terrorists could recover corpses, thaw them and gain access to smallpox, but searchers found no trace of the virus.

The United States could be very susceptible to a smallpox attack. Much of the U.S. population has not been vaccinated against smallpox -- routine vaccinations stopped in 1972 -- and it is unclear if those vaccinated prior to that still retain immunity from the deadly disease. President George W. Bush's plan to vaccinate healthcare workers and first responders against smallpox appears to have all but halted. Only a fraction of the anticipated 500,000 people targeted to be vaccinated received the medication.

Ambrose's article also cited an outbreak in Saginaw, Mich., involving 34 people and detailed in a 1901 issue of the New York Medical Journal. That outbreak appears to have originated in a Saginaw woman who developed smallpox after receiving a letter from her boyfriend, a soldier in Alaska who had written the letter while infected with the disease himself.

The other smallpox outbreak occurred at the headquarters of the Mormon church in Nottingham, England, Ambrose wrote. A report in the April 1901 issue of the British Medical Journal attributes that incident to letters from Salt Lake City, where hundreds of smallpox cases had been reported in recent months.

Dr. D.A. Henderson, professor of medicine at the Center for Biosecurity at the University of Pittsburgh Medical Center, said under normal circumstances there probably was very little, if any, risk of an infected person transmitting smallpox through the mail.

He said it was highly possible the cases described in the medical journal articles had not been properly investigated and there could have been other ways people became infected that did not involve contaminated letters. When he was involved in efforts to eradicate smallpox globally, he said, no instances were ever reported of infections that could be traced back to infected mail items.

Henderson did say he thought it was possible terrorists could transmit smallpox through the mail by aerosolizing the virus, similar to what was done in the anthrax attacks, which infected 18 people and killed five.

"They could do that, oh yeah, no question," Henderson told UPI.

He said it was less likely to happen with smallpox than with anthrax, however, due to difficulties of obtaining the virus in the first place, the technical knowledge required to work with it, and the dangers of self-infection.

Henderson noted, however, officials involved in the Russian Bioweapons program have admitted in recent years they produced very fine, tiny-particle smallpox and conducted outdoors experiments with it in 1971. He said it is not known whether the efforts infected anyone, but it demonstrates the feasibility of aerosolizing the deadly virus.

Henderson said if smallpox was stabilized properly, it probably could survive a trip through the mail system, "but it wouldn't survive as well as anthrax."

Bob Anderson, a spokesman for the U.S. Postal Service, said in terms of precautionary measures to prevent biological weapons from being spread through the mail system, the only monitoring systems in place test for anthrax.

"The system is expandable -- meaning the equipment is capable of being configured to test for the presence of other biohazards in the mail -- but there are no plans to do so at this time," Anderson told UPI.

The Postal Service also irradiates some federal mail to kill potential bioweapons, but this process is used only on government mail headed for federal agencies in the Washington area, he said.

Henderson said he did not know if irradiation would kill the smallpox virus.

--

Steve Mitchell is UPI's Medical Correspondent.

Copyright 2005 by United Press International.

Don't accept any mail from them.

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i,ll keep that in mind!!

Wonderful Just when you thought it was safe to use snail mail again!

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