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October 19, 2006, 9:29 PM CT

How Pathogens Spread In Human Body

How Pathogens Spread In Human Body
Scientists at the University of Cambridge have discovered a new, more accurate, method of mapping how bacteria spread within the body, a breakthrough that could lead to more effective therapys and prevention of certain bacterial infections.

Dr. Pietro Mastroeni, Professor Duncan Maskell at the Centre for Veterinary Science, and their teams have pioneered the integration of mathematical models with observational data to predict the spread of individual bacteria within the human body. Their findings are published in the recent issue of PLoS Biology.

The work analyses the spread and distribution of Salmonella in the body, which is a bacterium that causes typhoid fever and food borne gastroenteritis in humans and animals, with severe medical and veterinary consequences and threats for the food industry. The work is of broad significance as these novel research approaches are applicable to a multitude of pathogenic microorganisms.

These studies indicate that individual bacteria and their progenies cleverly escape from host cells and distribute to new sites of the body, continuously staying one step ahead of the immune response. The type of spread varies between different bacteria, thus posing challenges for the rational therapy or prevention of these infections.........

Posted by: Mark      Permalink         Source


October 16, 2006, 10:05 PM CT

How Ebola And Marburg Cause Disease

How Ebola And Marburg Cause Disease Ebola Virus
Scientists in the Greene Infectious Disease Laboratory at Columbia University's Mailman School of Public Health, the Centers for Disease Control and Prevention, and the Caribbean Primate Research Center have discovered a key mechanism by which the Filoviruses, Ebola and Marburg, cause disease. The identification of an amino acid sequence in Filoviruses that results in the rapid depression of immunological response is described in the December 2006 issue of The FASEB Journal. Using this information, scientists can begin to develop new drugs to stop these devastating diseases.

Filoviruses, named for their threadlike appearance in electron microscopy (filo= thread in Latin), are linked to outbreaks of fatal hemorrhagic fever in sub-Saharan Africa. Viral hemorrhagic fevers are of specific concern because they are linked to high morbidity and mortality (up to 80% mortality rates) and the potential for rapid dissemination through human-to-human transmission. The term "viral hemorrhagic fever" characterizes a severe multisystem syndrome linked to fever, shock, and bleeding caused by infection with one of many viruses, including the Filoviruses Ebola and Marburg.

Both humans and apes are susceptible to viral hemorrhagic fevers, and it is speculated that filovirus infections account at least in part for the recent decline in the gorilla and chimpanzee population in central Africa. There is no cure or approved vaccine for either Marburg or Ebola virus. Immunosuppression occurs early after infection and allows the viruses to reproduce rapidly and cause disease.........

Posted by: Mark      Permalink         Source


October 15, 2006, 7:25 PM CT

Promise For Herpes Vaccine

Promise For Herpes Vaccine Bill Halford
A study by a Montana State University researcher suggests a new avenue for developing a vaccine against genital herpes and other diseases caused by herpes simplex viruses.

As per a research findings published earlier this year in the Virology Journal, MSU virologist William Halford showed that mice vaccinated with a live, genetically-modified herpes simplex virus type 1 (HSV-1) showed no signs of disease 30 days after being exposed to a especially lethal "wild-type" strain of the virus.

In contrast, a second group of mice that received a more conventional vaccine died within six days of being exposed to the same "wild-type" strain.

"We have a clear roadmap for producing an effective live vaccine against genital herpes," said Halford, who works in MSU's Department of Veterinary Molecular Biology. "Eventhough my studies were performed with HSV-1, the implications for HSV-2-induced genital herpes are clear. Overall the two viruses are about 99 percent genetically identical".

An estimated 55 million Americans carry herpes simplex virus type 2 (HSV-2), which causes genital herpes. Infection is life-long. Approximately 5 percent of those with genital herpes - 2 million to 3 million Americans - suffer outbreaks one to four times annually. A vaccine offering life-long protection does not exist.........

Posted by: Mark      Permalink         Source


October 13, 2006, 4:53 AM CT

Studying Pediatric AIDS Vaccine

Studying Pediatric AIDS Vaccine
Researchers at Makerere University, in Kampala, Uganda, along with researchers from Johns Hopkins and other institutions worldwide, have begun the first clinical safety trial in Africa of a vaccine to prevent mother-to-child transmission of HIV through breastfeeding. Breast milk is a leading route of infection in the developing world, as per the United Nations World Health Organization, which estimates that each day 1,800 newborns are infected with the AIDS virus, 30 percent to 40 percent by virus carried in their mother's milk.

Enrollment of the first newborn took place at Mulago Hospital in Kampala. The so-called phase I study is designed to test the safety of injecting newborns with the vaccine, formally known as ALVAC-HIV (vCP1521). If the vaccine is found to be safe in this study, and if it is later shown to be effective in reducing the chance of infants' becoming infected during breastfeeding, scientists estimate that it could potentially stop up to 8,000 of Uganda's 22,000 infections a year in children. Initial results are expected by mid-2007.

"A vaccine is the easiest way to help prevent mother-to-child transmission of the disease, as healthy alternatives to breastfeeding, such as infant formula, are not available or affordable to most new mothers in the developing world, a number of of whom do not know they are HIV positive," says study protocol chair and pediatric infectious disease specialist Laura Guay, M.D., who will lead Hopkins' efforts.........

Posted by: Mark      Permalink         Source


October 12, 2006, 4:42 AM CT

Refocusing On Patients With HIV, Hepatitis

Refocusing On Patients With HIV, Hepatitis
As HIV patients live longer thanks to advanced therapies, scientists are looking for better ways to treat accompanying maladies such as hepatitis that traditionally were not emphasized.

"People are living longer with HIV now, but then we see people developing complications from liver disease due to hepatitis," said Dr. Mamta Jain, assistant professor of internal medicine at UT Southwestern Medical Center. "Before we had effective HIV treatment, there was no interest in treating hepatitis C because the thought was the patient would die of AIDS. Well, they're not dying of AIDS, so we are making an effort to try to treat more patients for hepatitis C".

Other diseases, such as cirrhosis or hepatocellular cancers, progress faster in co-infected HIV and hepatitis patients. As a result, health-care providers are trying to intervene as early as possible, said Dr. Jain, who specializes in infectious diseases.

Dr. Jain oversees a co-infection clinic at Parkland Memorial Hospital where patients are reviewed for hepatitis and HIV and can participate in clinical trials. Generally, co-infection rates range from 10 percent to 33 percent of HIV patients. Rates run at about 25 percent at the clinic in Parkland, which is the teaching hospital for UT Southwestern.

UT Southwestern has several ongoing clinical trials for which doctors are recruiting potential patients. The latest study involves whether giving hepatitis C, or HCV, medications early on during HIV disease speeds recovery or improves hepatitis therapies.........

Posted by: Mark      Permalink         Source


October 11, 2006, 5:17 AM CT

Hiv Gets A Makeover

Hiv Gets A Makeover Tweaking HIV. A newly engineered version of the AIDS virus, dubbed stHIV, replicates robustly in rhesus monkey cells.
The slow pace of AIDS research can be pinned, in no small part, on something akin to the square-peg-round-hole conundrum. The HIV-1 virus won't replicate in monkey cells, so scientists use a monkey virus - known as SIVmac, or the macaque version of simian immunodeficiency virus - to test potential therapies and vaccines in animals. But therapies and vaccines that are effective on SIV don't necessarily translate into human success. Now, using a combination of genetic engineering and forced adaptation, scientists at Rockefeller and the Aaron Diamond AIDS Research Center have created a version of the AIDS virus that replicates vigorously in both human and monkey cells - an advance that has the potential to revolutionize vaccine research.

In a paper published in today's issue of Science, Paul Bieniasz, associate professor and head of the Laboratory of Retrovirology, describes how he and colleagues maneuvered around the intrinsic immunity of primate cells by replacing just a few parts of the human virus - the ones responsible for blocking replication in monkey cells - with components from SIV. "Overall, the virus is a mixture of engineering and forced evolution," Bieniasz says. "It sounds simple, in theory, but it took us two years to do".

Bieniasz and Theodora Hatziioannou, a research scientist in the lab and the paper's first author, had to overcome two major obstacles: the first was a protein called TRIM5 that, in monkeys, recognizes the outer shell or "capsid" of HIV-1 but not that of SIV. By swapping out the capsid region of the HIV-1 genome for that of the monkey virus, and then selectively growing the viruses that replicated most robustly, over several generations Hatziioannou created an HIV-1 mutant that could evade the monkey cells' TRIM5 recognition.........

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October 10, 2006, 10:23 PM CT

Poultry And Antibiotic Resistance

Poultry And Antibiotic Resistance
Clinic researcher and colleagues have found.

Results of the nearly $1.4 million three-year study, funded by the Centers for Disease Control and Prevention, Atlanta, Georgia, are in the November 1 issue of The Journal of Infectious Diseases.

Edward Belongia, M.D., Marshfield Clinic Research Foundation, Marshfield, Wis., and colleagues examined poultry exposure as a risk factor for antibiotic resistance in Enterococcus faecium, a gut bacterium that is increasingly the cause of infections in hospitals. The investigation team focused on use of a growth-promoting antibiotic, called virginiamycin, in poultry.

Virginiamycin is closely correlation to quinupristin-dalfopristin, an antibiotic licensed to treat patients with serious, antibiotic-resistant infections. The drug is prescribed under the brand name Synercid.

As per Belongia, "There is a relative lack of data on the impact of antibiotic use in livestock and its relationship to antibiotic resistance in humans, but there is a fair amount of indirect evidence suggesting that antibiotic use could pose a risk to human health".

"We've known for a long time that resistant bacteria can be found on retail poultry products, but our study is one of the first to show an association between human carriage of antibiotic resistance genes and eating poultry or handling raw poultry.........

Posted by: Mark      Permalink         Source


October 9, 2006, 9:12 PM CT

Progress In HIV Research

Progress In HIV Research
How a harmless virus called GB Virus type C (GBV-C) protects against HIV infection is now better understood. Scientists at the Department of Veterans Affairs (VA) Iowa City Health Care System and the University of Iowa have identified a protein segment that strongly inhibits HIV from growing in cell models.

The team observed that an 85-amino acid segment within a GBV-C viral protein called NS5A greatly slows down HIV from replicating in cells grown in labs. The study results will appear online this week in the Proceedings of the National Academy of Sciences.

The finding builds on earlier VA and UI work showing that people with HIV who also are infected GBV-C live longer than those infected only with HIV, said Jinhua Xiang, M.D., a VA research health scientific specialist, UI researcher and the current study's principal author.

GBV-C and its role in HIV infection have been studied for nearly a decade by Xiang, along with another study author Jack Stapleton, M.D., staff doctor and researcher at the VA Iowa City Health Care System and professor of internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine.

"Identifying a specific protein made by GBV-C that inhibits HIV growth in cell culture strengthens the argument that GBV-C is responsible for the prolonged survival observed in several studies of HIV-positive people," Xiang said. "Understanding how the protein works may allow us to develop target-specific therapies that can mimic these effects and inhibit HIV.........

Posted by: Mark      Permalink         Source


October 9, 2006, 8:35 PM CT

About Antibiotic Resistance In Hospitals

About Antibiotic Resistance In Hospitals
In one of the first national studies on guidelines that control antibiotics and antibiotic resistance in hospitals, researchers from the Indiana University School of Medicine, the Regenstrief Institute, Inc. and the Richard Roudebush Veterans.

Administration Medical Center report that hospitals that follow national guidelines on controlling antibiotic use have lower rates of antibiotic resistance.

According to a research findings published in the recent issue of Infection Control and Hospital Epidemiology, the researchers studied four major types of antibiotic resistance at almost 450 hospitals, looking at what each hospital did to control antibiotic use and how this affected the rate of antibiotic resistance.

"We saw in this study, as in other work we have done, that antibiotic resistance is increasing rapidly. This increase is seen in all types of hospitals across the country - large and small, teaching and non-teaching, VA and non-VA," said Bradley N. Doebbeling, M.D., M.Sc., who led the study. He directs the IU Center for Health Services and Outcomes Research at the Regenstrief Institute and the IU School of Medicine. He also directs the VA Center for Implementing Evidence-Based Practice.

The study looked at measures to prevent development of antibiotic resistance as well as ways to stop its spread. The researchers reported that if hospitals implemented specific measures to control the use of antibiotics they were more likely to have succeeded in controlling antibiotic resistance.........

Posted by: Mark      Permalink         Source


October 4, 2006, 9:56 PM CT

A Biocontrol Agent That Doesn't Trigger Antibiotic Resistance

A Biocontrol Agent That Doesn't Trigger Antibiotic Resistance
A failed experiment turned out to be anything but for bacteriologist Marcin Filutowicz.

As he was puzzling out why what should have been a routine procedure wouldn't work, he made a discovery that led to the creation of a new biological tool for destroying bacterial pathogens - one that doesn't appear to trigger antibiotic resistance.

The discovery also led to the startup of a promising new biotechnology firm that has already brought Wisconsin a dozen new, high-paying, highly skilled jobs. Filutowicz is a professor of bacteriology in the University of Wisconsin-Madison College of Agricultural and Life Sciences.

His inspiration came one morning in 1999 when he was puzzling over a failed experiment. A researcher in his lab had been trying to insert two different mutations into an ordinary bacterial plasmid - a routine task for the experienced scientist - but every attempt failed to produce a live bacterium.

Plasmids are circular DNA molecules that are different from chromosomal DNA, the genetic material that encodes the instructions for life in all cells. Plasmids are small, non-chromosomal DNA molecules. They are common in bacteria. The genes in plasmids often encode information that confers some selective advantage to their hosts - such as the ability to resist antibiotics.........

Posted by: Mark      Permalink         Source



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Did you know?
Scientists at Baylor College of Medicine in Houston have found a genetic marker that may identify individuals at greater risk for life-threatening infection from the West Nile virus. Results of the study are reported in the Nov. 15 print edition of Journal of Infectious Diseases.

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