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January 18, 2006, 0:17 AM CT

Complex Infection Fighting Mechanisms

Complex Infection Fighting Mechanisms Image courtesy of Yale University
Yale School of Medicine scientists report in Nature Immunology how infection fighting mechanisms in the body can distinguish between a virus and the healthy body, shedding new light on auto immune disorders.

The infection fighters in question, toll-like receptors (TLRs), function by recognizing viral, bacterial or fungal pathogens and then sending signals throughout the immune system announcing that an infection has occurred.

Viruses change features to avoid being recognized, thereby triggering the immune response. But TLRs recognize the highly conserved features of pathogens, features that are often difficult to change without affecting the punch of the pathogen, said lead author of the study, Gregory Barton of the University of California at Berkeley who performed the research while in the Section of Immunobiology at Yale School of Medicine.

He said that one exception to the general view of how TLRs work is the way TLRs recognize viruses since viruses lack the unique features of bacterial or fungal pathogens. Because of this, the immune system has had to find other ways to recognize viral infection.

"In particular, the DNA or RNA that comprise viral genomes can stimulate certain TLRs," Barton said. "This strategy comes at an enormous cost. By targeting the DNA or RNA of viruses, the immune system runs the risk of accidentally recognizing its own DNA and RNA as foreign and inappropriately making an immune response against itself. This autoimmune condition is called systemic lupus erythematosus or SLE, and can be devastating for those unfortunate enough to suffer from it".........

Posted by: Mark      Permalink


January 15, 2006, 2:46 PM CT

Physicians Who Treat World Travelers

Physicians Who Treat World Travelers
Diseases know no borders, and as international business and personal travel continues to become more common, the borderlines become even more blurred. Physicians who specialize in travel and tropical medicine, like Phyllis E. Kozarsky, MD, professor of medicine, Emory University School of Medicine, now have new data that will help guide their therapy of international travelers.

Data on more than 17,000 ill returning travelers collected through the GeoSentinel Surveillance Network, an established network of International Society of Travel Medicine clinics, show, for the first time, that travelers to different parts of the developing world face varying but significant risks. The study appears in the Jan. 12 issue of "The New England Journal of Medicine."

The Emory TravelWell Clinic, located at Emory Crawford Long Hospital, is part of the GeoSentinel Surveillance Network, and Dr. Kozarsky, the clinic director, is a co-author of the study and a founder of the network.

"This data will not only guide me and my colleagues in travel and tropical medicine, but it will help internal medicine specialists and emergency physicians who may be faced with treating patients who present with unusual or exotic diseases," says Dr. Kozarsky.

"This information gives us a blueprint of what to look for when it comes to diagnosing sick travelers, based on where they have been," says lead author David O. Freedman, MD, director of the University of Alabama at Birmingham Travel Medicine Clinic. "Doctors -- travel medicine specialists in particular -- can use the destination-specific differences we've found to guide the diagnosis and therapy of ill travelers, meaning they can order the correct tests and begin the correct treatment while waiting for confirmation."........

Posted by: Mark      Permalink


January 11, 2006, 8:13 PM CT

Resistant Bacteria In Intensive Care Units

Resistant Bacteria In Intensive Care Units
A dangerous drug-resistant bacterium is becoming more prevalent in a number of intensive care units, according to an article in the Feb. 1 issue of Clinical Infectious Diseases, now available online.

Methicillin-resistant Staphylococcus aureus (MRSA) is responsible for a variety of infections that patients often acquire in the hospital. Skin infections are the most common, but MRSA can also infect the heart, the lungs, and the digestive tract. The emergence of MRSA and other drug-resistant bacteria may be due in part to over-prescribing and overuse of antibiotics.

Scientists at the Centers for Disease Control and Prevention examined MRSA data from more than 1,200 intensive care units (ICUs) from 1992 to 2003. They found that in 1992, 36 percent of S. aureus isolates were drug-resistant; but in 2003, 64 percent of isolates were MRSA, an increase of about 3 percentage points per year.

Despite the increase in MRSA prevalence, there was also a decrease in MRSA that was resistant to multiple drugs. The scientists hypothesize that the influx of MRSA strains from the community might have replaced those multidrug-resistant strains associated with the hospital.

"Unlike traditional MRSA the community strain is very fit - it causes infection in healthy people," said CDC epidemiologist Dr. Monina Klevens. "When it is introduced into a hospital, where ill patients are more vulnerable to infection, it has the potential to cause significant morbidity and mortality".........

Posted by: Mark      Permalink


January 9, 2006, 9:48 PM CT

Optimizing Immune Response Viral Infections

Optimizing Immune Response Viral Infections Gordon Freeman, PhD
Like boxers wearied by a 15-round bout, the immune system's CD8 T cells eventually become "exhausted" in their battle against persistent viral infection, and less effective in fighting the disease.

In a study would be published Dec. 28 on the journal Nature's website, scientists at Dana-Farber Cancer Institute and Emory University have traced the problem to a gene that turns off the infection-fighting drive of CD8 T cells in mice. The discovery raises the possibility that CD8 cell exhaustion can be reversed in human patients, reinvigorating the immune system's defenses against chronic viral infections ranging from hepatitis to HIV, the virus that causes AIDS.

"CD8 T cells that have fought viral infections retain a 'memory' of the viruses they've encountered, so they can rapidly respond to new infections from those viruses," says the study's author, Gordon Freeman, PhD, of Dana-Farber. In the case of chronic infection, however, senior author Rafi Ahmed, PhD, of Emory, has shown that memory cells become exhausted and lose the capacity to respond to the virus. Why this occurs, on a molecular level, has been unclear.

To find the cause, Freeman and colleagues conducted a "microarray" experiment measuring the activity of thousands of genes in normal memory CD8 T cells in mice and in "exhausted" versions of those cells. They found that a gene known as PD-1 was much more active in the exhausted cells.........

Posted by: Scott      Permalink


December 28, 2005

Two Million Americans Carry MRSA

Two Million Americans Carry MRSA Image of MRSA courtesy of University of Iowa
New research estimates that about 2 million people carry a strain of drug-resistant bacteria in their noses. This research, which was conducted by the Centers for Disease Control and Prevention (CDC), is the first reliable nationwide estimate of colonization with Staphylococcus aureus, including methicillin-resistant Staphylococcus aureus (MRSA). It is published in the Jan. 15 issue of The Journal of Infectious Diseases, now available online.

Those colonized with normal strains of staph are at higher risk of infection with the bacterium, which can lead to conditions ranging from mild skin infections to fatal toxic shock syndrome. MRSA causes more difficult-to-treat and, sometimes, more virulent illnesses. MRSA was once primarily a problem in hospitals, but is now a growing problem in communities around the country.

Matthew J. Kuehnert, MD, and his colleagues collected samples from nearly 10,000 participants in the 2001-2002 National Health and Nutritional Examination Survey, a representative sample of the U.S. population.

Nearly one-third were found to be colonized with staph. Prevalence was highest among males and children between 6 and 11 years old. MRSA prevalence was 0.8 percent. MRSA was highest among women and those older than 60, but those colonized with strains usually associated with community-associated MRSA were more likely to be younger and black.

Overall, strains and toxins previously found to be associated with community-associated MRSA were unusual. The genetic diversity of strains was remarkable-about half of isolates, including MRSA strains, had unique molecular fingerprinting patterns, and some fell outside recognized groups.

"There is a lot about staph colonization we don't know," Dr. Kuehnert said. "Interestingly, carriage of certain strains do seem to vary by sociodemographics, particularly age and race. We need to learn more in order to allow design of new, more effective interventions," he added, including vaccines or antimicrobial therapy. "Data from subsequent survey years may determine whether there are ongoing trends in colonization".........

Mark      Permalink


December 28, 2005

Eradication of Polio Nears

Eradication of Polio Nears
Polio is on track to become only the second disease ever eradicated. In two studies in the Dec. 15 issue of The Journal of Infectious Diseases, now available online, researchers are working to ensure that once it is gone, it stays gone. One study reduces concerns that people whose immune systems were weakened by HIV would re-introduce poliovirus into the community. The other study looks at the how switching forms of vaccine from a live, attenuated vaccine to an inactivated version may affect communities.

Oral polio vaccine (OPV), one of the vaccines instrumental in driving the disease to near-eradication, contains weakened live virus strains. The vaccine is highly effective, easy to administer, relatively inexpensive, and has been used for more than 40 years. Those given the vaccine excrete, or "shed," virus in their stool. There is some concern over the use of OPV, however, because vaccine-derived poliovirus (VDPV) can occasionally cause another form of polio.

Furthermore, in rare cases, immunodeficient persons have shown prolonged shedding of VDPV, which may be transmitted to contacts, thus potentially re-introducing polio into the community. Concerns had been raised that this issue would be a particular challenge in countries with high HIV prevalence.

Karen Hennessey, PhD, MSPH, and his colleagues in Cote d'Ivoire and at the Centers for Disease Control and Prevention examined the duration of shedding of oral poliomyelitis vaccine by individuals with HIV infection.

Dr. Hennessey and his colleagues tested stool specimens at various intervals following vaccination. Out of a total of 419 adults with HIV infection, no poliovirus was isolated from any of the specimens. Because of these results, it is likely that fewer than 1 percent of adults with HIV infection experience prolonged virus shedding when exposed to OPV, "and therefore probably represent minimal risk of re-introducing vaccine virus into the population after poliovirus has been eradicated," the authors concluded.........

Mark      Permalink


December 28, 2005

Defeating Malarial Parasite Defense

Defeating Malarial Parasite Defense
The world's deadliest malaria parasite, Plasmodium falciparum, sneaks past the human immune system with the help of a wardrobe of invisibility cloaks. If a person's immune cells learn to recognize one of the parasite's a number of camouflage proteins, the surviving invaders can swap disguises and slip away again to cause more damage. Malaria kills an estimated 2.7 million people annually worldwide, 75 percent of them children in Africa.

Howard Hughes Medical Institute (HHMI) international research scholars in Australia have determined how P. falciparum can turn on one cloaking gene and keep dozens of others silent until each is needed in turn. Their findings, published in the December 28, 2005, issue of Nature, reveal the mechanism of action of the genetic machinery thought to be the key to the parasite's survival.

A DNA sequence near the start of a cloaking gene, known as the gene's promoter, not only turns up production of its protein, but also keeps all other cloaking genes under wraps, according to Alan Cowman and Brendan Crabb, HHMI international research scholars at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, and their co-authors. "The promoter is all you need for activation and silencing," Cowman said. "It's the main site of action where everything is happening."

Malaria parasites enter human blood from infected mosquitoes. The organisms invade and promptly remodel red blood cells. They decorate the surface of the cells they occupy with a protein called PfEMP1, made by the var gene family.

Using this versatile surface protein, the parasite evades the host's immune system using two basic strategies. First, the protein sticks infected red blood cells to the blood vessel lining, removing the infected cells from circulation, where they would probably be destroyed.........

Mark      Permalink


December 25, 2005, 10:32 AM CT

Merry Christmas To All Our Readers

Merry Christmas To All Our Readers
Medicineworld wishes all our readers merry Christmas.

Oh, jingle bells, jingle bells

Jingle all the way

Oh, what fun it is to ride

In a one horse open sleigh

Jingle bells, jingle bells

Jingle all the way

Oh, what fun it is to ride

In a one horse open sleigh........

Daniel      Permalink


December 23, 2005

Epstein-Barr Virus In Blood Cancers

Epstein-Barr Virus In Blood Cancers
Earlier this year, scientists at the University of Pennsylvania School of Medicine identified a link between a critical cancer pathway and an Epstein-Barr Virus (EBV) protein known to be expressed in many EBV-associated cancers. Their findings demonstrated a new mechanism by which EBV can transform human B cells from the immune system into malignant cells, which can lead to B-cell lymphomas. Now, they have found that the viral protein--called EBNA3C (for EBV nuclear antigen)--mediates the degradation of the retinoblastoma protein, an important molecular brake for cell proliferation.

Erle S. Robertson, PhD, an Associate Professor of Microbiology who leads the Tumor Virology Program at Penn's Abramson Cancer Center, and MD/PhD student Jason Knight, published their results last week in the Proceedings of the National Academy of Sciences.

The retinoblastoma protein (Rb) is a major regulator of several genes in charge of cell proliferation and cell-cycle regulation. In the nucleus, Rb normally binds to E2F, turning off genes involved with cell proliferation. Using human cell cultures infected with the Epstein-Barr virus, the researchers found that EBNA3C recruits a group of molecules called the SCF complex, which attaches ubiquitin to Rb. This inadvertently tags Rb for degradation by the proteosome machinery, the cell's recycling plant. With Rb out of the way, the cell now reproduces uncontrollably.

"It's as simple as that, but it's a major mystery solved that a number of scientists have been working on for at least 15 years," says Robertson.

EBV, a member of the herpesvirus family and one of the most common human viruses, plays a role in cancers such as lymphoproliferative diseases in transplant or AIDS patients, Burkitt's lymphoma, Hodgkin's lymphoma, and nasopharyngeal carcinoma, and also causes the well-known disease infectious mononucleosis. As a number of as 95 percent of adults 20 years and older have been infected with EBV, but show no symptoms.........

Daniel      Permalink


December 21, 2005

Marine Bacteria Compound For Multiple Myeloma

Marine Bacteria Compound For Multiple Myeloma Dharminder Chauhan, PhD
An anti-cancer compound derived from bacteria dwelling in ocean-bottom sediments appears in laboratory tests to be a potent killer of drug-resistant multiple myeloma cells, and potentially with less toxicity than current therapys, report Dana-Farber Cancer Institute scientists in the recent issue of Cancer Cell.

The experimental compound, NPI-0052, has been found to block or inhibit cancer cells' proteasomes from working effectively. The proteasome work as a cell's "garbage disposal," chewing up and disposing of old, unwanted proteins. With their proteasome jammed, cells die from the backup of damaged proteins.

"Proteasome inhibition is a key therapeutic target and bortezomib (Velcadeā„¢) was the first in a new class of compounds in multiple myeloma. NPI-0052 is a novel proteasome inhibitor with a chemical structure and action that is distinct from bortezomib, and has the promise of being even more effective for patients," says Kenneth Anderson, MD, director of the Jerome Lipper Multiple Myeloma Center at Dana-Farber, and senior author of the report.

The compound will be moved into Phase I clinical trials in early 2006, say officials of Nereus Pharmaceuticals in San Diego, the developer of NPI-0052. The compound will be tested as a single agent and subsequently in combination with other therapys.

Multiple myeloma is a currently incurable cancer of the bone marrow that causes a plunge in the production of vital red and white blood cells. Eventhough relatively rare, it is the second most common type of blood cancer and accounts for 11,000 deaths annually in the United States. Bortezomib, approved by the Food and Drug Administration in 2003 for relapsed myeloma patients and subsequently for patients who have received at least one previous therapy, demonstrated in clinical trials that it extended the time to disease progression and also improved survival.........

Daniel      Permalink



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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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