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No Sex For 40 Million Years? No Problem

Posted by tumicrobiology on March 20, 2007

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A group of organisms that has never had sex in over 40 million years of existence has nevertheless managed to evolve into distinct species, says new research published today. The study challenges the assumption that sex is necessary for organisms to diversify and provides scientists with new insight into why species evolve in the first place 

The research, published in PLoS Biology, focuses on the study of bdelloid rotifers, microscopic aquatic animals that live in watery or occasionally wet habitats including ponds, rivers, soils, and on mosses and lichens. These tiny asexual creatures multiply by producing eggs that are genetic clones of the mother — there are no males. Fossil records and molecular data show that bdelloid rotifers have been around for over 40 million years without sexually reproducing, and yet this new study has shown that they have evolved into distinct species.

Using a combination of DNA sequencing and jaw measurements taken using a scanning electron microscope, the research team examined bdelloid rotifers living in different aquatic environments across the UK, Italy and other parts of the world. They found genetic and jaw-shape evidence that the rotifers had evolved into distinct species by adapting to differences in their environment.

Dr Tim Barraclough from Imperial College London’s Division of Biology explained: “We found evidence that different populations of these creatures have diverged into distinct species, not just because they become isolated in different places, but because of the differing selection pressures in different environments.

“One remarkable example is of two species living in close proximity on the body of another animal, a water louse. One lives around its legs, the other on its chest, yet they have diverged in body size and jaw shape to occupy these distinct ecological niches. Our results show that, over millions of years, natural selection has caused divergence into distinct entities equivalent to the species found in sexual organisms.”

Previously, many scientists had thought that sexual reproduction was necessary for speciation because of the importance of interbreeding in explaining speciation in sexual organisms. Asexual creatures like the bdelloid rotifers were known not to be all identical, but it had been argued that the differences might arise solely through the chance build-up of random mutations that occur in the ‘cloning’ process when a new rotifer is born. The new study proves that these differences are not random and are the result of so-called ‘divergent selection’, a process well known to cause the origin of species in sexual organisms.

Dr Barraclough adds: “These really are amazing creatures, whose very existence calls into question scientific understanding, because it is generally thought that asexual creatures die out quickly, but these have been around for millions of years.

“Our proof that natural selection has driven their divergence into distinct species is another example of these miniscule creatures surprising scientists — and their ability to survive and adapt to change certainly raises interesting questions about our understanding of evolutionary processes.”

Note: This story has been adapted from a news release issued by Imperial College London.

Science Daily


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Study: Antiviral protein may fight Ebola

Posted by tumicrobiology on March 20, 2007

German scientists have found an antiviral protein shown to inhibit other viruses might protect against Ebola and Marburg virus infections.

The Ebola and Marburg viruses belong to the Filoviridae family and cause severe hemorrhagic fever in humans and non-human primates. Filovirus infections are characterized by high fever, hemorrhages and shock and are responsible for mortality rates up to 90 percent. Currently, there is no vaccine or therapy available for treating infected patients.

In a previous study researchers found the zinc finger antiviral protein, or ZAP, capable of inhibiting Moloney murine leukemia virus and Sindbis virus replication.

In the new study, ZAP was tested for its antiviral activity in cells infected with Ebola and Marburg. Results showed up to 95 percent inhibition of Ebola, while Marburg was less significantly inhibited suggesting the antiviral effectiveness of ZAP may depend on the filovirus species.

The study conducted at the Bernhard-Nocht Institute for Tropical Medicine in Hamburg is reported in the Journal of Virology.

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Bacterial Virus Gene Confers Disease Resistance In Tall Fescue Grass

Posted by tumicrobiology on March 20, 2007

Researchers at North Carolina State University have discovered that inserting a specific gene from a bacterial virus into tall fescue grass makes the grass resistant to two of its biggest enemies
The NC State researchers showed that the inserted gene – the T4 lysozyme gene, a gene found in bacteriophages, or bacterial viruses – conferred high resistance to gray leaf spot disease in six of 13 experimental grasses. Three of the six resistant grasses also showed high resistance to brown patch disease. These two diseases are arguably the most important – and severe – fungal diseases affecting tall fescue grass.

The finding has the potential to have wide applications in engineering resistance to a variety of fungal diseases in not only tall fescue grass – the most widely planted turfgrass in North Carolina and a commonly utilized grass in the southeastern United States – but various other crops.

The collaborative research involves four faculty members: Dr. Ron Qu in the Department of Crop Science, Drs. H. David Shew and Lane Tredway from the Department of Plant Pathology, and Dr. Eric Miller, in the Department of Microbiology. The research was mainly performed by Dr. Shujie Dong, a post-doctoral researcher who was a graduate student of Qu’s, with assistance from two other scientists in Qu’s lab – Drs. Jianli Lu and Elumalai Sivamani.

About half of the turfgrass planted in North Carolina – one million acres – is tall fescue grass, a cool-season grass that has a high tolerance for the heat and drought of North Carolina summers, Tredway says. It is ubiquitous in the Southeast, found on lawns, golf courses and commercial acreages.

Gray leaf spot disease is caused by the Magnaporthe grisea fungus, the pathogen that also causes rice blast – the major disease of rice plants. Gray leaf spot causes round or oval tan spots that turn gray when there’s high humidity. It infects blades to make the grasses die rapidly.

Brown patch disease, caused by the soil-dwelling fungus Rhizoctonia solani, a major pest to various plant species, brings about circular, brown lesions on grass. Lawns with brown patch disease appear wilted, even if watered sufficiently, the researchers say.

Miller, the microbiologist, says that the bacterial viruses exist widely in different environments, and produce an array of products that are harmful to bacteria; as viruses attempt to spread, which they need to do in order to survive and thrive, the T4 lysozyme gene produces the enzymes that chew through the bacterial cell walls.

Miller says that the lysozyme now made by the grass does essentially the same thing to a fungus when it tries to infect, thereby providing anti-fungal properties in tall fescue and allowing the grass to withstand fungal disease.

Tredway says the benefits of potential applications may be felt economically and environmentally.

“A lot of money is spent on fungicides, which also have an impact on the environment,” he said. “Disease-resistant plants have the potential to reduce those economic and environmental impacts for many years.”

Qu says that future research will replicate this experiment in the field, rather than just in the lab, and that other disease resistance genes show anti-fungal properties in tall fescue. He also hopes to study how the group’s genetically altered plants interact with other important fungal diseases to further test their anti-fungal mettle.

Much of the work was funded by NC State’s Center for Turfgrass Environmental Research and Education and the Turfgrass Council of North Carolina.

Reference: “Expression of the Bacteriophage T4 Lysozyme Gene in Tall Fescue Confers Resistance to Gray Leaf Spot and Brown Patch Diseases”

Authors: Shujie Dong, H. David Shew, Lane P. Tredway, Jianli Lu, Elumalai Sivamani, Eric S. Miller and Rongda Qu, North Carolina State University

Published: February 2007 in Transgenic Research

Note: This story has been adapted from a news release issued by North Carolina State University.

Source: North Carolina State University

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Protein Found In Chickens May Help Protect Against Food-Borne Pathogens

Posted by tumicrobiology on March 20, 2007

Researchers from The Netherlands have identified a protein in the digestive tract of chickens that may serve as an antimicrobial agent against food-borne pathogens. They report their findings in the March 2007 issue of the journal Antimicrobial Agents and Chemotherapy

Food-borne pathogens, responsible for most cases of food poisoning in developed countries, are commonly affiliated with poultry products including chicken. Therapeutic doses of antibiotics in chicken feed have been administered since the 1950s, but are now discouraged due to increasing rates of antibiotic resistance.

In the study researchers tested for B-defensin gallinacin-6 (Gal-6) protein expression in chickens and explored antimicrobial activity against gram-positive and gram-negative bacteria as well as yeast. Researchers observed high expression of Gal-6 in the esophagus and crop and moderate expression in the glandular stomach. Colony-counting tests showed strong bactericidal activity against Campylobacter jejuni, Salmonella enterica serovar Typhimurium, Clostridium perfringens, and Escherichia coli, all major food-borne pathogens. Fungicidal activity was also noted. In a kill-curve study results showed treatment with Gal-6 reduced C. perfringens survival within sixty minutes.

“In conclusion, to our knowledge, this is the first report of a chicken B-defensin highly expressed in the digestive tract and displaying strong bactericidal activity against food-borne pathogens.” say the researchers.

(A. van Dijk, E.J.A. Veldhuizen, S.I.C. Kalkhove, J.L.M. Tjeerdsma-van Bokhoven, R.A. Romijn, H.P. Haagsman. 2006. The B-defensin gallinacin-6 is expressed in the chicken digestive tract and has antimicrobial activity against food-borne pathogens. Antimicrobial Agents and Chemotherapy, 51. 3: 912-922.)

Note: This story has been adapted from a news release issued by American Society for Microbiology. (Science Daily — )

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One more site for you

Posted by tumicrobiology on January 3, 2007

Dear all,

 Biology, Health and Medicine for the Third World has

come forth with another site that may be helpful to you.

Door to Science.”

 It’s url in .com is : itsnotsecret.blogspot

We hope you know about: healthandbiology.blogspot




All sites are to be opened as “”

Make maximum use of our joint venture.

All the best

Gaffer, NMDF

Posted in Gaffer's | 6 Comments »

An Important Notice

Posted by tumicrobiology on December 20, 2006

Dear all, 

We, in collaboration with our partner HealthandBiology, are going to launch our next site very soon.

There will be more features and more gifts to you!

A gate way to the Nepali journals and much more. We are negotiating with Nepali journal publishers.

You will be fascinated with what we are bringing, if we succeed.

Pray for our success.

Thanking you,

Gaffer, NMDF

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HIV Patients Have Increased Risk Of Pneumonia, Death Following Surgery

Posted by tumicrobiology on December 20, 2006

Science Daily HIV-infected patients undergoing surgical procedures may be more likely to develop pneumonia after surgery and to die within 12 months than those without HIV, according to a report in the December issue of Archives of Surgery, one of the JAMA/Archives journals. In addition, HIV patients with a preoperative viral load (number of copies of the virus in the blood) greater than 30,000 per milliliter appear to have increased risk of surgical complications.

Since the development of medication regimens known as highly active antiretroviral therapy (HAART), HIV has become a chronic, manageable condition, according to background information in the article. “Consequently, many HIV-infected patients elect to undergo surgical procedures to correct physical ailments that would not have been treated previously, and undergo operative interventions in lieu of medical therapies for certain conditions,” the authors write.

Michael A. Horberg, M.D., M.A.S., and colleagues at Kaiser Permanente Medical Care Program–Northern California, Oakland, studied surgical outcomes in 332 HIV-infected patients who underwent a variety of procedures (including abdominal, orthopedic and heart surgeries) between 1997 and 2002. For comparison, the researchers selected a group of 332 patients who did not have HIV but were the same age and sex and had a similar procedure at around the same time and at the same location as one of the HIV-infected patients. The investigators then used health plan databases to obtain clinical information about the HIV patients’ disease and to track whether any of the patients had complications after surgery or died within 12 months.

The surgical procedures analyzed included abdominal or pelvic procedures (80.8 percent), cardiac or breast procedures (8.4 percent) and orthopedic procedures (10.8 percent). Most complications–including infections and delayed wound healing–occurred equally frequently in patients with and without HIV. No difference between the two groups was found in the length of hospital stay, number of complications or need for additional procedures to treat complications. However, more HIV patients developed pneumonia (eight or 2.4 percent vs. one or .3 percent) and more died within 12 months (10 or 3 percent vs. two or .6 percent). “The causes of death varied” in HIV patients, the authors write. “While none of the causes appeared to be a direct consequence of the operation, two deaths were within 30 days of the operation.”

The researchers also examined risk factors for complications and death among HIV patients, including CD4 cell count response, a measure of the state of the immune system. The lower the CD4 count, the more likely a patient with HIV/AIDS is to develop secondary infections or illnesses. Those with a CD4 count of less than 50 cells per cubic millimeter of blood had more complications than those with higher CD4 counts. In addition, viral loads–measured as the number of copies of the virus in a milliliter of blood–of more than 30,000 were associated with a higher complication rate. Whether the patients were taking antiretroviral therapy did not appear to be related to their risk of developing complications. “Our results indicate that a higher HIV viral load seems to be a greater predictor of surgically related complications than either the CD4 cell count or the presence or absence of HAART use,” the authors write.

“Patients with HIV are living longer and regaining a substantial amount of immune function,” they conclude. “Many HIV-infected patients will require surgical attention because of a variety of disorders. In many cases, HIV serostatus [whether a person is infected with HIV or not] should not be a criterion when determining the need for surgery if patients have adequate viral control.”

Note: This story has been adapted from a news release issued by JAMA and Archives Journals.

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Bacterial infection ID method created

Posted by tumicrobiology on December 20, 2006

UPI— US scientists say they’ve developed a method of identifying specific sites of localized bacterial infections in living animals.
Bradley Smith of the University of Notre Dame and colleagues previously developed fluorescent molecular probes containing zinc that could be used to discriminate between common pathogenic bacteria, such as E. coli and Staphylococcus aureus, and mammalian cells.
In the new study, the scientists used the probes to pinpoint the sites of staph infections in laboratory mice. The scientists say physicians might have difficulty distinguishing localized bacterial infections from sites of sterile inflammation.
“Bacterial imaging is an emerging technology that has many health and environmental applications,” the researchers said. “For example, there is an obvious need to develop highly sensitive assays that can detect very small numbers of pathogenic bacterial cells in food, drinking water or biomedical samples. In other situations, the goal is to study, in vivo, the temporal and spatial distribution of bacteria in live animals.”
The study is described in a report scheduled for the Jan. 10 issue of the Journal of the American Chemical Society.
Copyright 2006 by United Press International. All Rights Reserved.

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Scientists Find Potential Weapon Against Tuberculosis Infection

Posted by tumicrobiology on December 14, 2006

The discovery of a unique copper-repressing protein in the bacterium that causes tuberculosis in humans may pave the way toward new strategies for halting tuberculosis infection.

Scientists have known that when macrophages – the host’s immune cells – swallow an invading bacterium, they dump excessive amounts of copper onto the invader in an effort to kill it. While all cells need copper to function, too much of the metal ion causes cell death.

“But the invaders fight back with their own defense,” says Adel Talaat, a microbiologist at the University of Wisconsin-Madison School of Veterinary Medicine. “They block the excess copper.”

In a paper published in the January 2007 issue of Nature Chemical Biology, Talaat and colleagues from Texas A&M University and University of Saskatchewan in Saskatoon, Canada describe a unique protein repressor that they have identified as the mechanism used by invading bacterium cells to fight off the host’s copper attack.

Prior to the discovery of this repressor protein, scientists did not know exactly how invading bacterium protected themselves from copper ions used by the body as a defense against infection.

“With this discovery, we can now pursue ways to deactivate the repressor protein,” says Talaat. “Our goal is to disable the tuberculosis bacterium from fighting back against the host body’s defense mechanisms, so that we can stop tuberculosis.”
Source: University Of Wisconsin-Madison

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Study: How shigella causes dysentery

Posted by tumicrobiology on December 14, 2006

French scientists say they believe they’ve discovered how shigella bacteria survive in the gut to be able to cause dysentery.

Laurence Arbibe and colleagues at the Pasteur Institute in Paris found a protein produced by shigella is injected into host cells and blocks production of immune signals required for preventing the infection.

Shigella affects millions of people worldwide, killing hundreds of thousands annually.

The researchers studied Shigella flexneri infection of human colon cells to understand the bacterial factors required to initiate disease. Shigella bacteria are known to inject up to 20 proteins into intestinal cells for the purpose of promoting infection and for dampening immune responses.

They found one of the injected proteins, OpsF, could prevent gut cells from switching on genes involved in immune responses. As a consequence, Shigella flexneri avoids being killed by their host’s immune cells and is able to spread throughout the gut.

The scientists say their study highlights the precision with which pathogens such as shigella can dramatically alter host cells. It also suggests blocking OspF may provide a target for treating bacterial dysentery.

The study is reported in the January issue of the journal Nature Immunology.

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Three studies focus on malaria parasite

Posted by tumicrobiology on December 14, 2006

The US and British scientists have produced three studies that independently characterize the genetic diversity of the parasite that causes malaria.

Two studies focused on Plasmodium falciparum, the most deadly of the Plasmodium species known to cause human malaria, while the other study compares it with the related Plasmodium reichenowi, which infects chimpanzees.

Overall, the scientists say the data constitute a valuable resource that should improve understanding of drug resistance in malaria and identify candidate targets for vaccines.

Dyann Wirth and colleagues at the Harvard School of Public Health produced a genome-wide map of diversity in P. falciparum, including full sequencing of 16 new and geographically diverse strains and targeted sequencing of 54 other worldwide isolates.

Xin-zhuan Su, Philip Awadalla and colleagues at the U.S. National Institutes of Health focus on sequencing genomic regions coding for proteins within 4 P. falciparum isolates.

In the third study, Manolis Dermitzakis, Matthew Berriman and colleagues at the Wellcome Trust Sanger Institute in Hinxton, England, provide the first sequence of the P. reichenowi strain, as well as the sequence of two P. falciparum strains.

All three papers appear in the January issue of Nature Genetics.

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Flu Shot Effective Against Drifted Influenza, Nasal Spray Vaccine Less So

Posted by tumicrobiology on December 14, 2006

During a year in which the circulating strains of influenza showed genetic differences from the strains in vaccines, the traditional killed-virus flu shot was found to be effective in preventing influenza in healthy adults. The live attenuated-virus nasal spray vaccine also prevented illnesses but was less effective.

Both outcomes were determined by laboratory confirmation of flu infection, a University of Michigan study found.

Earlier studies had suggested that the nasal spray, sold by MedImmune as FluMist, might offer better protection against drifted viruses that had genetically changed between vaccine formulation and annual influenza activity. The nasal spray, which is based on a live but weakened virus, was 86 percent protective in one study conducted in children during a major drift year. However, FluMist had not previously been studied head-to-head against the shot in adults with laboratory confirmation.

The killed-virus flu shot is usually billed as 70 to 90 percent effective against circulating strains that are well matched to vaccine strains. During the 2004-2005 flu season, a University of Michigan team found that the killed-virus flu shot was 75 percent effective against a moderately-drifted type A virus and two types of B virus. The standard formulation of both the flu shot and the nasal spray vaccine includes two types of A influenza and one B, but in the 2004-05 season, there were two B strains circulating and one type A.

“On the other hand, FluMist was 48 percent effective. These results may only apply to the 2004-05 flu season,” said Dr. Arnold S. Monto, professor of epidemiology. “In other years the results may be different. We need a more specific understanding of which viral changes matter and which don’t. There are many things about vaccine protectiveness that we still don’t completely understand.”

“It may be that the difference in effectiveness between the shot and the spray can be attributed to poorer protection against type B infections in participants given FluMist,” Monto said, but that’s not clear from this study.

The live attenuated vaccine marketed as FluMist was developed at the University of Michigan by Hunein “John” Massaab, professor emeritus of epidemiology. MedImmune produces it under a license with the University.

Monto’s research team is conducting a randomized, double-blind, placebo-controlled three-year trial with National Institutes of Health funding in which the two vaccines are being compared head-to-head and against a placebo. Prior to the 2004-05 flu season, they vaccinated 1,247 people aged 18 to 46 in four Michigan communities.

A source of confusion about vaccine effectiveness against drifted viruses may stem from study design. Many vaccine evaluation studies rely on a clinical diagnosis of “influenza-like illness,” or measures of the immune response to infection in the blood. For the present study, Monto and lead author Suzanne Ohmit, assistant research scientist in epidemiology, took throat swab specimens from participants experiencing flu symptoms and analyzed them, using virus isolation and PCR techniques, to determine if influenza virus was causing the illness.

Monto and Ohmit suspect that the adult participants in their study in 2004-05 had enough prior experience with influenza that the live attenuated virus may have failed to infect their nasal passages and initiate an immune response as it is intended to do. However, both still believe that the nasal spray is very effective in children and may be more effective than the killed vaccine in the young.

“FluMist works very well in children with naive immune systems,” Ohmit said. The FDA approval of FluMist limits its use to people between age 5 and 49 years.

In another paper in the same edition of the New England Journal of Medicine, FluMist was administered to school children and the children were followed to see if they and their families had been protected against flu. The study’s authors conclude that vaccinating children had some protective effect on the children and their families, confirming a notion of “herd immunity” first tested by Arnold Monto in a 1970 influenza vaccine study.

Without having children in their study, Monto and Ohmit can’t tell whether the two vaccines would have conferred different protection in 2004-05 in that age group. However, data from a study conducted in 2004-05 in children aged 6 to 59 months by MedImmune, suggested that FluMist offered significantly greater protection than the flu shot. A MedImmune study discussed in October at a Toronto conference also found that FluMist was more successful at initiating antibody response than the traditional shot in young children.

Monto and Ohmit will continue to follow study participants vaccinated in Fall 2005 , without vaccinating them this year, to see whether the shot or the spray offer long-term protection.

The paper “Prevention of Antigenically Drifted Influenza by Inactivated and Live Attenuated Vaccines,” appears in the Dec. 14 issue of the New England Journal of Medicine.
Source: University of Michigan

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Snottites, Other Biofilms Hasten Cave Formation

Posted by tumicrobiology on December 14, 2006

Biofilms, which are complex layered communities of sulfur-consuming microbes, increase the rate of cave formation, but may also shed light on other biofilms, including those that grow on teeth and those that corrode steel ships hulls, according to a team of geologists
Cave biofilms are simpler than the microbes that occur in soils where there can be hundreds of thousands of species,” says Dr. Jennifer L. Macalady, assistant professor of geosciences, Penn State. “Some cave biofilms have very few species, 10 to 20. The more complex ones have 100s or 1,000s.”

The researchers investigated the Frasassi cave system located north of Rome and south of Venice in Italy. These limestone caves are like New Mexico’s Carlsbad Caverns and Lechuguilla

Cave, but in those caves, sulfur entered the caves from oil and gas reserves, while in Italy, the sulfur source is a thick gypsum layer below. Having sulfur in the environment allows these biofilms to grow.

Most limestone caves form when rainwater and runoff permeate the caves from above. Water and carbon dioxide mix to form carbonic acid, a very weak acid, that erodes the limestone cave walls. In sulfidic caves, water enters the caves from below, carrying hydrogen sulfide. Microbes in the biofilms use the sulfur for energy and produce sulfuric acid, a very strong acid.

“One type of biofilm, called a snottite because of its appearance, has a pH of zero or one,” says Daniel S. Jones, graduate student in geosciences. “This is very, very acidic.”

Carbonic acid cave systems lose about a third of an inch of wall every thousand years, while sulfuric acid cave systems lose about two and a third inches or six times as much in the same time. The researchers are interested in the make-up of the biofilms and how they cycle sulfur.

Biofilms are made up of thin layers of microbe species that can be very different. All require water, but some biofilms live in the pools, lakes and streams in caves and others live on the damp walls. The layers against the rock surface use oxygen and hydrogen sulfide for energy and produce sulfuric acid. The layer on the outside does as well, but, because middle layers exist, there is an opportunity for microbes that find oxygen poisonous to thrive. These middle layers may convert the sulfuric acid to hydrogen sulfide, creating a complete sulfur cycle in a few microns.

In dental biofilms, the microbes on the teeth are the ones that produce the acids that cause cavities, while the ones on the top create the right conditions for the acid-producing microbes to survive. Cave biofilm layers also fulfill different niches in their very tiny environment.

“Stream biofilms are responsible for the majority of sulfide disappearance in streams,” Jones told attendees today (Dec. 11) at the fall meeting of the American Geophysical Meeting in San Francisco.

Because the cave biofilms are relatively simple, it will be easier to connect the various microbe species to the geochemistry involved. While this work is not yet complete, the researchers are working on the problem. Dr. Greg K. Druschel, assistant professor of geology, University of Vermont, used microelectrode voltammetry to try to determine exactly which biofilm layers produce acids. The levels of hydrogen sulfide and sulfuric acid change, depending on which layer is tested.

“There is also a question about where these microbes originate,” says Macalady. “We do not know if they are always in rocks or if they are transported from somewhere else to establish themselves.”

No matter the answer, the biofilms probably begin growing in tiny cracks in the rock and eventually create some of the largest cave systems in the world. Cave biofilms are also the bottom of the food chain for cave ecosystems. They provide food for a variety of spiders, flat worms, pill bugs and amphipods — shrimp like crustaceans — that form a blind and pigmentless community.

“The only other place we find sulfur-based ecosystems is near the deep sea vents on the ocean floor,” says Jones.

Understanding how cave biofilms dissolve calcium carbonate may help us to understand the communities around ocean floor vents, but it may also, eventually, lead to understanding how biofilms dissolve calcium phosphate on teeth and the steel hulls of ships.

Macalady, Jones and Druschel worked with two undergraduate students: Daniel Eastman, University of Vermont, and Lindsey Albertson, Brown University. The National Science Foundation and NASA Astrobiology institute supported this research.

Source: Penn State

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Male Circumcision Reduces HIV Risk, Study Stopped Early

Posted by tumicrobiology on December 14, 2006

A University of Illinois at Chicago study has been stopped early due to preliminary results indicating that medical circumcision of men reduces their risk of acquiring HIV during heterosexual intercourse by 53 percent.

The study’s independent Data Safety and Monitoring Board met Dec. 12 to review the interim data. Based on the board’s review, the National Institutes of Health halted the trial and recommended that all men enrolled in the study who remain uncircumcised be offered circumcision.

“Circumcision is now a proven, effective prevention strategy to reduce HIV infections in men,” said Robert Bailey, professor of epidemiology in the UIC School of Public Health and principal investigator of the study.

The clinical trial, funded by the National Institute of Allergy and Infectious Diseases and the Canadian Institute of Health Research, enrolled 2,784 HIV negative, uncircumcised men between 18 and 24 years old in Kisumu, Kenya.

Half the men were randomly assigned to circumcision, half remained uncircumcised. All men enrolled in the study received free HIV testing and counseling, medical care, tests and treatment for sexually transmitted infections, condoms and behavioral risk counseling for 24 months.

Study results show that 22 of the 1,393 circumcised men in the study contracted HIV, compared to 47 of the 1,391 uncircumcised men. In other words, circumcised men had 53 percent fewer HIV infections than uncircumcised men.

Until now, public health organizations have not supported circumcision as a method of HIV prevention due to a lack of randomized controlled trials.

“With these findings, the evidence is now available for donor and normative agencies, like WHO and UNAIDS, to actively promote circumcision in a safe context and along with other HIV prevention strategies,” Bailey said.

“Circumcision cannot be a stand-alone intervention. It has to be integrated with all the other things that we do to prevent new HIV infections, such as treating sexual transmitted diseases and providing condoms and behavioral counseling,” Bailey said. “We can’t expect to just cut off a foreskin and have the guy go on his merry way without additional tools to fight against getting infected.”

Opponents of circumcision have speculated that circumcised men may feel they are not at risk of contracting HIV and may be more likely to engage in risky behavior. The Kenya study suggests that circumcision did not increase risky behavior among circumcised or uncircumcised men, according to Bailey.

“Both uncircumcised and circumcised men are reducing their sexual risk behavior,” he said, “which indicates that our counseling is doing some good.”

The study also evaluated the safety of circumcision in a community health clinic with specially trained practitioners. There were no severe or lasting complications from circumcision. However, 1.7 percent of surgeries resulted in mild complications, such as bleeding or infection.

Bailey said that promoting circumcision in Africa must be done in conjunction with proper technical training and medical tools, equipment and supplies necessary to perform large numbers of circumcisions safely.

“Already, there are large numbers of boys and young men who are seeking circumcision in areas of Africa where men are not traditionally circumcised,” he said. “The danger is that unqualified practitioners will fill a niche by providing circumcision, but with much higher complication rates.”

An estimated 30 million people in Africa are infected with HIV/AIDS and more than 90 percent of HIV infections in adults result from heterosexual intercourse. In Kisumu, the third-largest city in Kenya, an estimated 26 percent of uncircumcised men are HIV infected by age 25.

“This study will likely not have a large impact on the incidence of HIV/AIDS in the United States or Europe where heterosexual transmission of HIV is low compared with areas like sub-Saharan Africa and parts of Asia,” Bailey said. “However, there are other proven health benefits of circumcision, including better hygiene, fewer urinary tract infections, and less risk of cervical cancer in the partners of circumcised men.”

The armamentarium of HIV prevention strategies is very small, according to Bailey. The only other strategy proven effective is the use of antiretroviral drugs to reduce transmission from mother to child.

If a significant proportion of men in a population get circumcised, it will have an enormous impact on preventing HIV infection in men, as well as reducing infections in women, Bailey said.

Co-investigators of the study include Stephen Moses and Ian Maclean at the University of Manitoba, Jekoniah Ndinya-Achola at the University of Nairobi, Corette Parker at Research Triangle International, Kawango Agot at UNIM Project, John Krieger at University of Washington, and Richard Campbell at UIC.

During the past two decades, more than 40 observational epidemiological studies and one previous clinical trial have reported an association between male circumcision and a reduced risk of HIV infection.

On Dec. 12, the NIH stopped another clinical trial of male circumcision undertaken by investigators in Uganda and at Johns Hopkins University, after the study’s Data Safety Monitoring Board reviewed the preliminary results and found a protective effect similar to that found in Bailey’s study.

Source: University of Illinois at Chicago
Date: December 13, 2006

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Natural Radioactivity Could Provide Microbes In The Deep Biosphere With Vitality

Posted by tumicrobiology on December 6, 2006

Source: Max-Planck-Gesellschaft

An international team of researchers from the USA and Germany has published an explanation for life in the deep biosphere in the journal Science. Using the latest technologies from biogeochemistry, molecular biology and microbiology, the scientists collected a wide range of samples from the bottom of the sea. After intensive analysis, Bo B. Jørgensen and Steven D´Hondt have now published a model with which they explain that microorganisms might survive due to the natural radioactivity deep under the sea floor (Science, 10th November 2006).

It is estimated today that between 10 and 50 percent of all the biomass on the Earth is found deep below ground. Researchers working with Steven D´Hondt from the University of Rhode Island, USA, and Bo B. Jørgensen from the Max Planck Institute for Marine Microbiology in Bremen have confirmed this in the course of the Ocean Drilling Program. On a voyage on the research ship “Joides Resolution” they found life up to 400 meters below the sea floor. Tests revealed that the drilled cores contained living microorganisms; contamination was ruled out. In the upper layers of sediment, the researchers counted up to 100 million unicellular organisms per millilitre; deeper, in the 35 million year old sediments on the Earth’s crust, they still found one million microorganisms. This is a puzzle for scientists: only the upper layers of these deposits are in contact with the water – so where does the energy to provide life in the depths of the sediment come from?

Taking as a basis the energy sources in the deposits that are available to the cells in the form of organic carbon compounds, it is possible to calculate that the cells could only divide every thousand years. This extremely long period for reproduction cannot be reconciled with current understanding of living cells.

Jørgensen and D’Hondt are now proposing, on the basis of their data, a process which could represent an alternative source of energy for life deep under large sections of the Pacific – natural radioactivity. Water is broken down by radioactive radiation, which arises during the decomposition of naturally occurring potassium, thorium and uranium isotopes. This process (radiolysis) creates hydrogen and oxygen. Estimates of the energy balance show that this process can supply sufficient energy for the microorganisms. This would make life forms in the Deep Biosphere independent of the processes on the Earth’s surface. The authors point out that an exotic habitat like this could also have developed on other planets, far away from any suns.

In December 2006 the researchers will be taking the drilling ship “RV Roger Revelle” to the South Pacific. There, far away from the continental shelves, the quantity of carbon compounds which could serve the microorganisms as a basis for life is very low. This makes the researchers all the more curious about the sediment samples from the bottom of the sea.

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Scientists spot unknown gene interaction

Posted by tumicrobiology on December 6, 2006

Italian genetic researchers say they’ve made a discovery that might provide an important tool for controlling and treating breast cancer.

Scientists at Milan’s National Tumor Institute discovered proteins produced by the genes HER-2 and FHIT interact in a way that encourages tumor growth, the Italian news agency ANSA reported Wednesday. The researchers determined HER-2 prevents FHIT from blocking cell proliferation. Without FHIT’s action, cells can multiply quickly and end up producing a tumor.

“The analysis carried out for our research shows how the activity of HER-2 leads to the degradation of FHIT,” Sylvie Menard, head of experimental oncology at INT, told ANSA.

Medical researchers previously determined breast tumor development was often accompanied by an overproduction of proteins by the HER-2 gene. It is also known that in 70 percent of breast cancer cases, FHIT has stopped working for some reason.

Menard told ANSA it should be possible to find pharmaceuticals to prevent FHIT degradation, thereby slowing the development of tumors.

The research appears in the current issue of the journal of the American Academy of the Sciences.

Copyright 2006 by United Press International. All Rights Reserved.

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Method for detection and identification of multiple chromosomal integration sites in transgenic animals created with lentivirus

Posted by tumicrobiology on December 4, 2006

Elizabeth C. Bryda, Michael Pearson, Yuksel Agca, and Beth A. Bauer

BioTechniques® December 2006
Volume 41, Number 6: pp 715-719

Transgene delivery systems, particularly those involving retroviruses, often result in the integration of multiple copies of the transgene throughout the host genome. Since site-specific silencing of trangenes can occur, it becomes important to identify the number and chromosomal location of the multiple copies of the transgenes in order to correlate inheritance of the transgene at a particular chromosomal site with a specific and robust phenotype. Using a technique that combines restriction endonuclease digest and several rounds of PCR amplification followed by nucleotide sequencing, it is possible to identify multiple chromosomal integration sites in transgenic founder animals. By designing genotyping assays to detect each individual integration site in the offspring of these founders, the inheritance of transgenes integrated at specific chromosomal locations can be followed efficiently as the transgenes randomly segregate in subsequent generations. Phenotypic characteristics can then be correlated with inheritance of a transgene integrated at a particular chromosomal location to allow rational selection of breeding animals in order to establish the transgenic line.


Production of genetically engineered animals by pronuclear injection or retroviral delivery systems has been a successful strategy for generating animal models to better understand the functionality of genes. In transgenic animals created by embryo microinjection, the site of integration of the transgene within the genome is a random event. Thus, when multiple embryos have been injected or infected with the same DNA, the integration site will be different in each founder animal. When the integration events have occurred at the one-cell stage, they should exhibit germline transmission with the potential to be inherited by the founder’s offspring. If the integration occurs at a later stage, the resulting mosaic founder may or may not exhibit germline transmission of the transgene. In the case of pronuclear injection, there is typically one insertion site, although multiple transgene copies are often found in a tandem array at that integration site (1).

Lentivirus transgenesis is becoming an increasingly attractive alternative to pronuclear injection because it is more efficient in terms of successful transgene incorporation into the host genome, less invasive to the embryo, and technically less demanding to perform (2). Lentiviral delivery systems have been used successfully to generate transgenic mice, rats, pigs, and cattle (2–7). The disadvantage of lentivirus is that there are often multiple integration events with random transgene insertions on several chromosomes.

Independent of the method of transgene delivery, the insertion site can have profound effects on transgene expression. This can lead to phenotypic effects in the transgenic animal that are not due to the transgene per se, but are a consequence of the integration site, a phenomenon referred to as position effect (8). It is critical to correlate phenotype with genotype, particularly in animals created via lentivirus transgenesis, since not all copies of the transgene may be contributing equally to the phenotype.

Determining transgene integration sites is challenging. A number of PCR-based methods, often referred to as chromosome walking techniques, have been developed to isolate DNA fragments adjacent to known sequences, including inverse PCR (9), ligation-mediated PCR (LMPCR) (10), randomly primed PCR (RP-PCR) (11,12), and T-linker PCR (13). The method described in this paper incorporates several elements of these techniques in a unique way that allows the capture of DNA fragments containing the chromosomal region flanking the transgene. Our method enables quick and inexpensive determination of multiple independent transgene integration sites in founder animals and their offspring. Here, we demonstrate that this method is useful for identifying and monitoring multiple transgene integration sites in transgenic animals created using lentivirus.



Lewis rat lines carrying an enhanced green fluorescent protein (EGFP) transgene were created by using the EGFP DNA construct and experimental protocol described by Lois et al. (2). Transgene positive founder animals were identified using an EGFP PCR assay (14). To assess GFP expression, tail biopsies were examined for fluorescence under a Nikon SMZ1500 UV dissecting scope (Nikon Instruments, Melville, NY, USA). Founders (F0) were bred to wild-type Lewis rats obtained from Harlan Sprague Dawley (Indianapolis, IN, USA) to generate the N1. N1 animals were genotyped using integration site-specific PCR assays. Selected N1 animals were mated to wild-type Lewis rats to generate the N2. N2 animals were genotyped using integration site-specific genotyping assays, and GFP expression was confirmed. Several of these lines (F455.5, F456.9, F458.7, F463.1, and F463.5) demonstrated stable transmission of the integration site-specific transgene coupled with robust GFP expression and were donated to the Rat Research and Resource Center (RRRC) at the University of Missouri. All other rat lines and mouse strains used are available either through the RRRC (Web site (external)) for rats or the University of Missouri/Harlan Mutant Mouse Regional Resource Center (MMMRC; Web site (external)) for mice.

Preparation of DNA

DNA was isolated from tail biopsies using the DNeasy® Tissue kit (Qiagen, Valencia, CA, USA). Restriction endonuclease digestion was performed with PstI and HhaI (Figure 1, step 1). These enzymes were chosen because they created 3′ overhangs and their recognition sites were not present within the transgene sequence. Three micrograms genomic DNA were digested with 20 U enzyme in a total reaction volume of 30 μL as recommended by the manufacturer. Reactions were incubated for 2 h for partial digestion.

PCR Amplification and Linker Ligation

Three transgene-specific nested primers were designed to both the 5′ and 3′ regions of the transgene using PrimerQuest available from Integrated DNA Technologies (IDT; Coralville, IA, USA). Primer 1 was farthest from the junction between the known transgene sequence and the unknown integration site, whereas primer 3 was closest (Figure 1). All gene-specific primers were designed to have an optimum melting temperature (Tm) of 60°C, optimum primer length of 24 bp, and an optimum % GC content of 50. Y-linker and primer sequences for the Y-linker and their relationships are provided in Figure 2. Y-linker A (Figure 2) contains a terminal inverted T at the 3′ end to inhibit extension by DNA polymerases. The Y-linker was prepared by combining equal volumes of 8 μM Y-linker A and 8 μM Y-linker E, incubating at 95°C for 5 min, and then letting the reaction cool on the benchtop. The sequences of the genespecific primers used for the lentivirus-generated rat lines are available upon request or are listed under the genotyping assay for the specific lines at Web site (external). Primers and linkers were synthesized by IDT.

All PCRs were performed in a 25-μL volume containing 2.5 μL 10× FastStart Taq with 20 mM MgCl2 (Roche Diagnostics, Indianapolis, IN, USA), 0.2 mM each dNTP, 1.6 μM each primer, and 1.25 U FastStart Taq buffer. In the first PCR, 1 μL restriction digest from above and transgenespecific primer 1 were used, and a single round of PCR was performed with the following thermal cycling conditions: 94°C for 10 min, 60°C for 1 min, and 72°C for 10 min (Figure 1, step 2). Following amplification, a 10-μL reaction containing 7 μL this PCR, 1 μM Y-linker, 400 U T4 DNA Ligase (New England BioLabs, Ipswich, MA, USA), and 1 μL 10× T4 DNA Ligase buffer supplied with the enzyme was incubated at 16°C for 16 h (Figure 1, step 3). Transgene-specific primer 2, Y-primer D, and 1 μL ligase reaction were used in the second PCR with the following cycling conditions: 94°C for 5 min, 20 cycles of 94°C for 30 s, 60°C for 30 s, 72°C for 1.5 min, and one cycle of 72°C for 10 min (Figure 1, step 4). The same cycling conditions were used in the third PCR. This final reaction utilized transgene-specific primer 3, Y-primer G, and 1 μL from the second PCR (Figure 1, step 5).

PCR Product Purification and Analysis

Amplification products from the third PCR were separated by gel electrophoresis on 1%-3% agarose gels, and individual products were gel-purified using QIAquick® Gel Extraction kit (Qiagen). When multiple bands were detected, all bands were isolated. The nucleotide sequence of each amplification product was determined using the transgene-specific primer 3 as a sequencing primer (Figure 1, step 6). Nucleotide sequencing was performed either at our DNA Core (University of Missouri-Columbia) or by SeqWright (Houston, TX, USA). The nucleotide sequences were aligned and examined to confirm the presence of the expected known transgene sequence and determine the flanking sequence representing the insertion site. The insertion site sequence was analyzed using Basic Local Alignment Search Tool (BLAST) (15) to determine the chromosomal location of the transgene.


Lentivirus was used as a delivery system to create Lewis rat lines carrying an EGFP transgene (2). A total of nine transgene positive founder (F0) animals were recovered. While all nine founders were positive for the presence of the EGFP transgene, eight founders expressed EGFP based on epifluorescent microscopy of tail biopsies, while one founder (456) had no detectable fluorescence (Table 1). Our method for determining chromosomal integration sites was used to identify the chromosomal location(s) of the transgene in each of the nine founders. PCR products ranged in size from 100–1000 bp. Longer PCR fragments were generally necessary for determining the insertion site when the region contained repetitive elements. Several sites were successfully identified with recovered products as small as 110 bp, which included as little as 20 bp genomic sequence. For seven of the founders, we identified one to four integration sites depending on the founder. We failed to identify the integration site in two founders using PstI and HhaI digestion, and we did not pursue these further. It is possible that by using other restriction enzymes with 4–6 bp recognition sites or increasing PCR extension times to generate larger products, we would have successfully identified the integration sites in these founder lines. For seven lines, site-specific genotyping assays were developed for every integration site identified in the founder. In one case (463), we recovered genomic sequence that matched a sequence found on many chromosomes, so we could not assign a chromosomal location to this integration site. Nonetheless, the genotyping assay based on this sequence allowed the transgene integration site to be followed not only in the founder but in his offspring.

To follow segregation of the integration sites, the offspring from matings between each of the seven founders and wild-type Lewis rats were monitored for presence and expression of the transgene at each integration site using the site-specific genotyping assays and microscopic examination for GFP fluorescence. One founder (452) was infertile. For the remaining six founder lines, offspring were obtained, and both the insertion sites and the GFP expression were determined.

Founder 455 had two independent transgene insertion sites: one on chromosome 1, and a second on chromosome 5. When this founder was mated to a wild-type Lewis animal, two N1 offspring were recovered. One N1 carried the chromosome 1 integration site, but did not have detectable GFP expression. Lack of expression may have been due to positional effects. The other N1 carried the chromosome 5 integration site and did have GFP expression. The chromosome 5 transgene positive N2 offspring (n = 5) continued to have high fluorescence, demonstrating that GFP expression in this line was associated with the chromosome 5 transgene, and could be stably transmitted from generation to generation. This illustrates the importance of determining which transgene insertion site was correlated with GFP expression in order to successfully maintain a GFP-expressing line.

Line 456, which carried two transgene insertion sites, was unusual in that the founder did not display GFP fluorescence. Of the offspring recovered from this founder, three carried the chromosome 17 transgene insertion only and one carried the chromosome 9 transgene insertion only. While animals carrying the chromosome 17 insertion did not have detectable fluorescence, robust GFP fluorescence was seen in the animal that inherited the chromosome 9 transgene insertion. The chromosome 9 transgene positive N2 animals continued to have high fluorescence, demonstrating that GFP expression in this line was associated with the chromosome 9 transgene. We speculate that GFP expression was suppressed at the chromosome 17 insertion due to a position effect and that the founder was mosaic for the chromosome 9 insertion, resulting in undetectable GFP expression. In subsequent generations, inheritance of the chromosome 9 insertion was germline, and expression occurred in all cells leading to detectable fluorescence.

For line 458, three insertion sites were detected. By correlating GFP expression with inheritance of the various transgene insertion sites, it was possible to show that the chromosome 7 integration gave good GFP expression. This was confirmed in N2 animals (n = 10) carrying only the chromosome 7 integration. It should be noted that while none of the N1 animals carried the chromosome 10 integration site, this site was confirmed in the original founder by integration site-specific genotyping. It is possible that the founder was mosaic for the chromosome 10 integration site.

For line 459, which had a single detected transgene insertion on chromosome 2, two offspring were recovered that inherited the chromosome 2 transgene insertion site. However, neither of these animals exhibited GFP fluorescence. This could be due to a positional effect associated with the particular insertion site on chromosome 2 coupled with inheritance through the male lineage, or alternatively, we may have missed an insertion site in founder 459 that was associated with the fluorescence seen in the founder, which was not inherited by these two offspring.

Founder 463 had the greatest number of insertion sites; by continuing to correlate GFP expression with inheritance of specific transgene insertion sites, it was possible by the N2 generation to identify animals with single transgene insertion sites that maintained high GFP expression.

In addition to the lentivirus experiment described above, we have successfully used this technique to determine the lentivirus integration sites and to generate rat lines with single transgene integration sites for a Sprague-Dawley GFP transgenic (RRRC: 0065), derived from the line created by Lois et al. (2), and a rat model containing the human presenilin-1 gene (RRRC: 0061). To test whether our method for identifying insertion sites had broader application beyond just determining chromosomal locations of lentivirus transgene integration, we attempted to identify the transgene integration site of three additional rodent strains: (i) a mouse transgenic strain (MMRRC: 000366-MU/H) carrying the EGFP gene on the FVB inbred genetic background (16); (ii) a knockout mouse line (MMRRC: 000352-MU/H) involving the acetylcoenzyme A dehydrogenase long chain gene (Acadl), which carries a duplication of exons 3 and 4 with insertion of the neocassette into the approximately 11 kb intron 4 (17); and (iii) a transgenic rat line (RRRC: 0043), which contains a mutated version of the human HLA-B2705 gene on a Lewis genetic background (18). In the case of the FVB-EGFP strain and the Acadl knockout strain, we were able to determine precisely the insertion site on chromosome 3 and within the large Acadl intron 4, respectively. Our method failed for the HLA-B2705 transgenic rat line, which has a high transgene copy number (24 copies) in homozygous animals (18). The insertions are integrated at a single locus (18), and the multiple copies have probably integrated as concatamers.

A major advantage of determining the precise chromosomal integration site in animals created via pronuclear injection is that genotyping assays can be developed that allow animals heterozygous for a transgene to be easily distinguished from homozygous animals. Without this type of information, PCR-based genotyping assays can distinguish only whether animals carry the transgene. While it is possible to use Southern blot analysis and densitometry to measure transgene copy number as an alternative method to distinguish homozygotes from heterozygotes, it is laborious, timeconsuming, and not practical for many labs.

In summary, we have described a quick and straightforward method for determining the location of multiple chromosomal integration sites in animals created by lentivirus transgenesis. Our studies underline the need to carefully correlate a particular integration site with gene expression over multiple generations in order to create stable models. We have also found that this method has applicability for detecting transgene integration sites in other cases of random integration, but is probably limited to situations where very few tandem copies of the transgene have been integrated at the insertion site.


E.C.B. and M.P contributed equally to this work. This work was supported in part by grants from the National Institutes of Health (NIH; U42 RR014821 and P40 RR16939). We thank James Sparks for technical assistance and Howard Wilson for assistance with graphics.


The authors declare no competing interests.


1. Lo, C.W., M. Coulling, and C. Kirby. 1987. Tracking of mouse cell lineage using microinjected DNA sequences: analyses using genomic Southern blotting and tissue-section in situ hybridizations. Differentiation 35:37-44.

2. Lois, C., E.J. Hong, S. Pease, E.J. Brown, and D. Baltimore. 2002. Germline transmission and tissue-specific expression of transgenes delivered by lentiviral vectors. Science 295:868-872.

3. Hofmann, A., B. Kessler, S. Ewerling, M. Weppert, B. Vogg, H. Ludwig, M. Stojkovic, M. Boelhauve, et al. 2003. Efficient transgenesis in farm animals by lentiviral vectors. EMBO Rep. 4:1054-1060.

4. Whitelaw, C.B., P.A. Radcliffe, W.A. Ritchie, A. Carlisle, F.M. Ellard, R.N. Pena, J. Rowe, A.J. Clark, et al. 2004. Efficient generation of transgenic pigs using equine infectious anaemia virus (EIAV) derived vector. FEBS Lett. 571:233-236.

5. Pfeifer, A., M. Ikawa, Y. Dayn, and I.M. Verma. 2002. Transgenesis by lentiviral vectors: lack of gene silencing in mammalian embryonic stem cells and preimplantation embryos. Proc. Natl. Acad. Sci. USA 99:2140-2145.

6. Hofmann, A., V. Zakhartchenko, M. Weppert, H. Sebald, H. Wenigerkind, G. Brem, E. Wolf, and A. Pfeifer. 2004. Generation of transgenic cattle by lentiviral gene transfer into oocytes. Biol. Reprod. 71:405-409.

7. van den Brandt, J., D. Wang, S.H. Kwon, M. Heinkelein, and H.M. Reichardt. 2004. Lentivirally generated eGFP-transgenic rats allow efficient cell tracking in vivo. Genesis 39:94-99.

8. Clark, A.J., P. Bissinger, D.W. Bullock, S. Damak, R. Wallace, C.B. Whitelaw, and F. Yull. 1994. Chromosomal position effects and the modulation of transgene expression. Reprod. Fertil. Dev. 6:589-598.

9. Rosenthal, A. 1992. PCR amplification techniques for chromosome walking. Trends Biotechnol. 10:44-48.

10. Rosenthal, A. and D.S. Jones. 1990. Genomic walking and sequencing by oligocassette mediated polymerase chain reaction. Nucleic Acids Res. 18:3095-3096.

11. Shyamala, V. and G.F. Ames. 1989. Genome walking by single-specific-primer polymerase chain reaction: SSP-PCR. Gene 84:1-8.

12. Parker, J.D., P.S. Rabinovitch, and G.C. Burmer. 1991. Targeted gene walking polymerase chain reaction. Nucleic Acids Res. 19:3055-3060.

13. Yuanxin, Y., A. Chengcai, L. Li, G. Jiayu, T. Guihong, and C. Zhangliang. 2003. Tlinker-specific ligation PCR (T-linker PCR): an advanced PCR technique for chromosome walking or for isolation of tagged DNA ends. Nucleic Acids Res. 31:e68.

14. Lai, L., K.W. Park, H.T. Cheong, B. Kuhholzer, M. Samuel, A. Bonk, G.S. Im, A. Rieke, et al. 2002. Transgenic pig expressing the enhanced green fluorescent protein produced by nuclear transfer using colchicine-treated fibroblasts as donor cells. Mol. Reprod. Dev. 62:300-306.

15. Altschul, S.F., W. Gish, W. Miller, E.W. Myers, and D.J. Lipman. 1990. Basic local alignment search tool. J. Mol. Biol. 215:403-410.

16. Kisseberth, W.C., N.T. Brettingen, J.K. Lohse, and E.P. Sandgren. 1999. Ubiquitous expression of marker transgenes in mice and rats. Dev. Biol. 214:128-138.

17. Kurtz, D.M., P. Rinaldo, W.J. Rhead, L. Tian, D.S. Millington, J. Vockley, D.A. Hamm, A.E. Brix, et al. 1998. Targeted disruption of mouse long-chain acyl-CoA dehydrogenase gene reveals crucial roles for fatty acid oxidation. Proc. Natl. Acad. Sci. USA 95:15592-15597.

18. Taurog, J.D., S.D. Maika, N. Satumtira, M.L. Dorris, I.L. McLean, H. Yanagisawa, A. Sayad, A.J. Stagg, et al. 1999. Inflammatory disease in HLA-B27 transgenic rats. Immunol. Rev. 169:209-223.

Received 6 July 2006; accepted 22 August 2006.

Address correspondence to Beth A. Bauer or Yuksel Agca, University of Missouri-Columbia, Department of Veterinary Pathobiology, 1600 E. Rollins St., Columbia, MO 65211, USA. e-mail:; e-mail:

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Painkillers May Threaten Power Of Vaccines

Posted by tumicrobiology on November 29, 2006

With flu-shot season in full swing and widespread anticipation of the HPV vaccine to prevent cervical cancer, a new University of Rochester study suggests that using common painkillers around the time of vaccination might not be a good idea
Researchers showed that certain nonsteroidal anti-inflammatory drugs (NSAIDs), also known as cyclooxygenase inhibitors, react with the immune system in such a way that might reduce the effectiveness of vaccines.

The research has widespread implications: study authors report that an estimated 50 to 70 percent of Americans use NSAIDs for relief from pain and inflammation, even though NSAIDs blunt the body’s natural response to infection and may prolong it.

“For years we have known that elderly people are poor responders to the influenza vaccine and vaccines in general,” said principal investigator Richard P. Phipps, Ph.D., a professor of Environmental Medicine, and of Microbiology and Immunology, Oncology and Pediatrics. “And we also know that elderly people tend to be heavy users of inhibitors of cyclooxygenase such as Advil, aspirin, or Celebrex. This study could help explain the immune response problem.”

The study is available online in the Dec. 1, 2006, Journal of Immunology, and was funded in part by the National Institutes of Health.

When a person is vaccinated, the goal is to produce as many antibodies as possible to effectively neutralize the infection. To do this, white blood cells called B-lymphocytes, or B cells, spring into action to produce those antibodies. B cells also serve as the immune system’s memory for future protection against the illness.

But Phipps and colleagues discovered that human B cells also highly express the cyclooxygenase-2 (cox-2) enzyme, which is not intrinsically bad unless it is overproduced, causing pain and fever. So, when a person takes a drug to block the cox-2 enzyme — and thereby reduce pain and fever — the drug also reduces the ability of B cells to make antibodies.

“The next step is to figure out the worst time to take drugs that inhibit cox-2 in the context of getting vaccinated. Is it the day before, the day of, or the day after” The timing is likely to be very important,” Phipps said. “But meanwhile, we believe that when you reach for the medicine cabinet to reduce pain at the injection site, that is probably the wrong thing to do.”

The findings are based on laboratory studies of blood samples from people who participated in early clinical trials for the HPV vaccine, and on studies of mice.

For the animal portion of the study, researchers vaccinated normal mice and mice engineered to be cox-2 deficient with a component form of the HPV vaccine. They analyzed the amount of antibodies the animals produced, focusing on the critical virus-neutralizing antibodies. The cox-2 deficient mice made 50 to 70 percent less of these key antibodies.

The same experiment was done on preserved blood samples from people who had been vaccinated against HPV-16, the strain linked to cervical cancer. Scientists reactivated the B cells in the blood samples and watched them churn out antibodies, as expected. But when researchers treated the B cells with a cox-2 inhibiting drug, the cells significantly diminished their production of antibodies — showing that cox-2 is essential for an optimal immune response against HPV 16.

This study is not questioning the effectiveness of the newly marketed HPV vaccine, the Rochester scientists said. They pointed out that in many clinical trials involving thousands of women, the vaccine offered complete protection against the development of cervical cancer. And presumably some of these women were taking NSAIDs at the time.

“There’s no doubt the HPV vaccine showed 100 percent efficacy. Still, our data does suggest that it might be wise to limit the use of NSAIDs when you receive any vaccine,” said co-author Robert Rose, Ph.D., associate professor of Medicine and Microbiology and Immunology at the University of Rochester, and one of the virologists whose work led to the development of the new cancer vaccine.

Scientists do not completely understand the mechanism by which cox-2 influences the immune response in humans. They do believe the response may depend upon the dose and frequency of NSAID use.

The negative effects of blocking cox-2 could be more pronounced in people with compromised immune systems, such as AIDS or cancer patients, the study noted. Moreover, if a vaccine is in short supply and needs to be given in lower-than-optimal doses, taking an NSAID could hamper the immune response even more.

In addition to Phipps and Rose, graduate student Elizabeth Ryan was a co-author on the study, with assistance from students Matt Bernard and Christine Malboef.

Source: University of Rochester Medical Center

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Causes Of Global Death And Disease In The Next 25 Years

Posted by tumicrobiology on November 29, 2006

In 1993, the World Bank sponsored the 1990 Global Burden of Disease study carried out by researchers at Harvard University and the World Health Organization (WHO). This study provided the first comprehensive global estimates of death and illness by age, sex, and region. It also provided projections of the global burden of disease and mortality up to 2020. The study and its projections have been crucial in national and international health policy planning. Colin Mathers and Dejan Locar (from the World Health Organization, Geneva) have now updated the projections based on 2002 data on mortality and burden of disease and published their results in the international open-access journal PLoS Medicine.

As for the earlier report, the researchers used projections of socio-economic development to model future patterns of mortality and illness for three different scenarios: a baseline scenario, a pessimistic scenario that assumes a slower rate of socio-economic development, and an optimistic scenario that assumes a faster rate of growth.

They predict that between 2002 and 2030 under all three scenarios life expectancy will increase around the world, fewer children under the age of 5 years will die, and the proportion of people dying from non-communicable diseases such as heart disease and cancer will increase. Although deaths from infectious diseases will decrease overall, HIV/AIDS deaths will continue to increase. Despite this increase, 50% more people are predicted to die of tobacco-related disease than of HIV/AIDS in 2015. By 2030, the three leading causes of illness will be HIV/AIDS, depression, and ischemic heart disease in the baseline and pessimistic scenarios. In the optimistic scenario, road-traffic accidents (which increase with socioeconomic development) will replace heart disease as the number 3 killer.

In an accompanying editorial, the PLoS Medicine editors ask whether they are publishing “the right stuff”, i.e. research and commentary whose goal it is to reduce mortality and suffering from the most relevant conditions–and whether research funding and health expenditure are consistent with these results.

Citation: Mathers CD, Loncar D (2006) Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 3(11): e442. (

Source: Public Library of Science

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Mass Extinction 250 Million Years Ago Sparked Dramatic Shift To Complex Marine Ecosystems

Posted by tumicrobiology on November 29, 2006

The earth experienced its biggest mass extinction about 250 million years ago, an event that wiped out an estimated 95% of marine species and 70% of land species. New research shows that this mass extinction did more than eliminate species: it fundamentally changed the basic ecology of the world’s oceans.

Ecologically simple marine communities were largely displaced by complex communities. Furthermore, this apparently abrupt shift set a new pattern that has continued ever since. It reflects the current dominance of higher-metabolism, mobile organisms (such as snails, clams and crabs) that actually go out and find their own food and the decreased diversity of older groups of low-metabolism, stationary organisms (such as lamp shells and sea lilies) that filter nutrients from the water.

So says research published in Science on November 24, 2006. An accompanying article suggests that this striking change escaped detection until now because previous research relied on single numbers–such as the number of species alive at one particular time or the distribution of species in a local community–to track the diversity of marine life. In the new research, however, scientists examined the relative abundance of marine life forms in communities over the past 540 million years.

One reason they were able to do this is because they tapped the new Paleobiology Database (, a huge repository of fossil occurrence data. The result is the first broad objective measurement of changes in the complexity of marine ecology over the Phanerozoic.

“We were able to combine a huge data set with new quantitative analyses,” says Peter J. Wagner, Associate Curator of Fossil Invertebrates at The Field Museum and lead author of the study. “We think these are the first analyses of this type at this large scale. They show that the end-Permian mass extinction permanently altered not just taxonomic diversity but also the prevailing marine ecosystem structure.”

Specifically, the data and analyses concern models of relative abundance found in fossil communities throughout the Phanerozoic. The ecological implications are striking. Simple marine ecosystems suggest that bottom-dwelling organisms partitioned their resources similarly. Complex marine ecosystems suggest that interactions among different species, as well as a greater variety of ways of life, affected abundance distributions. Prior to the end-Permian mass extinction, both types of marine ecosystems (complex and simple) were equally common. After the mass extinction, however, the complex communities outnumbered the simple communities nearly 3:1.

The other authors are Scott Lidgard, Associate Curator of Fossil Invertebrates at The Field Museum, and Matthew A. Kosnik, from the School of Marine and Tropical Biology at the James Cook University in Townsville, Queensland, Australia.

“Tracing how marine communities became more complex over hundreds of millions of years is important because it shows us that there was not an inexorable trend towards modern ecosystems,” Wagner said. “If not for this one enormous extinction event at the end of the Permian, then marine ecosystems today might still be like they were 250 million years ago.”

These results also might provide a wake-up call, Wagner added: “Studies by modern marine ecologists suggest that humans are reducing certain marine ecosystems to something reminiscent of 550 million years ago, prior to the explosion of animal diversity. The asteroid that wiped out the dinosaurs couldn’t manage that.”

Lidgard added, “When Pete walked into my office with his preliminary results, I simply couldn’t believe them. Paleontologists had long recognized that ecosystems had become more complex, from the origin of single-celled bacteria to the present day. But we had little idea of just how profoundly this one mass extinction–but not the others like it–changed the marine world.”

Source: Field Museum

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Evolution Of Typhoid Bacteria: Researchers Warn Of Increased Spread Of Resistant Strains

Posted by tumicrobiology on November 29, 2006

In a study published in the latest issue of Science (24 November, 2006), an international consortium from the Max-Planck Society, Wellcome Trust Institutes in Britain and Vietnam, and the Institut Pasteur in France have elucidated the evolutionary history of Salmonella Typhi. Typhi is the cause of typhoid fever, a disease that sickens 21 million people and kills 200,000 worldwide every year. The results indicate that asymptomatic carriers played an essential role in the evolution and global transmission of Typhi. The rediscovered importance of the carrier state predicts that treatment of acute disease, including vaccination, will not suffice to eradicate this malady. The results also illuminate patterns leading to antibiotic resistance after the indiscriminate use of antibiotics. Fluoroquinolone treatment in southern Asia over two decades has resulted in the emergence of multiple, independent nalidixic acid-resistant mutants, of which one group, H58, has multiplied dramatically and spread globally. The prevalence of these bacteria hampers medical cure of clinical disease via antibiotics.

Typhoid fever remains a major health problem in the developing world and continues to cause disease in Europe and on the american continent. The evolutionary history and population structure of Typhi were poorly understood, partly because these bacteria show little genetic diversity. Now a team led by Mark Achtman and Philippe Roumagnac from the Max Planck Institute for Infection Biology, Berlin, has applied population genetic experience from prior work with Yersinia pestis, Escherichia coli, Helicobacter pylori and Neisseria meningitidis to provide novel insights into the evolution of this pathogen. The team combined its resources to assemble for the first time a globally representative collection of 105 strains of Typhi and investigated the sequence diversity within 90,000 base pairs per strain. Eighty-eight informative sequence differences were detected, showing that the population structure has evolved over the last 10,000 to 43,000 years. Amazingly, the ancestral strain continues to exist today, as do many of its direct descendents, indicating a neutral population structure, whereas normally selective forces lead to extinction of intermediate genotypes. Furthermore, these bacteria are distributed globally, demonstrating that Typhi has spread inter-continentally on multiple occasions.

The authors propose that the unusual population structure of Typhi reflects long-term carriage by asymptomatic carriers, who reached public notoriety at the beginning of the 20th century with “Mr. N the milker” in England and Typhoid Mary (Mary Mallon) in the U.S.A. These individuals infected 100s of people over the decades while they worked in the food production industry. Healthy carriers may have allowed Typhi to survive in hunter-gatherer populations prior to the Neolithic expansion of city states and facilitated its intercontinental spread. Healthy carriers are also consistent with the observation that individual genotypes of Typhi persist for many decades within each country.

Increasing resistance to antibiotics in recent decades has hampered efforts of clinicians to cure typhoid fever. The indiscriminate use of fluoroquinolones, which is a cost-effective, standard treatment for typhoid fever, has been accompanied by a frightening increase in the numbers of resistant Typhi. Investigations of a large strain collection from southern Asia revealed that many different genotypes independently acquired resistance to nalidixic acid, a quinolone. One of these genotypes, H58, has become predominant throughout southern Asia and has even spread to Africa. In Vietnam, up to 95% of Typhi are now resistant to nalidixic acid and many other antibiotics. Although these cases can still be treated with newer antibiotics, those antibiotics are much more expensive than standard fluoroquinolones, which raises the cost of medical treatment. Furthermore, it is likely that Typhi will develop resistance to these antibiotics as well.

The combination of these investigations raises problems for public health measures. Indiscriminate antibiotic usage results in real-time evolution of bacteria that resist treatment. Furthermore, the healthy carrier state provides a safe reservoir for these bacteria which allows them to evade short-term antibiotic treatment and vaccination, indicating that typhoid fever will remain a major health problem for the foreseeable future.

The research was carried out collaboratively by the Max Planck Institute for Infection Biology in Berlin, the Wellcome Trust Sanger Institute, Hinxton Hall, the Institut Pasteur, Paris, and the Oxford University Clinical Research Unit, Ho Chi Minh City, with assistance from hospitals in Ho Chi Minh City and Hanoi and the International Vaccine Institute in Seoul. Financial support was by the Wellcome Trust, UK.

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Nepal Microbiology Discussion Forum (NMDF)

Posted by tumicrobiology on November 22, 2006

Now from TUMDF we have been NMDF. You will get a lot of things from us. Just wait.

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Scientists Explore Function Of ‘Junk DNA’

Posted by tumicrobiology on November 22, 2006

University of Iowa scientists have made a discovery that broadens understanding of a rapidly developing area of biology known as functional genomics and sheds more light on the mysterious, so-called “junk DNA” that makes up the majority of the human genome.

The team, led by Beverly Davidson, Ph.D., a Roy J. Carver Biomedical Research Chair in Internal Medicine and UI professor of internal medicine, physiology and biophysics, and neurology, have discovered a new mechanism for the expression of microRNAs — short segments of RNA that do not give rise to a protein, but do play a role in regulating protein production. In their study, Davidson and colleagues not only discovered that microRNAs could be expressed in a different way than previously known, they also found that some of the junk DNA is not junk at all, but instead consists of sequences that can generate microRNAs.

Davidson and her colleagues, including Glen Borchert, a graduate student in her lab, investigated how a set of microRNAs in the human genome is turned on, or expressed. In contrast to original assertions, they discovered that the molecular machinery used to express these microRNAs is different than that used to express RNA that encodes proteins. Expression of the microRNAs required an enzyme called RNA Polymerase III (Pol III) rather than the RNA Polymerase II (Pol II), which mediates expression of RNA that encode proteins. The study is published in Nature Structural and Molecular Biology Advance Online Publication (AOP) on Nov. 12.

“MicroRNAs are being shown to play roles in cancer and in normal development, so learning how these microRNAs are expressed may give us insight into these critical biological processes,” said Borchert, who is lead author of the study. “Up to now it’s been understood that one enzyme controls their expression, and we now show that in some cases it’s a completely different one.”

Genes that code for proteins make up only a tiny fraction of the human genome. The function of the remaining non-coding sequence is just beginning to be unraveled. In fact, until very recently, much of the non-coding sequence was dismissed as junk DNA. In 1998, scientists discovered that some DNA produced small pieces of non-coding RNA that could turn off, or silence, genes. This discovery won Andrew Fire and Craig Mello the 2006 Nobel Prize for medicine or physiology. Since their discovery, the field has exploded and small, non-coding RNAs have been shown to play an important role in development and disease in ways that scientists are only just beginning to understand.

“Not so many years ago our understanding was that DNA was transcribed to RNA, which was then translated to protein. Now we know that the levels of control are much more varied and that many RNAs don’t make protein, but instead regulate the expression of proteins,” Davidson explained. “Non-coding RNA like microRNAs represent a set of refined control switches, and understanding how microRNAs work and how they are themselves controlled is likely to be very important in many areas of biology and medicine.”

Over 450 microRNAs have been identified in the human genome. Learning how they are turned on and in what cells and what they do, may allow scientists to turn that knowledge to their advantage as a medical tool.

In addition to Davidson and Borchert, William Lanier, a graduate student in the UI Department of Biological Sciences, was also part of the research team. The study was funded in part by the National Institutes of Health.

Source: University of Iowa
Date: November 21, 2006

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New Protective Action For Powerful Anti-HIV Factor Identified

Posted by tumicrobiology on October 30, 2006

Scientists at the Gladstone Institute of Virology and Immunology (GIVI) have identified a previously unknown function of APOBEC3G (A3G), a protein that acts against HIV, a finding that may lead to new approaches for controlling HIV infection.

The work is published today, Oct. 2, 2006, in Proceedings of the National Academy of Sciences, USA.

The research, conducted by scientists in the laboratory of GIVI Director Warner C. Greene, MD, PhD, explains why CD4 T cells — the immune system cells targeted by HIV — are sometimes so susceptible to HIV infection and at other times are highly resistant.

Scientists have known that resistant CD4 T cells, called “resting cells,” are made up predominantly of CD4+ T cells that are in an inactive state, awaiting a stimulus to move into action. In these cells, A3G blocks HIV at an early step in its life cycle. However, when resting CD4 T cells are stimulated by a foreign protein or other signal, A3G is rapidly recruited into large RNA protein complexes within the cells. This change neutralizes the anti-HIV properties of A3G, opening the door to HIV infection.

In the current study, the researchers set out to decipher the protein and RNA components of the A3G RNA protein complexes. In so doing, Ya-Lin Chiu, PhD, a postdoctoral fellow in Greene’s laboratory, determined that the complexes help to prevent a threat within cells posed by a class of “jumping genes,” or retro-elements, which are sequences of DNA that change position within the genome, causing mutations, activating or inactivating other genes, or duplicating themselves, thereby increasing the quantity of DNA in each cell.

As with HIV, the replication and movement of these retro-elements to new chromosomal sites with potentially damaging effect involves copying DNA into RNA and then back into DNA again. The A3G RNA protein complex, Chiu determined, interrupts this retro-element replication cycle by binding the retro-element RNAs and sequestering them in the cytoplasm away from the nuclear machinery required for copying the RNA back into DNA and inserting the retro-element at a new chromosomal site.

Understanding A3G’s role in activated CD4 T cells could lead to a new strategy against HIV.

“If we can find a way to partially block A3G assembly into the large complexes during CD4 T cell activation, we could both preserve the potent anti-HIV effect of the small form of A3G and the protective function of the large A3G complex against select mobile genetic elements,” Greene said. Gladstone scientists are now exploring various ways to achieve this desired balance.

Other authors on the study were Gladstone postdoctoral fellows Mario Santiago PhD, and Vanessa B. Soros, PhD, and H. Ewa Witkowska and Steven C. Hall of the University of California, San Francisco, and Cécile Esnault and Thierry Heidmann from the Institut Gustave Roussy in Villejuif, France. Funding for the study came from the National Institutes of Health, San Francisco Women’s HIV Interdisciplinary Network, the American Foundation for AIDS Research, UCSF-GIVI Center for AIDS Research, Ligue Nationale Contre le Cancer, Sandler Family Foundation and the J. David Gladstone Institutes. The Gladstone Institute of Virology and Immunology is one of three research institutes of The J. David Gladstone Institutes, a private, nonprofit biomedical research institution. It is affiliated with UCSF, a leading university that consistently defines health care worldwide by conducting advanced biomedical research, educating graduate students in the health professions and life sciences, and providing complex patient care.

Source: University of California – San Francisco
Date: October 30, 2006

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Headway Against Hepatitis C: Study Shows Liver Damage Can Be Reversed

Posted by tumicrobiology on October 30, 2006

Saint Louis University Liver Center scientists are presenting research today on a more effective way to treat hepatitis C patients who have been unresponsive to current drug therapies.

They have shown that a cocktail of ribavirin and Infergen, a highly potent Interferon, is nearly twice as effective at controlling hepatitis C than standard treatments.

They are sharing their findings at the annual American Association for the Study of Liver Diseases meeting in Boston.

“The results are promising,” says Bruce R. Bacon, M.D., principal investigator and director of the division of gastroenterology and hepatology at Saint Louis University School of Medicine. “This group of non-responders is a very challenging population to treat, and we found that patients who followed through with the therapy had a response nearly twice that of previous trials looking at this population.”

Saint Louis University Liver Center researchers led a study of more than 500 patients with hepatitis C at 40 sites, 77 percent of whom had advanced fibrosis. Fourteen percent of patients taking 9mcg of Infergen daily and 20 percent taking 15 mcg were virus negative after six months.

A quarter of the non-cirrhotic patients receiving Infergen were also virus negative after 24 weeks. The optimal response to antiviral therapy is for the hepatitis C viral RNA to become undetectable on treatment and to remain undetectable for at least another six months off therapy; this is referred to as a sustained virologic response, essentially a cure of the disease. Rates of sustained virologic response are still to be determined in this ongoing study.

Infergen is a highly potent type of interferon currently used for adult patients with chronic hepatitis C three times a week, Bacon says. This trial is expected to be completed in 2007.

An estimated 3.9 million Americans have hepatitis C. About 250,000 who have been offered therapy are unresponsive to current drug therapies, and the number is growing by 50,000 annually, according to the CDC.

Second Study Shows Liver Damage Can Be Reversed

In another study being presented at the AASLD conference, SLU researchers found that liver damage may be able to be reversed in patients with chronic hepatitis C who have undergone successful therapy.

“They are not only at a very low risk for relapse but may also see improvements to their liver,” says lead author Adrian Di Bisceglie, M.D., professor in the division of gastroenterology and hepatology at Saint Louis University School of Medicine.

Researchers studied the long-term effects in 150 patients with chronic hepatitis C following therapy. The level of liver damage in 79 percent of patients with stage 2 or worse fibrosis greatly improved and was unchanged in the rest of the patients.

“Little is known about how these patients fare after their treatment,” says Di Bisceglie, M.D., also acting chair of the department of internal medicine at SLU. “This is the largest study of its kind to examine just how much improvement patients with hepatitis C have five years after a sustained virologic response, and the results are very encouraging.”

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