False-colored scanning electron micrograph of HIV particles (yellow) infecting a human H9 T cell (blue, turquoise)
Success in the laboratory suggests that a new compound can point the way to preventing active tuberculosis in people infected with the latent form of the bacterium, says a team led by researchers at Weill Cornell Medical College in New York City. A drug with such properties could also be useful in treating people who already have tuberculosis by shortening the lengthy treatment period. The discovery also points to new ways of thinking about fighting bacterial infection, which is becoming increasingly resistant to traditional antibiotics.
MIT researchers have uncovered a critical difference between flu viruses that infect birds and humans, a discovery that could help scientists monitor the evolution of avian flu strains and aid in the development of vaccines against a deadly flu pandemic.
The researchers found that a virus’s ability to infect humans depends on whether it can bind to one specific shape of receptor on the surface of human respiratory cells.
Scientists have genetically engineered a mosquito to release a sea-cucumber protein into its gut which impairs the development of malaria parasites, according to research out today (21 December) in PLoS Pathogens. Researchers say this development is a step towards developing future methods of preventing the transmission of malaria.
University of Illinois at Chicago researchers have identified new sites on the bacterial cell’s protein-making machinery where antibiotics can be delivered to treat infections.
Continue reading “Researchers Find Promising New Targets for Antibiotics”
Biology textbooks are blunt—neutrophils are mindless killers. These white blood cells patrol the body and guard against infection by bacteria and fungi, identifying and destroying any invaders that cross their path. But new evidence, which may lead to better drugs to fight deadly pathogens, indicates that neutrophils might actually distinguish among their targets.
Scientists working in Switzerland, Vietnam and the United States say they have isolated antibodies that they hope could offer protection against several different strains of the virus simultaneously. Antibodies are used by our immune system to neutralise bacteria and viruses – in this case, the scientists have isolated antibodies that bird flu survivors in Vietnam produced to fight off the disease. Professor Antonio Lanzavecchia, at the Institute for Research in Biomedicine in Switzerland, says the antibodies have already proven effective in the lab and in mice and he is confident that they could be used in humans.
Read rest of the story at BBC News site.
In a study of non-human primates infected with the influenza virus that killed 50 million people in 1918, an international team of scientists has found a critical clue to how the virus killed so quickly and efficiently. Writing this week (Jan. 18, 2007) in the journal Nature, a team led by University of Wisconsin-Madison virologist Yoshihiro Kawaoka reveals how the 1918 virus – modern history’s most savage influenza strain – unleashes an immune response that destroys the lungs in a matter of days, leading to death.
The finding is important because it provides insight into how the virus that swept the world in the closing days of World War I was so efficiently deadly, claiming many of its victims people in the prime of life. The work suggests that it may be possible in future outbreaks of highly pathogenic flu to stem the tide of death through early intervention.
Continue reading “Study uncovers a lethal secret of 1918 influenza virus”
When a cell has to destroy any of its organelles or protein aggregates, it envelops them in a membrane, forming an autophagosome, and then moves them to another compartment, the lysosome, for digestion. Two years ago, Rockefeller University assistant professor Christian Münz showed that this process, called autophagy, sensitizes cells for recognition by the immune system’s helper T cells. But he didn’t know how often this pathway is used or how efficient it is. Now, a new study published online today in the journal Immunity goes a long way toward addressing these questions and shows that the pathway is so common that it could be a valuable new way of boosting vaccine efficacy.
A moderate exercise program may reduce the incidence of colds. A study published in the November issue of The American Journal of Medicine, led by researchers at Fred Hutchinson Cancer Research Center, found that otherwise sedentary women who engaged in moderate exercise had fewer colds over a one year period than a control group.
Continue reading “New study indicates moderate exercise may protect against colds”
An analysis of mice infected with the reconstructed 1918 influenza virus has revealed that although the infection triggered a very strong immune system response, the response failed to protect the animals from severe lung disease and death.
Continue reading “Reconstructed 1918 influenza virus induces immune response that fails to protect”
For many years, researchers believed that stem cells in the bone marrow spent most of their existence in a slumber-like state, unaware of — and unaffected by — the daily battles fought by the body's immune system.
Scientists at the Oklahoma Medical Research Foundation have discovered that marrow stem cells — undifferentiated cells that eventually give rise to the blood cells that fight infection — possess receptors that recognize bacteria and viruses. When activated, these receptors kick the stem cells and immature blood cells into action, enlisting them to help fight whatever pathogen is attacking the body.
Scientists reveal the structure of a protein that packages the viral genome and helps viruses to replicate while avoiding human immune reactions
Ebola, measles and rabies are serious threats to public health in developing countries. Despite different symptoms all of the diseases are caused by the same class of viruses that unlike most other living beings carry their genetic information on a single RNA molecule instead of a double strand of DNA. Now researchers from the Institut de Virologie Moléculaire et Structurale [IVMS] and the Outstation of the European Molecular Biology Laboratory [EMBL] in Grenoble have obtained a detailed structural picture of a protein that allows the rabies virus to withstand the human immune response and survive and replicate in our cells.
The study that is published in this week’s online edition of Science suggests new potential drug targets in rabies and sheds light on how similar approaches can help fighting other viral diseases.
Continue reading “Cracking a virus protection shield”
New insights into how a subpopulation of helper T-cells provides immunity and promotes survival following infection with an AIDS-like virus offer a new means of predicting an AIDS vaccine's effectiveness, a discovery that could help scientists as they test these vaccines in clinical trials.
Despite lack of a key component of the immune system, a line of genetically engineered mice can control chronic herpes virus infections, researchers at Washington University School of Medicine in St. Louis have found.
Scientists can't prove it yet, but they suspect the missing immune system component, a group of molecules known as the Major Histocompatibility Complex (MHC) Class Ia, has a previously unrecognized backup that is similar enough to step in and fill the void left by its absence. If so, that backup may become a new focus for efforts to design antiviral vaccines.
Continue reading “Mice Lacking Key Immune Component Still Control Chronic Viral Infections”
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 to be published Dec. 28 on the journal Nature’s website, researchers 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.
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 many 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.
An international consortium of researchers led by the University of Manchester has cracked the gene code behind a key family of fungi, which includes both the leading cause of death in leukaemia and bone marrow transplant patients and an essential ingredient of soy sauce.
The ‘genome sequences’ or genetic maps for the fungi Aspergillus fumigatus, Aspergillus nidulans and Aspergillus oryzae are published on 22 December in Nature magazine. Despite being from the same fungal family, they have been found to be as genetically different as fish and man.
Cleistothecium – sexual spore container, false coloured from Aspergillus nidulans. (Courtesy of Professor Rheinhard Fischer, Institut für Angewandte Biowissenschaften Abt. für Angewandte Mikrobiologie der Universität Karlsruh, with whom copyright remains)
Scientists from the Max Planck Institute for Infection Biology in Berlin discovered why lung, but not skin, anthrax infections are lethal. As reported in the newest issue of PloS Pathogen (November 2005) Neutrophils, a form of white blood cells, play a key role in anthrax infections. They can kill Bacillus anthracis by producing a protein called alpha-defensin. This discovery might now pave the way towards the development of new therapies for the fatal lung form of anthrax.
Continue reading “Researchers discover a protein which is deadly for anthrax”