Want to get a lot of money thrown at immunology? Show that sex can not only be exhausting, if you do it right, it can also cause drops in the immune system.
According to a study in Journal of Evolutionary Biology, when fruit flies mate the females' genes are activated to roughly the same extent as when an immune reaction starts. Using a combination of behavioral studies and genomic technology, so-called microarrays, researchers at Uppsala University can show how fruit fly females are affected by mating.
"We monitor how genetic expression is impacted by mating and show that the most common process that is affected is the immune defense system," says Ted Morrow at the Department of Ecology and Evolution, Uppsala University.
The Rift Valley fever virus is a mosquito-borne African virus that causes fever in humans, inflicting liver damage, blindness and even death on a small percentage of the people it infects. Rift Valley fever also afflicts cattle, goats and sheep, resulting in a nearly 100 percent abortion rate in these animals. Its outbreaks periodically cause economic devastation in parts of Kenya, Somalia, Sudan and Zimbabwe, and bioterrorism experts warn that its introduction to the United States would cripple the North American beef industry.
Researchers at the University of Texas Medical Branch at Galveston say they have discovered a key tactic that the Rift Valley fever virus uses to disarm the defenses of infected cells.
Parents and advocates who believe vaccines cause autism were dealt a double blow this week. On the scientific front, a discredited 1998 study that launched the vaccine-autism debate onto the forefront made headlines, and on the legal front, a special U.S. court ruled that vaccines are not to blame for the disease.
Could a hereditary illness ever spread by contamination? Researchers at the CNRS Laboratoire d’enzymologie et biochimie structurales, studying Huntington’s disease in collaboration with Professor Ron Kopito’s team at Stanford University, have shown that the normal form of huntingtin protein
can acquire an abnormal form without any modification of its genetic code. These researchers observed that clumps of abnormal huntingtin protein, characteristic of Huntington’s disease, could induce clumping in the normal form of the protein.
In recent decades, viral epidemics have risen in ferocity and quantity in continents around the globe. More and more people in not only places like Africa and South America, but also in Asia and parts of Europe have been affected by the spread of emergent and prolific viral diseases.
Influenza is and remains a disease to reckon with. Seasonal epidemics around the world kill several hundred thousand people every year. In the light of looming pandemics if bird flu strains develop the ability to infect humans easily, new drugs and vaccines are desperately sought. Researchers at the European Molecular Biology Laboratory (EMBL) and the joint Unit of Virus Host-Cell Interaction (UVHCI) of EMBL, the University Joseph Fourier (UJF) and the National Centre for Scientific Research (CNRS), in Grenoble, France, have now precisely defined an important drug target in influenza. In this week's Nature they publish a high-resolution image of a crucial protein domain that allows the virus to hijack human cells and multiply in them.
Whenever humans create a new antibiotic, deadly bacteria can counter it by turning into new, indestructible super-bugs. That's why bacterial infection is the number one killer in hospitals today. But new research from Tel Aviv University may give drug developers the upper hand in outsmarting bacteria once and for all.
The secret weapon against a colony of bacteria may be to stress it with its own protection system, which forces it to reduce its population through ... cannibalism.
In the year of the 200th anniversary of the birth of Darwin, researchers using comparative genomics have uncovered genetic clues about why some strains of the pathogen that causes Q fever, Coxiella burnetii, are more virulent than others.
Relevant? Well, sort of, though genetics came after Darwin, but the evolution of the pathogen makes it relevant and it also gives us a chance to remind you about Darwin Day here on February 12th.
All life depends on peaceful coexistence with a swarm of microbial life inside us that performs vital services from helping to convert food to energy to protection from disease. With the help of a squid that uses a luminescent bacterium to create a predator-fooling light organ and a fish that uses a different strain of the same species of bacteria like a flashlight to illuminate the dark nooks of the reefs where it lives, scientists have found that gaining a single gene is enough for the microbe to switch host animals.
Mold is icky. However, it has yielded one of the most important advances in medicine: antibiotics. There was a time when penicillin was the cure-all antibiotic, capable of quelling almost any one-celled invader.
However, today this is not the case. Today’s bacteria are getting faster, stronger and more resistant to even our most aggressive antibiotics. This has prompted scientists to look in other nooks and crannies of our world to find the next solution to our growing resistant population of angry bacteria.