Genetic Mutations Could Increase Risk of Cytomegalovirus Infection
December 20th 2016Experimenting with human cells and mice, Johns Hopkins researchers have found that a genetic mutation that alters a protein called NOD1 may increase susceptibility to human cytomegalovirus (CMV) infection. CMV is a common pathogen that infects almost 60 percent of adults in the U.S., according to the Centers for Disease Control and Prevention (CDC), and can lead to devastating developmental defects in fetuses and severe disease in people with weakened immune systems.
Researchers Strengthen the Case for Sexual Transmission of Zika Virus
December 20th 2016Aedes aegypti mosquitoes harboring parasitic Zika virus (ZIKV) are the primary transmitters of virus to humans, potentially causing catastrophic congenital microcephaly in babies born to women bitten by infected mosquitoes. But confirmation earlier this year by the Centers for Disease Control and Prevention (CDC) that ZIKV can also be sexually transmitted raised new alarm that virus could be passed between sexual partners in venues far from mosquito habitats.
Sunlight Energizes Infection-Fighting T Cells
December 20th 2016Georgetown University Medical Center researchers have found that sunlight, through a mechanism separate than vitamin D production, energizes T cells that play a central role in human immunity. Their findings, published today in Scientific Reports, suggest how the skin, the body’s largest organ, stays alert to the many microbes that can nest there.
El Nino Fueled Zika Outbreak, Study Suggests
December 20th 2016Scientists at the University of Liverpool have shown that a change in weather patterns, brought on by the El Niño of 2015, fueled the Zika outbreak in South America. The findings were revealed using a new epidemiological model that looked at how climate affects the spread of Zika virus by both of its major vectors, the yellow fever mosquito (Aedes aegypti) and the Asian tiger mosquito (Aedes albopictus).
Researchers Map Genome-Wide Changes That Drive T Cell Maturation and Exhaustion
December 19th 2016In a bid to better understand the gene expression patterns that control T cell activity, researchers at the La Jolla Institute for Allergy and Immunology mapped genome-wide changes in chromatin accessibility as T cells respond to acute and chronic virus infections. Their findings, published in the Dec. 20, 2016 issue of Immunity, shed light on the molecular mechanisms that determine the fate of T lymphocytes and open new approaches to clinical intervention strategies to modulate T cell activity and improve immune function.
DNA Markers Distinguish Between Harmless and Deadly Bacteria
December 19th 2016The virulent pathogen that causes the disease tularemia, or "rabbit fever," was weaponized during past world wars and is considered a potential bioweapon. Through a new study of the coccobacillus Francisella, Los Alamos National Laboratory researchers are working to use DNA markers to discern related but relatively harmless species as they are identified and to provide a means to distinguish them from the harmful F. tularensis.
Important Element of Immune Defense Against Fungal Infections is Discovered
December 19th 2016Fungal infections are a serious health risk. They can be harmful especially to patients whose immune system is compromised through illness or chemotherapy. A team working at the Technical University of Munich (TUM) has discovered an important mechanism in the body's defenses against fungi. The discovery explains, among other things, why people with certain genetic variations are more susceptible to fungal infections.
Gut Bacteria May Hold Key to Treating Autoimmune Disease
December 19th 2016Defects in the body’s regulatory T cells cause inflammation and autoimmune disease by altering the type of bacteria living in the gut, researchers from The University of Texas Health Science Center at Houston have discovered. The study, “Resetting microbiota by Lactobacillus reuteri inhibits T reg deficiency-induced autoimmunity via adenosine A2A receptors,” which will be published online December 19 in the Journal of Experimental Medicine, suggests that replacing the missing gut bacteria, or restoring a key metabolite called inosine, could help treat children with a rare and often fatal autoimmune disease called IPEX syndrome.