Lymphocytic choriomeningitis, or LCM, is a rodent-borne viral infectious disease that presents as aseptic meningitis (inflammation of the membrane, or meninges, that surrounds the brain and spinal cord), encephalitis (inflammation of the brain), or meningoencephalitis (inflammation of both the brain and meninges). Its causative agent is the lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae that was initially isolated in 1933. Although LCMV is most commonly recognized as causing neurological disease, as its name implies, infection without symptoms or mild febrile illnesses are common clinical manifestations. Additionally, pregnancy-related infection has been associated with congenital hydrocephalus, chorioretinitis, and mental retardation.
Scientists at The Scripps Research Institute have determined the atomic structure of a protein that the Lassa fever virus uses to make copies of itself within infected cells.
SIGA Technologies, Inc., a company specializing in the development of pharmaceutical agents to combat bio-warfare pathogens, announced today the successful completion of its fourth human clinical trial, supporting the safety and tolerability of the anticipated clinical dose of ST-246®, SIGA's lead smallpox antiviral drug candidate.
In an acute viral infection, most of the white blood cells known as T cells differentiate into cells that fight the virus and die off in the process. But a few of these "effector" T cells survive and become memory T cells, ensuring that the immune system can respond faster and stronger the next time around.
A team of researchers from The Wistar Institute has identified a protein that could serve as a target for reprogramming immune system cells exhausted by exposure to chronic viral infection into more effective "soldiers" against certain viruses like HIV, hepatitis C, and hepatitis B, as well as some cancers, such as melanoma.
A new study by scientists at the University of Iowa shows why muscle membranes don't rupture when healthy people exercise.
Rapamycin, a drug given to transplant recipients to suppress their immune systems, has a paradoxical effect on cells responsible for immune memory, scientists at the Emory Vaccine Center have discovered.
Scientists at Columbia University's Mailman School of Public Health, the South African National Institute for Communicable Diseases of National Health Laboratory Service (NICD-NHLS), the U.S. Centers for Disease Control and Prevention, and Roche's 454 Life Sciences Corporation have discovered the new virus responsible for a highly fatal hemorrhagic fever outbreak in Zambia and South Africa in late 2008.
The reason deadly infections like human immunodeficiency virus (HIV) and hepatitis C never go away is because these viruses disarm the body's defense system.
A main reason why viruses such as HIV or hepatitis C persist despite a vigorous initial immune response is exhaustion. The T cells, or white blood cells, fighting a chronic infection eventually wear out.
By blocking PD-1 (programmed death-1), an immune receptor molecule known to inhibit the immune response to chronic viral infections, scientists have safely and significantly reduced the plasma viral load and also prolonged survival of rhesus macaque monkeys severely infected with simian immunodeficiency virus (SIV), the nonhuman primate version of human immunodeficiency virus (HIV).
Like tuning a violin to produce strong, elegant notes, researchers at The Wistar Institute have found multiple receptors on the outside of the body's killer immune system cells which they believe can be selectively targeted to keep the cells in superb infection- and disease-fighting condition.
In a November 16 advance, online publication of the journal Nature, the researchers say their discovery revamps common beliefs about how such potentially lethal infections may be ravaging the brain and suggests the possibility of new treatments.
One of the biggest challenges to treating infectious diseases and developing preventive vaccines is the ability of many chronic infections to suppress the immune T-cell response over time.
A case involving seven transplant recipients killed by a rodent-borne virus that they apparently acquired from donated and infected human organs has prompted a recommendation that regulatory authorities require suppliers of pet rodents to screen their colonies for the virus.
In the latest news on the subject, experts now believe they can link at least six deaths of organ transplant patients to a rodent virus, which raises questions about whether others may have gone undetected and whether the germ also could spread through blood transfusions.
Three transplant patients have died as a result of receiving an organ from a donor who had unknowingly been infected with a common rodent virus. A fourth patient who received a kidney from the organ donor is recovering.
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