Thus, RV differentially interacts with primary human B cells depending on their tissue of origin and differentiation stage, and it affects their capacity to modulate the local and systemic immune responses.”
“Venezuelan equine encephalitis virus (VEEV) is a mosquito-borne RNA virus

of the genus Alphavirus that is responsible for a significant disease burden in Central and South America through sporadic outbreaks into human and equid populations. For humans, 2 to 4% of cases are associated with encephalitis, and there is an overall case mortality rate of approximately 1%. In mice, replication of the virus within neurons of the central nervous system find more (CNS) leads to paralyzing, invariably lethal encephalomyelitis. However, mice infected with certain attenuated mutants of the virus are able to control the infection within the CNS and recover. selleck inhibitor To better define what role T cell responses might be playing in this process, we infected B cell-deficient mu

MT mice with a VEEV mutant that induces mild, sublethal illness in immune competent mice. Infected mu MT mice rapidly developed the clinical signs of severe paralyzing encephalomyelitis but were eventually able to control the infection and recover fully from clinical illness. Recovery in this system was T cell dependent and associated with a dramatic reduction in viral titers within the CNS, followed by viral MM-102 price persistence in the brain. Further comparison of the relative roles of T cell subpopulations within this system revealed that CD4(+) T cells were better producers of gamma interferon (IFN-gamma) than CD8(+/-)

T cells and were more effective at controlling VEEV within the CNS. Overall, these results suggest that T cells, especially CD4(+) T cells, can successfully control VEEV infection within the CNS and facilitate recovery from a severe viral encephalomyelitis.”
“Epigenomic settings control gene regulation in both developing and postmitotic tissue, whereas abnormal regulation of epigenomic settings has been implicated in many developmental and neurological disorders. Evidence is emerging for the roles of epigenetic mechanisms in the mature nervous system, in the dynamic processes of learning and memory. The discovery of the involvement of DNA methylation and histone acetylation and methylation in neuronal processing provides a possible answer to the long-standing riddle of how memories persist in a biological system whose cellular composition is in a constant state of flux and renewal. This mini review focuses on present research in DNA methylation and histone posttranslational modifications in learning and memory, age-related cognitive decline, and related pathological disorders. NeuroReport 21:909-913 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.