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Biotech / Medical : Regeneron Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?

To: Miljenko Zuanic who wrote (399)	2/28/2000 7:43:00 PM
From: Miljenko Zuanic	Respond to of 3557

Just parking. Note: CNTF and AXOKINE promote neuronal survival, so this my be one of the cytokine signaling path. Nothing to be concerned about, because HSV-1 reactivation by Axokine is transient in nature. Mechanisms of Herpes Simplex Virus Latency Clarified -------------------------------------------------------------------------------- WESTPORT, Feb 28 (Reuters Health) - The herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) gene promotes neuronal survival in rabbits after viral infection by inhibiting apoptosis, according to a report in the February 25th issue of Science. The LAT gene, which is abundantly transcribed during latent HSV-1 infections, is necessary for efficient HSV reactivation. And it "probably plays a role in a number of other functions that allow the herpes virus to persist in the body," Dr. Steven Wechsler from Cedars-Sinai Medical Center in Los Angeles, California told Reuters Health. Dr. Wechsler and a multicenter team explored the function of LAT by comparing the trigeminal ganglia of rabbits infected by wild-type HSV-1 with those of rabbits infected by a herpes virus lacking the LAT gene, which is designated LAT2903. "Extensive apoptosis was observed in 66% of the sections from dLAT2903 (LAT-negative) infected rabbits, versus only 4% of the sections from uninfected rabbits or rabbits infected with wild-type [HSV-1]," the authors report. These experiments suggested that "apoptosis was more likely, by a factor of 2 to 16, in rabbit trigeminal ganglia infected with the LAT-negative mutant." Further, when the researchers used an expression plasmid to introduce the LAT gene into primary human lung cells, monkey kidney cells, and murine neuroblastoma cells, the cells were protected against several different chemicals that induce apoptosis. "Our results suggest that LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis," the authors conclude. This indicates that "suppressing apoptosis is an important mechanism by which LAT enhances HSV-1 reactivation." "In addition, the ability of LAT to prevent HSV-1-induced apoptosis may be important in preventing the virus from causing extensive neuronal damage and subsequent neuronal disorders." The researchers suggest three mechanisms by which this anti-apoptosis function could promote reactivation: by providing more latently infected neurons for future reactivations; by protecting neurons in which reactivation occurs; and by protecting previously uninfected neurons during a reactivation. Dr. Wechsler says that the findings do not have immediate clinical implications. "We're trying to understand the mechanisms of reactivation," he said. "If our theory about LAT is true, we might be able to work toward blocking that particular function of the LAT gene." Science 2000;287:1500-1503.