A common brain virus that is usually harmless in adults but can be devastating in early development not only causes deterioration of infected cells but also affects nearby non-infected brain cells, which may explain why it is so destructive, a Yale School of Medicine researcher reports in the Journal of Virology.
The virus, cytomegalovirus (CMV), can cause disorders such as hydrocephalus, epilepsy, learning disabilities and deafness by infecting the developing brain. It also infects the brain in organ transplant recipients and those with HIV infection who have compromised immune systems.
In the early stages of infection, CMV targets astrocytes, which are important in neuronal development and intercellular communication within the brain. Astrocytes respond to and release transmitters such as glutamate and extracellular ATP through increases in intracellular calcium. Astrocytes also make long-distance calls to each other, so to speak, and modulate synaptic transmission between neurons.
Anthony van den Pol, professor of neurosurgery and senior author of the study, and lead author Winson Ho, a student at the School of Medicine, used digital imaging to examine mouse brain cells infected by mouse CMV. They found that the virus weakened long-distance glial intercellular communication and neuronal synaptic signaling, even in bystander cells that had no sign of infection.
"The 'bystander effects' we observed would tend to cause further deterioration of cellular communication in the brain in addition to the problems caused by the loss of directly infected cells," van den Pol says. "These effects might help explain why CMV is the leading viral cause of neurological dysfunction in the developing brain."
In a paper published earlier this year in the Journal of Virology, van den Pol's lab showed that interferon in the brain can reduce proliferation of CMV, which might then reduce the problems in cellular communication precipitated by the virus.
-- By Jacqueline Weaver
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