For more than a decade a research group led by Walter Atwood, professor of medical science, has doggedly pursued the workings of the JC polyomavirus, which causes a disease called PML that fatally degrades the central nervous system of patients with weakened immune systems. In a study published online Oct. 2 in the Journal of Virology, his team describes how the virus gains entry into cells: It breaks in via certain receptors of the neurotransmitter serotonin called 5-HT2 receptors. In lab experiments funded by the National Institutes of Health, Atwood, Benedetta Assetta (lead author and graduate student), and their co-authors showed this by inserting more than a dozen different serotonin receptors into cells that normally can’t be infected. Of all 14 receptors, only the three 5HT-2 receptors facilitated infection. The research, Atwood said, could lead to improved treatment for PML, for instance by informing how existing drugs work.“The present study provides new insights on three different serotonin receptors which are potential drug targets,” Atwood said. “Several 5-HT2 receptor inhibitors, both selective and non-selective, are FDA-approved and commonly used to treat neurological disorders. One of these drugs, mirtazapine, has been administered in patients with PML and results have been mixed, but it does appear that the use of mirtazapine is most successful if administered early at the onset of PML symptoms.” The researchers are now looking at why these three specific serotonin receptors facilitate infection, while the others do not.