Drs. David Fredricks and Keith Jerome, investigators in the Clinical Research Division, are recipients of Program Committee Choice awards from the Infectious Diseases Society of America. The $2,500 awards, presented at the society's annual meeting in Boston earlier this month, recognize research excellence of abstracts submitted to the conference. Fredricks and Jerome were two of three awardees chosen from more than 1,200 presenters at the meeting.
Fredricks received the award for research involving the use of sensitive DNA detection methods to identify the types of bacteria associated with bacterial vaginosis, a condition that can lead to infections of the female reproductive system.
Although certain species of bacteria have been associated with the condition, previous studies to identify the bacteria responsible for the condition have focused on the ability to culture the microbes in the laboratory.
Because many bacterial species cannot be successfully cultivated in the lab, Fredricks used polymerase chain reaction (PCR) and fluorescence in situ hybridization (FISH) to analyze vaginal fluid from women with and without bacterial vaginosis. He identified an average of 14 bacterial species present in women with the condition, including several novel types that had never before been cultivated. Several of these species may play a role in the condition.
Jerome, his former postdoctoral fellow Dr. George Zahariadis and colleagues were recognized for their research to discover how herpes simplex virus (HSV)-infected cells interfere with the function of immune-system cells known as T cells.
Viruses use many strategies to protect infected cells from recognition by T cells, which normally seek out and destroy virus-infected cells. The basis for the ability of HSV-infected cells to disrupt T-cell signaling — thus interfering with their function — has not been defined. Jerome and colleagues found that HSV infection triggers a dissociation of a protein called HSP90 from two other proteins — p56lck and Raf — that are necessary for proper T-cell signaling. The work may lead to new strategies to prevent T-cell inhibition by HSV-infected cells.