Researchers at Albert Einstein College of Medicine of Yeshiva University in New York City have discovered a novel strategy for preventing infections due to the highly common herpes simplex viruses, the microbes responsible for causing genital herpes (herpes simplex virus 2) and cold sores (herpes simplex virus 1). The finding, published online on March 18, 2013 in The FASEB Journal, could lead to new drugs for treating or suppressing herpes virus infections. "We've essentially identified the molecular "key" that herpes viruses use to penetrate cell membranes and infect cells of the human body," said Betsy Herold, M.D., professor of pediatrics (infectious diseases), of microbiology & immunology and of obstetrics & gynecology and women's health at Einstein and attending physician of pediatrics, The Children's Hospital at Montefiore. Herpes viruses are known to infect skin cells as well as cells lining the cervix and the genital tract. A 2006 JAMA study estimated that nearly 60 percent of U.S. men and women between the ages of 14 and 49 carry the HSV-1 virus. The Centers for Disease Control (CDC) estimated that about 1 in 6 Americans (16.2 percent) between 14 and 49 are infected with herpes simplex virus type 2 (HSV-2), according to a 2010 national health survey. HSV-2 is a lifelong and incurable infection that can cause recurrent and painful genital sores and can make those infected with the virus two-to-three times more likely to acquire HIV, the virus that causes AIDS. Dr. Herold and her colleagues had previously shown that infection by the herpes viruses depends on calcium released within the cells. In this study, they found that calcium release occurs because the viruses activate a critical cell-signaling molecule called Akt at the cell membrane.
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