LAUSR

The 7th annual symposium of the Colorado Alphaherpesvirus Latency Society (CALS) convened 70 investigators who have authored over 2473 PubMed-listed publications involving herpesvirology and who traveled 110,408 miles from 3 continents, 6 countries, and 22 states. The 2-day symposium consisted of 26 oral presentations by investigators to discuss advances in the research of herpes simplex types 1 and 2, varicella zoster virus, bovine herpesvirus virus type 1, pseudorabies virus, and simian varicella virus latency. In addition, 18 promising graduate students and postdoctoral fellows presented posters, each preceded by a short oral summary, and a small group of exceptional undergraduates whose interest in herpesvirology is just beginning were also hosted. New this year was a special session led by volunteers with first-hand experience in NIH grant reviews to discuss the inner workings of an NIH study section. This year marked the beginning of the Don Gilden Memorial Lectureship, a grassroots endeavor initiated and generously supported by fellow alphaherpesvirus experts who wish to continue Dr. Gilden’s desire to underscore the value of neuroscientists outside the field of virology in broadening the knowledge base. The inaugural Don Gilden Memorial Lecture, presented by Dr. Paola Sandroni from the Mayo Clinic, provided an overview of disorders of the autonomic nervous system. While an early spring blizzard prevented the musical tribute that traditionally follows the presentation, all enjoyed the silent ambiance of the quaint mountain town covered with snow. The relaxed setting of The Christiania Lodge and The Tivoli Lodge, nestled in the heart of the Colorado Rocky Mountains, provided an ideal location to establish new collaborations, strengthen existing partnerships, and train the next generation of clinical/basic research scientists devoted to the ultimate elimination of disease caused by alphaherpesvirus reactivation (Fig. 1). A brief summary of the presentations follows: Andrea S. Bertke, Virginia Tech, explored the effects of various environmental triggers on HSV-1 and HSV-2 reactivation in different types of peripheral neurons. Previous studies have shown that the viruses preferentially replicate and establish latency in different types of sensory neurons, as well as in neurons of the autonomic nervous system. To determine in which types of neurons HSV-1 and HSV-2 reactivate in response to triggers commonly associated with recurrent disease, this laboratory infected primary adult murine sensory and autonomic neuronal cultures, and either treated them with stress hormones or deprived them of target-derived neurotrophic factors to simulate epithelial injury. Deprivation of neurotrophic factors neurturin and glial cell-derived neurotrophic factor induced reactivation of HSV-1 and HSV-2 in sensory neurons expressing glial family receptors, while nerve growth factor deprivation led only to HSV-1 reactivation in sympathetic neurons. Treatment with stress hormones epinephrine (EPI) and corticosterone (CORT) selectively induced HSV-1 or HSV-2 reactivation; HSV-1 only reactivated in sympathetic neurons in response to EPI or CORT, while HSV-2 reactivated in both sensory and autonomic neurons but only in response to CORT. Thus, HSV-1 and HSV-2 reactivate from different types of sensory and autonomic neurons in * Randall J. Cohrs [email protected]