Thor Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPain. Author manuscript; obtainable in PMC 2014 December

Thor Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPain. Author manuscript; obtainable in PMC 2014 December 01.Bruehl et al.Pagea additional complete understanding of pathways underlying these associations have to await future studies.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSupplementary MaterialRefer to Net version on PubMed Central for supplementary material.AcknowledgmentsThis project was supported in part by grants R01-DA031726 (SB), R01-NS050578 (SB), R01-NS046694 (SB), R01-MH071260 (SB), P30-AG036445 (TATW), and T32-GM07347 (MEK). This perform was also supported by Vanderbilt CTSA grant UL1TR000445 from the National Center for Advancing Translational Sciences/NIH. The dataset utilized for the analyses described was in part obtained from Vanderbilt University Healthcare Center’s BioVU which is supported by institutional funding and by the Vanderbilt CTSA grant UL1TR000445 from NCATS/NIH. The content material is solely the responsibility in the authors and doesn’t necessarily represent the official views on the NIH. The authors have no conflicts of interest. The authors gratefully acknowledge the contributions with the Vanderbilt University Center for Human Genetics Research DNA Resources Core as well as the help of Dr. Holli Hutcheson Dilks in designing the tag SNP panel.
Interactions amongst Herpesvirus Entry Mediator (TNFRSF14) and Latency-Associated Transcript during Herpes Simplex Virus 1 LatencySariah J. Allen,a Antje Rhode-Kurnow,b Kevin R. Mott,a Xianzhi Jiang,c Dale Carpenter,c J. Ignacio Rodriguez-Barbosa,d Clinton Jones,e Steven L. Wechsler,c,f Carl F. Ware,b Homayon GhiasiaCenter for Neurobiology and Vaccine Development, Division of Surgery, Cedars-Sinai Health-related Center, Los Angeles, Mps1 custom synthesis California, USAa; Laboratory of Molecular Immunology, Infectious and Inflammatory Diseases Center, Sanford-Burnham Healthcare Investigation Institute, La Jolla, California, USAb; Gavin Herbert Eye Institute, University of California, Irvine, College of Medicine, Irvine, California, USAc; Immunobiology Laboratory, Institute of Biomedicine, University of Leon, Campus de Vegazana, Leon, Spaind; College of Veterinary Beta-secretase supplier Medicine and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Lincoln, Nebraska, USAe; Department of Microbiology and Molecular Genetics, and Center for Virus Study, University of California, Irvine, Irvine, California, USAfHerpesvirus entry mediator (HVEM) is 1 of a number of cell surface proteins herpes simplex virus (HSV) utilizes for attachment/entry. HVEM regulates cellular immune responses and can also increase cell survival. Interestingly, latency-associated transcript (LAT), the only viral gene consistently expressed for the duration of neuronal latency, enhances latency and reactivation by promoting cell survival and by helping the virus evade the host immune response. Nonetheless, the mechanisms of these LAT activities aren’t well understood. We show right here for the first time that one particular mechanism by which LAT enhances latency and reactivation seems to be by upregulating HVEM expression. HSV-1 latency/reactivation was significantly decreased in Hvem / mice, indicating that HVEM plays a substantial role in HSV-1 latency/reactivation. Moreover, LAT upregulated HVEM expression for the duration of latency in vivo and also when expressed in vitro in the absence of other viral factors. This study suggests a mechanism whereby LAT upregulates HVEM expression potentially through binding of two LAT modest noncoding RNAs for the HVEM pr.