Thor Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPain. Author manuscript; out there in PMC 2014 December 01.Bruehl et al.Pagea more complete understanding of pathways underlying these associations need to await future studies.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSupplementary MaterialRefer to Internet version on PubMed Central for supplementary material.AcknowledgmentsThis project was supported in component by grants R01-DA031726 (SB), R01-NS050578 (SB), R01-NS046694 (SB), R01-MH071260 (SB), P30-AG036445 (TATW), and T32-GM07347 (MEK). This operate was also supported by Vanderbilt CTSA grant UL1TR000445 from the National Center for Advancing Translational Sciences/NIH. The dataset used for the analyses described was in portion obtained from Vanderbilt University Healthcare Center’s BioVU that 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 will not necessarily represent the official views on the NIH. The authors have no conflicts of interest. The authors gratefully acknowledge the contributions from the Vanderbilt University Center for Human Genetics Analysis DNA Resources Core and the help of Dr. Holli Hutcheson Dilks in designing the tag SNP panel.
Interactions amongst Herpesvirus Entry Mediator (TNFRSF14) and Latency-Associated Transcript through 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 Improvement, Division of Surgery, Cedars-Sinai Healthcare Center, Los Angeles, Succinate Receptor 1 Agonist manufacturer California, USAa; Laboratory of Tau Protein Inhibitor list Molecular Immunology, Infectious and Inflammatory Ailments Center, Sanford-Burnham Medical Investigation Institute, La Jolla, California, USAb; Gavin Herbert Eye Institute, University of California, Irvine, School of Medicine, Irvine, California, USAc; Immunobiology Laboratory, Institute of Biomedicine, University of Leon, Campus de Vegazana, Leon, Spaind; College of Veterinary Medicine and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Lincoln, Nebraska, USAe; Department of Microbiology and Molecular Genetics, and Center for Virus Investigation, University of California, Irvine, Irvine, California, USAfHerpesvirus entry mediator (HVEM) is 1 of quite a few cell surface proteins herpes simplex virus (HSV) utilizes for attachment/entry. HVEM regulates cellular immune responses and may also raise cell survival. Interestingly, latency-associated transcript (LAT), the only viral gene regularly expressed during neuronal latency, enhances latency and reactivation by promoting cell survival and by assisting the virus evade the host immune response. On the other hand, the mechanisms of those LAT activities are not nicely understood. We show here for the initial time that one particular mechanism by which LAT enhances latency and reactivation seems to become by upregulating HVEM expression. HSV-1 latency/reactivation was significantly reduced in Hvem / mice, indicating that HVEM plays a significant function in HSV-1 latency/reactivation. In addition, LAT upregulated HVEM expression in the course of latency in vivo as well as when expressed in vitro within the absence of other viral elements. This study suggests a mechanism whereby LAT upregulates HVEM expression potentially via binding of two LAT modest noncoding RNAs for the HVEM pr.
