Ction,NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPain. Author
Ction,NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPain. Author manuscript; readily available in PMC 2014 December 01.Bruehl et al.Pagea more comprehensive 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 Internet version on PubMed Central for supplementary material.AcknowledgmentsThis project was supported in element by grants R01-DA031726 (SB), R01-NS050578 (SB), R01-NS046694 (SB), R01-MH071260 (SB), P30-AG036445 (TATW), and T32-GM07347 (MEK). This work was also supported by Vanderbilt CTSA grant UL1TR000445 in the National Center for Advancing Translational Sciences/NIH. The dataset used for the analyses described was in portion obtained from Vanderbilt BRD4 Inhibitor Storage & Stability University Health-related 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 of your authors and does not necessarily represent the official views from the NIH. The authors have no conflicts of interest. The authors gratefully acknowledge the contributions on the Vanderbilt University Center for Human Genetics Research DNA Sources Core and also the assistance of Dr. Holli Hutcheson Dilks in designing the tag SNP panel.
Interactions among 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 Development, Division of Surgery, Cedars-Sinai Healthcare Center, Los Angeles, LTC4 Antagonist list California, USAa; Laboratory of Molecular Immunology, Infectious and Inflammatory Illnesses Center, Sanford-Burnham Health-related 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; School 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 Study, University of California, Irvine, Irvine, California, USAfHerpesvirus entry mediator (HVEM) is a single of various cell surface proteins herpes simplex virus (HSV) utilizes for attachment/entry. HVEM regulates cellular immune responses and can also improve cell survival. Interestingly, latency-associated transcript (LAT), the only viral gene consistently expressed throughout neuronal latency, enhances latency and reactivation by promoting cell survival and by assisting the virus evade the host immune response. Having said that, the mechanisms of these LAT activities are certainly not properly understood. We show right here for the first time that 1 mechanism by which LAT enhances latency and reactivation appears to be by upregulating HVEM expression. HSV-1 latency/reactivation was substantially lowered in Hvem / mice, indicating that HVEM plays a important function in HSV-1 latency/reactivation. Furthermore, LAT upregulated HVEM expression throughout latency in vivo as well as when expressed in vitro in the absence of other viral elements. This study suggests a mechanism whereby LAT upregulates HVEM expression potentially by means of binding of two LAT tiny noncoding RNAs.
