Thor Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPain. Author manuscript; available in PMC 2014 December 01.Bruehl et al.Pagea far more complete understanding of pathways underlying these associations ought 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 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 element 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 is solely the responsibility with the authors and does not necessarily represent the official views with the NIH. The authors have no conflicts of interest. The authors gratefully acknowledge the contributions of your Vanderbilt University Center for Human Genetics Study DNA Sources Core and also the help of Dr. Holli Hutcheson Dilks in designing the tag SNP panel.
Interactions between Herpesvirus Entry Mediator (TNFRSF14) and Latency-Associated Transcript in the course of Herpes Simplex Virus 1 LatencySariah J. Allen,a Antje Rhode-Kurnow,b Kevin R. Mott,a Xianzhi Jiang,c Dale Carpenter,c J. Sorcin/SRI Protein web Ignacio Rodriguez-Barbosa,d Clinton Jones,e Steven L. Wechsler,c,f Carl F. Ware,b Homayon GhiasiaCenter for Neurobiology and Vaccine Development, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, Prostatic acid phosphatase/ACPP Protein Storage & Stability California, USAa; Laboratory of Molecular Immunology, Infectious and Inflammatory Illnesses Center, Sanford-Burnham Healthcare 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; Division of Microbiology and Molecular Genetics, and Center for Virus Investigation, University of California, Irvine, Irvine, California, USAfHerpesvirus entry mediator (HVEM) is one of several 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 consistently expressed during 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 well understood. We show right here for the initial time that 1 mechanism by which LAT enhances latency and reactivation seems to become by upregulating HVEM expression. HSV-1 latency/reactivation was substantially decreased in Hvem / mice, indicating that HVEM plays a substantial role in HSV-1 latency/reactivation. Moreover, LAT upregulated HVEM expression through latency in vivo and also when expressed in vitro in the absence of other viral aspects. This study suggests a mechanism whereby LAT upregulates HVEM expression potentially by means of binding of two LAT modest noncoding RNAs towards the HVEM pr.
