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The locus encompassing the latency-associated transcript of herpes simplex virus type 1 interferes with and delays interferon expression in productively infected neuroblastoma cells and trigeminal Ganglia of acutely infected mice
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Peng W Henderson G Inman M BenMohamed L Perng GC Wechsler SL Jones C 《Journal of virology》2005,79(10):6162-6171
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Huang Rongquan Zhou Xusha Ren Shuqi Liu Xianjie Han Zhiyuan Zhou Grace Guoying 《中国病毒学》2019,34(4):386-396
To date, 29 distinct microRNAs(miRNAs) have been reported to be expressed during herpes simplex virus infections.Sequence analysis of mature herpes simplex virus-1(HSV-1) miRNAs revealed five sets of miRNAs that are complementary to each other: miR-H6-5p/H1-3p, miR-H6-3p/H1-5p, H2-5p/H14-3p, miR-H2-3p/H14-5p, and miR-H7/H27.However, the roles of individual miRNAs and consequences of this complementarity remain unclear. Here, we focus on two of these complementary miRNAs, miR-H6-5p and miR-H1-3p, using loss-of-function experiments in vitro and in a mouse model of infection using an miRNA sponge approach, including tandem multiplex artificial miRNA-binding sequences that do not match perfectly to the target miRNA inserted downstream of a green fluorescent protein reporter gene. Infection with recombinant virus expressing the miR-H6-5p sponge reduced viral protein levels and virus yield.Decreased accumulation of viral proteins was also observed at early stages of infection in the presence of both an miR-H6-5p inhibitor and plasmid-expressed miR-H1-3p. Moreover, establishment of latency and reactivation did not differ between the recombinant virus expressing the miR-H6-5p sponge and wild-type HSV-1. Taken together, these data suggest that miR-H6-5p has an as-yet-unidentified role in the early stages of viral infection, and its complement miR-H1-3p suppresses this role in later stages of infection. This report extends understanding of the roles of miRNAs in infection by herpes simplex viruses, supporting a model of infection in which the production of virus and its virulent effects are tightly controlled to maximize persistence in the host and population. 相似文献
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Herpes simplex virus type 1 serum neutralizing antibody titers increase during latency in rabbits latently infected with latency-associated transcript (LAT)-positive but not LAT-negative viruses.
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Guey-Chuen Perng Susan M. Slanina Ada Yukht Homayon Ghiasi Anthony B. Nesburn Steven L. Wechsler 《Journal of virology》1999,73(11):9669-9672
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Jiang X Chentoufi AA Hsiang C Carpenter D Osorio N BenMohamed L Fraser NW Jones C Wechsler SL 《Journal of virology》2011,85(5):2325-2332
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Spontaneous reactivation of herpes simplex virus type 1 in latently infected murine sensory ganglia 总被引:2,自引:1,他引:1
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Margolis TP Elfman FL Leib D Pakpour N Apakupakul K Imai Y Voytek C 《Journal of virology》2007,81(20):11069-11074
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Latency-Associated Transcript (LAT) Exon 1 Controls Herpes Simplex Virus Species-Specific Phenotypes: Reactivation in the Guinea Pig Genital Model and Neuron Subtype-Specific Latent Expression of LAT
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Andrea S. Bertke Amita Patel Yumi Imai Kathleen Apakupakul Todd P. Margolis Philip R. Krause 《Journal of virology》2009,83(19):10007-10015
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A gene capable of blocking apoptosis can substitute for the herpes simplex virus type 1 latency-associated transcript gene and restore wild-type reactivation levels. 总被引:9,自引:0,他引:9
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Guey-Chuen Perng Barak Maguen Ling Jin Kevin R. Mott Nelson Osorio Susan M. Slanina Ada Yukht Homayon Ghiasi Anthony B. Nesburn Melissa Inman Gail Henderson Clinton Jones Steven L. Wechsler 《Journal of virology》2002,76(3):1224-1235
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Intrinsic immunity is a first-line intracellular defense against virus infection, and viruses have evolved mechanisms to counteract it. During herpes simplex virus (HSV) infection, nuclear domain 10 (ND10) components localize adjacent to incoming viral genomes and generate a repressive environment for viral gene expression. Here, we found that the ND10 component, alpha-thalassemia/mental retardation syndrome X-linked (ATRX) protein, is predicted to be a target of HSV-1 miR-H1 and HSV-2 miR-H6. These microRNAs (miRNAs) share a seed sequence and are abundant during lytic infection. Mimics of both miRNAs could deplete endogenous ATRX, and an miR-H1 mimic could repress the expression of a reporter linked to the 3' untranslated region of ATRX mRNA, identifying a cellular mRNA targeted by an HSV miRNA. Interestingly, ATRX protein and its mRNA were depleted in cells lytically infected with HSV, and ATRX protein was also depleted in cells infected with human cytomegalovirus. However, infection with an HSV-1 mutant lacking miR-H1 still resulted in ATRX depletion. This depletion was sensitive to a proteasome inhibitor and was largely ablated by a deletion of the gene encoding the immediate-early ICP0 protein. Additionally, a deletion of the gene encoding the tegument protein Vhs ablated most of the depletion of ATRX mRNA. Thus, HSV is equipped with multiple mechanisms to limit the expression of ATRX. As ATRX is implicated in repression of lytic viral gene expression, our results suggest roles for these different mechanisms during various phases of HSV infection. 相似文献