The 2.2-Kilobase Latency-Associated Transcript of Herpes Simplex Virus Type 2 Does Not Modulate Viral Replication, Reactivation, or Establishment of Latency in Transgenic Mice
نویسندگان
چکیده
منابع مشابه
The 2.2-kilobase latency-associated transcript of herpes simplex virus type 2 does not modulate viral replication, reactivation, or establishment of latency in transgenic mice.
To better understand the mechanisms responsible for the observed effects of deletions in the promoter region of the latency-associated transcript (LAT) gene in impairing herpes simplex virus (HSV) reactivation, we generated mice transgenic for a 5.5-kb HSV type 2 (HSV-2) genomic fragment spanning the major LAT, along with the LAT promoter and flanking regions, in the C57BL/6 background. The mic...
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The latency-associated transcript (LAT) gene the only herpes simplex virus type 1 (HSV-1) gene abundantly transcribed during neuronal latency, is essential for efficient in vivo reactivation. Whether LAT increases reactivation by a direct effect on the reactivation process or whether it does so by increasing the establishment of latency, thereby making more latently infected neurons available f...
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Herpes simplex virus type 1 establishes latent infections in sensory neurons. During latency only one locus, the latency-associated transcript (LAT), is abundantly transcribed. Several lines of evidence suggest that this locus is required for the efficient reactivation from latency in experimental models. However, it is not yet clear whether this is a direct effect on the reactivation process p...
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Background and Aims: The latency-associated transcript (LAT) transcribed by latent Herpes Simplex Virus type-1 in neuron cells are able to influence their host cell pathways. While the most of previous studies were focused on anti-apoptotic effects of LAT, our investigation is making an effort to explore LAT potency on cell cycle pathway in neuroblastoma cell lines. Methods: The evaluation of L...
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ژورنال
عنوان ژورنال: Journal of Virology
سال: 2001
ISSN: 0022-538X,1098-5514
DOI: 10.1128/jvi.75.17.8166-8172.2001