herpes simplex virus type-1 (hsv-1) causes a variety of diseases in human. this virus is a neurotropic pathogen of human that establishes latent infection in the sensory ganglia innervating the site of primary infection. a number of genes including icp34.5 control hsv-1 pathogenicity and icp34.5 has been identified as hsv-1 virulence gene. open reading frame p (orf p) is also a hsv-1 gene that ...

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...

The herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) is abundantly expressed in latently infected sensory neurons. In small animal models of infection, expression of the first 1.5 kb of LAT coding sequences is necessary and sufficient for wild-type reactivation from latency. The ability of LAT to inhibit apoptosis is important for reactivation from latency. Within the fir...

objective: infection with herpes simplex virus type 1 induces viral latency in neuron trigeminal ganglions. the late associated transcript (lat) is uniquely expressed in infected neural cells, however no coding protein associated with these transcripts has been identified in infected cells. it has been shown that six micrornas transcribed from lat have the capabilities to affect the cell signal...

The herpes simplex virus type 1 latency-associated transcript (LAT) inhibits apoptosis. We demonstrate here that LAT influences the accumulation of the Bcl-x(L) transcript versus the Bcl-x(S) transcript in Neuro-2A cells. Bcl-x(L) encodes an antiapoptotic protein, whereas Bcl-x(S) encodes a proapoptotic protein. Promoting the accumulation of Bcl-x(L) in neurons may inhibit apoptosis, thus enhan...

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...

Infection by herpes simplex virus type 1 (HSV-1) can cause clinical symptoms in the peripheral and central nervous system. Recurrent ocular shedding can lead to corneal scarring and vision loss making HSV-1 a leading cause of corneal blindness due to an infectious agent. The primary site of HSV-1 latency is sensory neurons within trigeminal ganglia. Periodically, reactivation from latency occur...

Only the latency-associated transcript (LAT) of the herpes simplex virus type 1 (HSV-1) genome is transcribed during latency, while the lytic genes are suppressed, possibly by LAT antisense mechanisms and/or chromatin modifications. In the present study, latently infected dorsal root ganglia were explanted to assess both relative levels of LAT and histone H3 (K9, K14) acetylation of the LAT loc...

Trigeminal ganglia (TG) from rabbits latently infected with either wild-type herpes simplex virus type 1 (HSV-1) or the latency-associated transcript (LAT) promoter deletion mutant 17DeltaPst were assessed for their viral chromatin profile and transcript abundance. The wild-type 17syn+ genomes were more enriched in the transcriptionally permissive mark dimethyl H3 K4 than were the 17DeltaPst ge...

Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. The latency-associated transcript (LAT) gene is required for wild-type reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT(-) virus but not with LAT(+) viruses. In addition, a pla...