Influence of Herpes Simplex Virus Latency-Associated Transcript (LAT) on the Distribution of Latently Infected Neurons

2007 ◽  
Author(s):  
Andrea S. Bertke
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Latency ◽  
Latently Infected ◽  
Simplex Virus

scholarly journals 17-β Estradiol Promotion of Herpes Simplex Virus Type 1 Reactivation Is Estrogen Receptor Dependent

2009 ◽  
Vol 84 (1) ◽  
pp. 565-572 ◽  
Author(s):  
Rodolfo D. Vicetti Miguel ◽  
Brian S. Sheridan ◽  
Stephen A. K. Harvey ◽  
Robert S. Schreiner ◽  
Robert L. Hendricks ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Viral Reactivation ◽  
Hormonal Contraceptives ◽  
Viral Gene ◽  
Dependent Manner ◽  
Ovariectomized Mice ◽  
Latently Infected ◽  
Simplex Virus

ABSTRACT Correlations between estrogen and herpes simplex virus (HSV) reactivation from latency have been suggested by numerous clinical reports, but causal associations are not well delineated. In a murine HSV-1 corneal infection model, we establish 17-β estradiol (17-βE) treatment of latently infected ovariectomized mice induces viral reactivation, as demonstrated by increased viral load and increased immediate-early viral gene expression in the latently infected trigeminal ganglia (TG). Interestingly, the increased HSV reactivation occurred in the absence of inhibition of viral specific CD8+ T-cell effector function. 17-βE administration increased HSV reactivation in CD45+ cell-depleted TG explant cultures, providing further support that leukocyte-independent effects on latently infected neurons were responsible for the increased reactivation. The drug-induced increases in HSV copy number were not recapitulated upon in vivo treatment of latently infected estrogen receptor alpha-deficient mice, evidence that HSV reactivation promoted by 17-βE was estrogen receptor dependent. These findings provide additional framework for the emerging conceptualization of HSV latency as a dynamic process maintained by complex interactions among multiple cooperative and competing host, viral, and environmental forces. Additional research is needed to confirm whether pregnancy or hormonal contraceptives containing 17-βE also promote HSV reactivation from latency in an estrogen receptor-dependent manner.

scholarly journals Experimental investigation of herpes simplex virus latency.

1997 ◽  
Vol 10 (3) ◽  
pp. 419-443 ◽  
Author(s):  
E K Wagner ◽  
D C Bloom
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Animal Models ◽  
Latent Infection ◽  
Cultured Cells ◽  
Early Stage ◽  
Clinical Manifestations ◽  
Cis Acting ◽  
Virus Latency ◽  
Simplex Virus

The clinical manifestations of herpes simplex virus infection generally involve a mild and localized primary infection followed by asymptomatic (latent) infection interrupted sporadically by periods of recrudescence (reactivation) where virus replication and associated cytopathologic findings are manifest at the site of initial infection. During the latent phase of infection, viral genomes, but not infectious virus itself, can be detected in sensory and autonomic neurons. The process of latent infection and reactivation has been subject to continuing investigation in animal models and, more recently, in cultured cells. The initiation and maintenance of latent infection in neurons are apparently passive phenomena in that no virus gene products need be expressed or are required. Despite this, a single latency-associated transcript (LAT) encoded by DNA encompassing about 6% of the viral genome is expressed during latent infection in a minority of neurons containing viral DNA. This transcript is spliced, and the intron derived from this splicing is stably maintained in the nucleus of neurons expressing it. Reactivation, which can be induced by stress and assayed in several animal models, is facilitated by the expression of LAT. Although the mechanism of action of LAT-mediated facilitation of reactivation is not clear, all available evidence argues against its involving the expression of a protein. Rather, the most consistent models of action involve LAT expression playing a cis-acting role in a very early stage of the reactivation process.

Retention of Nonlinear Viral DNA during Herpes simplex Virus Latency in vitro

Intervirology ◽  
1991 ◽  
Vol 32 (2) ◽  
pp. 69-75 ◽  
Author(s):  
Chris M. Preston ◽  
Jackie Russell
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Viral Dna ◽  
Virus Latency ◽  
Simplex Virus

scholarly journals Physical characterization of the herpes simplex virus latency-associated transcript in neurons.

1988 ◽  
Vol 62 (4) ◽  
pp. 1194-1202 ◽  
Author(s):  
E K Wagner ◽  
G Devi-Rao ◽  
L T Feldman ◽  
A T Dobson ◽  
Y F Zhang ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Physical Characterization ◽  
Virus Latency ◽  
Simplex Virus

scholarly journals Identification of a novel herpes simplex virus type 1 transcript and protein (AL3) expressed during latency

2009 ◽  
Vol 90 (10) ◽  
pp. 2342-2352 ◽  
Author(s):  
Tareq Jaber ◽  
Gail Henderson ◽  
Sumin Li ◽  
Guey-Chuen Perng ◽  
Dale Carpenter ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Neuroblastoma Cells ◽  
Productive Infection ◽  
Coding Sequences ◽  
Promoter Sequences ◽  
Mouse Neuroblastoma ◽  
Latently Infected ◽  
Simplex Virus

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 first 1.5 kb of LAT coding sequences and LAT promoter sequences, additional transcripts have been identified. For example, the anti-sense to LAT transcript (AL) is expressed in the opposite direction to LAT from the 5′ end of LAT and LAT promoter sequences. In addition, the upstream of LAT (UOL) transcript is expressed in the LAT direction from sequences in the LAT promoter. Further examination of the first 1.5 kb of LAT coding sequences revealed two small ORFs that are anti-sense with respect to LAT (AL2 and AL3). A transcript spanning AL3 was detected in productively infected cells, mouse neuroblastoma cells stably expressing LAT and trigeminal ganglia (TG) of latently infected mice. Peptide-specific IgG directed against AL3 specifically recognized a protein migrating near 15 kDa in cells stably transfected with LAT, mouse neuroblastoma cells transfected with a plasmid containing the AL3 ORF and TG of latently infected mice. The inability to detect the AL3 protein during productive infection may have been because the 5′ terminus of the AL3 transcript was downstream of the first in-frame methionine of the AL3 ORF during productive infection.

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