Investigation of Herpes Simplex Virus Latency in a Tissue Culture System

1993 ◽  
Vol 85 (s29) ◽  
pp. 36P-37P
Author(s):  
D R S Jamieson ◽  
J M Rhodes
1996 ◽  
Vol 77 (2) ◽  
pp. 199-209 ◽  
Author(s):  
A. H. Patel ◽  
J. H. Subak-Sharpe ◽  
N. D. Stow ◽  
H. S. Marsden ◽  
J. B. Maclean ◽  
...  

Author(s):  
Mariko Kobayashi ◽  
Ju-Youn Kim ◽  
Vladimir Camarena ◽  
Pamela C. Roehm ◽  
Moses V. Chao ◽  
...  

Author(s):  
K. Rekrut ◽  
K. Schleuter

Confirmation of herpes simplex virus (HSV) from genital lesions of obstetrical (OB) patients may affect both the management of the delivery and of the neonate.(l,2) During 1992 and 1993, 4,450 genital specimens from OB patients were submitted in viral transport media for herpes culture. The specimens were inoculated into MRC-5, Vero, and A-549 tissue culture tubes, incubated, and examined daily for 7 days for cytopathic effect (CPE). The original specimens were frozen at −70° C until final reports were issued. Culture tubes with CPE were tested by the Dupont Herpchek enzyme immuno assay (EIA) to confirm the presence of herpes simplex virus (HSV). (3,4) 170 OB patient specimens were positive by culture and confirmed by EIA.There were also 63 cultures exhibiting CPE ressembling HSV which were negative by EIA testing, which failed to pass in fresh tissue culture cells or progress to more enhanced CPE in culture. These original specimens were screened by electron microscopy after direct ultracentrifugation employing the Beckman airfuge with the EM 90 rotor on to formvar carbon-coated 300 mesh copper grids and negatively stained with 2% PTA.


1997 ◽  
Vol 10 (3) ◽  
pp. 419-443 ◽  
Author(s):  
E K Wagner ◽  
D C Bloom

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.


Intervirology ◽  
1991 ◽  
Vol 32 (2) ◽  
pp. 69-75 ◽  
Author(s):  
Chris M. Preston ◽  
Jackie Russell

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

2019 ◽  
Vol 94 (4) ◽  
Author(s):  
Navneet Singh ◽  
David C. Tscharke

ABSTRACT During herpes simplex virus (HSV) latency, the viral genome is harbored in peripheral neurons in the absence of infectious virus but with the potential to restart infection. Advances in epigenetics have helped explain how viral gene expression is largely inhibited during latency. Paradoxically, at the same time, the view that latency is entirely silent has been eroding. This low-level noise has implications for our understanding of HSV latency and should not be ignored.


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