Replication of thymidine kinase deficient herpes simplex virus type 1 in neuronal cell culture: Infection of the PC 12 cell

Rubenstein, Richard; Price, Richard W.

doi:10.1007/bf01310858

Cited by 12 publications

(5 citation statements)

References 34 publications

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“…However, unlike lentiviruses, these large dsDNA viruses encode dNTP biosynthesis proteins such as ribonucleotide reductase (RNR) and thymidine kinase (TK) that supply essential dNTP substrates for the viral DNA polymerase. Both of these genes are dispensable for HSV-1 viral replication in dividing cells, but are essential for replication under serum-starvation/non-dividing conditions where dNTP pools are limited [31], [32]. Thus, it is plausible that the dNTP biosynthesis machinery of dsDNA viruses promotes efficient replication in both dividing and non-dividing target cell types.…”

Section: Introductionmentioning

confidence: 99%

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

et al. 2013

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SAMHD1 is a newly identified anti-HIV host factor that has a dNTP triphosphohydrolase activity and depletes intracellular dNTP pools in non-dividing myeloid cells. Since DNA viruses utilize cellular dNTPs, we investigated whether SAMHD1 limits the replication of DNA viruses in non-dividing myeloid target cells. Indeed, two double stranded DNA viruses, vaccinia and herpes simplex virus type 1, are subject to SAMHD1 restriction in non-dividing target cells in a dNTP dependent manner. Using a thymidine kinase deficient strain of vaccinia virus, we demonstrate a greater restriction of viral replication in non-dividing cells expressing SAMHD1. Therefore, this study suggests that SAMHD1 is a potential innate anti-viral player that suppresses the replication of a wide range of DNA viruses, as well as retroviruses, which infect non-dividing myeloid cells.

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Section: Introductionmentioning

confidence: 99%

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

et al. 2013

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“…The cells were infected with HSV-1 strain KOS(M) (51) at a multiplicity of infection (MOI) of 1. Single-step growth curves confirmed that both differentiated and undifferentiated cells were permissive for HSV-1 infection (data not shown) (38). To examine the LAT gene transcripts expressed, total RNA was isolated from cells lysed in the presence of 5.5 M guanidinium isothiocyanate (Gibco-Bethesda Research Laboratories) by centrifugation through a cushion of cesium trifluoroacetate (Pharmacia-LKB).…”

mentioning

confidence: 86%

“…In this study, we have examined the stability and conformation of the 2-kb LAT gene transcript expressed in PC12 cells productively infected with HSV-1. PC12 cells differentiate into cells resembling sympathetic neurons after treatment with nerve growth factor (NGF) (21) and have been used by several investigators to study the interaction between HSV-1 and neuronal cells in culture (3,38,39). They support high levels of LAT promoter activity compared with other cell lines (5,29).…”

mentioning

confidence: 99%

Analysis of the 2-kilobase latency-associated transcript expressed in PC12 cells productively infected with herpes simplex virus type 1: evidence for a stable, nonlinear structure

Rødahl

Haarr

1997

J Virol

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The major latency-associated transcript (LAT) expressed in PC12 cells productively infected with herpes simplex virus type 1 is a 2-kb, nonpolyadenylated RNA molecule that accumulates in the nuclei of infected cells. In actinomycin D-treated cells, the 2-kb LAT gene transcript has a half-life considerably greater than 12 h. After polyacrylamide gel electrophoresis, two species of the transcript were observed, a major species that was retarded in the gel and a minor species that migrated as a 1.96-kb RNA molecule. RNase H digestion after hybridization of the RNA with an oligonucleotide complementary to positions ؊80 to ؊101 relative to the 3 end of the 2-kb LAT gene transcript changed the mobility of the retarded species into that of the rapidly migrating species. Our data indicate that the 2-kb LAT gene transcript expressed in productively infected PC12 cells is present in a stable, nonlinear form.

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“…However, in the rabbit model, Tk activity is not required for ganglionic infection [55]. Further studies using the mouse model demonstrate that only minimal Tk activity is sufficient for ganglionic infection [56] and that HSV-1 Tk -null virus can replicate in neuronal cells [57]. In addition, using PCR to increase the detection of virus DNA, low copies of HSV-1 Tk-null DNA were found in mouse TG following corneal infection [58].…”

Section: Seeding the Ganglion With Virusmentioning

confidence: 99%

Varicella Zoster Virus Latency

2011

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Primary infection by varicella zoster virus (VZV) typically results in childhood chickenpox, at which time latency is established in the neurons of the cranial nerve, dorsal root and autonomic ganglia along the entire neuraxis. During latency, the histone-associated virus genome assumes a circular episomal configuration from which transcription is epigenetically regulated. The lack of an animal model in which VZV latency and reactivation can be studied, along with the difficulty in obtaining high-titer cell-free virus, has limited much of our understanding of VZV latency to descriptive studies of ganglia removed at autopsy and analogy to HSV-1, the prototype alphaherpesvirus. However, the lack of miRNA, detectable latency-associated transcript and T-cell surveillance during VZV latency highlight basic differences between the two neurotropic herpesviruses. This article focuses on VZV latency: establishment, maintenance and reactivation. Comparisons are made with HSV-1, with specific attention to differences that make these viruses unique human pathogens.

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Replication of thymidine kinase deficient herpes simplex virus type 1 in neuronal cell culture: Infection of the PC 12 cell

Cited by 12 publications

References 34 publications

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

Host Factor SAMHD1 Restricts DNA Viruses in Non-Dividing Myeloid Cells

Analysis of the 2-kilobase latency-associated transcript expressed in PC12 cells productively infected with herpes simplex virus type 1: evidence for a stable, nonlinear structure

Varicella Zoster Virus Latency

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