Construction of recombinant herpes simplex virus type I expressing green fluorescent protein without loss of any viral genes

Tanaka, Michiko; Kodaira, Hiroshi; Nishiyama, Yukihiro; Sata, Tetsutaro; Kawaguchi, Yasushi

doi:10.1016/j.micinf.2004.01.011

Cited by 40 publications

(49 citation statements)

References 34 publications

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“…We determined the effect of XAV939 on HSV-1 replication by using Vero cells in a plaque reduction assay. The assay was performed according to a previously described method, with some modifications (65). In brief, Vero cells were grown as a monolayer in a 6-well plate.…”

Section: Cells and Virusesmentioning

confidence: 99%

Herpes Simplex Virus Requires Poly(ADP-Ribose) Polymerase Activity for Efficient Replication and Induces Extracellular Signal-Related Kinase-Dependent Phosphorylation and ICP0-Dependent Nuclear Localization of Tankyrase 1

Yamauchi

Kamakura

et al. 2012

J Virol

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Tankyrase 1 is a poly(ADP-ribose) polymerase (PARP) which localizes to multiple subcellular sites, including telomeres and mitotic centrosomes. Poly(ADP-ribosyl)ation of the nuclear mitotic apparatus (NuMA) protein by tankyrase 1 during mitosis is essential for sister telomere resolution and mitotic spindle pole formation. In interphase cells, tankyrase 1 resides in the cytoplasm, and its role therein is not well understood. In this study, we found that herpes simplex virus (HSV) infection induced extensive modification of tankyrase 1 but not tankyrase 2. This modification was dependent on extracellular signal-regulated kinase (ERK) activity triggered by HSV infection. Following HSV-1 infection, tankyrase 1 was recruited to the nucleus. In the early phase of infection, tankyrase 1 colocalized with ICP0 and thereafter localized within the HSV replication compartment, which was blocked in cells infected with the HSV-1 ICP0-null mutant R7910. In the absence of infection, ICP0 interacted with tankyrase 1 and efficiently promoted its nuclear localization. HSV did not replicate efficiently in cells depleted of both tankyrases 1 and 2. Moreover, XAV939, an inhibitor of tankyrase PARP activity, decreased viral titers to 2 to 5% of control values. We concluded that HSV targets tankyrase 1 in an ICP0-and ERK-dependent manner to facilitate its replication. Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), members of the Herpesviridae family (17), possess large DNA genomes, share virion structures and replication mechanisms, and establish lifelong latency in host cells. The HSV genome comprises a 152-kb double-stranded DNA molecule that encodes approximately 80 gene products expressed in a temporally regulated cascade (6, 68). HSV genes are classified into three groups: immediate-early, early, and late genes. Immediate-early genes are expressed first upon infection and encode several transactivators, which in turn initiate transcription of the other early and some late genes; the latter are called leaky late or ␥1 genes (12,20,48,73). Early gene products include viral DNA replication factors that initiate viral DNA synthesis, which in turn stimulate expression of ␥1 and true late (␥2) genes, encoding mainly virion structural proteins.The immediate-early viral proteins ICP4, ICP27, ICP0, and ICP22 allow the virus to create an environment conducive to infection and counteract the intrinsic ability of cells to inhibit viral infection (29,34,55,59). ICP4 and ICP27 play essential roles in stimulating robust viral gene expression (34). The immediateearly protein ICP0 activates viral and cellular gene expression and functions as an E3 ubiquitin ligase that degrades several cellular proteins (29). ICP0 targets the promyelocytic leukemia protein (PML), a major component of nuclear foci called ND10 bodies that repress viral gene expression. ICP0 interferes with several intrinsic host defense mechanisms, including the host interferon responses (29), thereby playing a major role in establishing permissive conditions for viral infec...

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Section: Cells and Virusesmentioning

confidence: 99%

Herpes Simplex Virus Requires Poly(ADP-Ribose) Polymerase Activity for Efficient Replication and Induces Extracellular Signal-Related Kinase-Dependent Phosphorylation and ICP0-Dependent Nuclear Localization of Tankyrase 1

Yamauchi

Kamakura

et al. 2012

J Virol

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“…HSV-1 YK333 was created by the intergenic insertion of a GFP-expressing cassette between UL3 and UL4 of the virus genome. Green fluorescence can be detected after HSV infects host cells and starts viral gene expression (60); however, since this event occurs before viral DNA replication, the GFP signal detected in these cells is not indicative of HSV-1 progeny production. The titers were determined by determining the standard 50% tissue culture infective dose (TCID 50 ) or PFU on Vero cells.…”

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confidence: 99%

APOBEC1-Mediated Editing and Attenuation of Herpes Simplex Virus 1 DNA Indicate That Neurons Have an Antiviral Role during Herpes Simplex Encephalitis

Gee

Ando

Kitayama

et al. 2011

J Virol

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APOBEC1 (A1) is a cytidine deaminase involved in the regulation of lipids in the small intestine. Herpes simplex virus 1 (HSV-1) is a ubiquitous pathogen that is capable of infecting neurons in the brain, causing encephalitis. Here, we show that A1 is induced during encephalitis in neurons of rats infected with HSV-1. In cells stably expressing A1, HSV-1 infection resulted in significantly reduced virus replication compared to that in control cells. Infectivity could be restored to levels comparable to those observed for control cells if A1 expression was silenced by specific A1 short hairpin RNAs (shRNA). Moreover, cytidine deaminase activity appeared to be essential for this inhibition and led to an impaired accumulation of viral mRNA transcripts and DNA copy numbers. The sequencing of viral gene UL54 DNA, extracted from infected A1-expressing cells, revealed G-to-A and C-to-T transitions, indicating that A1 associates with HSV-1 DNA. Taken together, our results demonstrate a model in which A1 induction during encephalitis in neurons may aid in thwarting HSV-1 infection.The human apolipoprotein B-editing catalytic polypeptide (ABOBEC) family is a group of zinc-dependent DNA and RNA cytidine deaminases and consists of AID, APOBEC1 (A1), APOBEC2 (A2), seven APOBEC3s (APOBEC3A [A3A] to A3H), and APOBEC4 (A4). A1, the first APOBEC to be discovered, is known to introduce a premature stop codon into host apolipoprotein B mRNA in the gastrointestinal tract, an event critical for lipid metabolism (17,40,61). The editing by A1 is highly precise and specifically converts C to U at position 6666 of the apolipoprotein B mRNA substrate (46). Along with APOBEC1 complementation factor (ACF), these two proteins constitute the minimal required components necessary for the editing of apolipoprotein B mRNA in vitro (37).Cytidine deaminases first came into the limelight as antiviral factors after A3G was identified as a cellular restriction factor capable of inhibiting HIV-1 dissemination in the absence of HIV-1 virus infectivity factor (Vif) (56). This molecule was later shown to inhibit retrovirus infection by inducing a massive hypermutation of the murine leukemia virus (MLV) genome (23). Further detailed studies revealed that APOBEC molecules are packaged into HIV-1 virions in virus producer cells via a specific interaction with Gag and viral RNA and then exert their deaminase activity in subsequent target cells on a single-stranded DNA (ssDNA) intermediate synthesized by reverse transcriptase (3, 28, 55). Editing can lead to nonsynonymous mutations, such as premature stop codons, in critical proteins (e.g., reverse transcriptase) necessary for virus replication and infectivity, severely impairing the next round of infection (54,64). Extensive studies to assess the antiviral nature of these APOBEC enzymes have been performed across a broad range of retroviruses and hepatitis B virus (HBV) (7,35,36,42,43,50,56,58).Herpes simplex virus (HSV) is an enveloped, double-stranded DNA (dsDNA) virus and a member of the genus Alphaherpe...

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“…Anti-HSV-1 activity was measured by plaquereduction assay (Tanaka et al, 2004). Vero cells (Tanaka et al, 2003) were grown to the confluent stage in 24-well titre plates, in Dulbecco's modified Eagles medium (Nacalai) supplemented with heat-treated fetal bovine serum (1 %).…”

Section: Methodsmentioning

confidence: 99%

A silkworm–baculovirus model for assessing the therapeutic effects of antiviral compounds: characterization and application to the isolation of antivirals from traditional medicines

Orihara

Hamamoto

Hiroshi

et al. 2008

Journal of General Virology

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Ganciclovir, foscarnet, vidarabine and ribavirin, which are used to treat viral infections in humans, inhibited the proliferation of a baculovirus (Bombyx mori nucleopolyhedrovirus) in BmN4 cells, a cultured silkworm cell line. These antiviral agents inhibited the proliferation of baculovirus in silkworm body fluid and had therapeutic effects. Using the silkworm infection model, the antiviral activity of Kampo medicines was screened and it was found that cinnamon bark, a component of the traditional Japanese medicine Mao-to, had a therapeutic effect. Based on the therapeutic activity, the antiviral substance was purified. Nuclear magnetic resonance analysis of the purified fraction revealed that the antiviral activity was due to cinnzeylanine, which has previously been isolated from Cinnamomum zeylanicum. Cinnzeylanine inhibits the proliferation of herpes simplex virus type 1 in Vero cells. These results suggest that the silkworm-baculovirus infection model is useful for screening antiviral agents that are effective for treating humans infected with DNA viruses.

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Construction of recombinant herpes simplex virus type I expressing green fluorescent protein without loss of any viral genes

Cited by 40 publications

References 34 publications

Herpes Simplex Virus Requires Poly(ADP-Ribose) Polymerase Activity for Efficient Replication and Induces Extracellular Signal-Related Kinase-Dependent Phosphorylation and ICP0-Dependent Nuclear Localization of Tankyrase 1

Herpes Simplex Virus Requires Poly(ADP-Ribose) Polymerase Activity for Efficient Replication and Induces Extracellular Signal-Related Kinase-Dependent Phosphorylation and ICP0-Dependent Nuclear Localization of Tankyrase 1

APOBEC1-Mediated Editing and Attenuation of Herpes Simplex Virus 1 DNA Indicate That Neurons Have an Antiviral Role during Herpes Simplex Encephalitis

A silkworm–baculovirus model for assessing the therapeutic effects of antiviral compounds: characterization and application to the isolation of antivirals from traditional medicines

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