Exogenous human immunodeficiency virus‐1 protein, tat, enhances replication of JC virus efficiently in neuroblastoma cell lines

Nukuzuma, Souichi; Kameoka, Masanori; Sugiura, Shigeki; Nakamichi, Kazuo; Nukuzuma, Chiyoko; Miyoshi, Isao; Takegami, Tsutomu

doi:10.1002/jmv.23239

Cited by 9 publications

(15 citation statements)

References 20 publications

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“…Cell proliferation was determined by measuring mitochondrial succinate dehydrogenase activity using an MTT assay as described previously [Nukuzuma et al, 2012]. IMR‐32 cells were plated into 96‐well microtiter plates at a concentration of 7.1 × 10 4 cells/well in 100 µl medium and incubated in the absence or presence of 3‐AB at a final concentration of 20 mM for 5 days at 37°C in a CO 2 incubator.…”

Section: Methodsmentioning

confidence: 99%

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Suppressive effect of PARP‐1 inhibitor on JC virus replication in vitro

Nukuzuma¹,

Kameoka

Sugiura

et al. 2012

Journal of Medical Virology

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The incidence of progressive multifocal leukoencephalopathy (PML) has increased due to the AIDS pandemic, hematological malignancies, and immunosuppressive therapies. Recently, the number of cases of monoclonal antibody-associated PML has increased in patients treated with immunomodulatory drugs such as natalizumab. However, no common consensus regarding PML therapy has been reached in clinical studies. In order to examine the suppression of JC virus (JCV) replication by 3-aminobenzamide (3-AB), a representative PARP-1 inhibitor, a DNA replication assay was carried out using the neuroblastoma cell line IMR-32 and IMR-adapted JCV. The suppression of JCV propagation by 3-AB was also examined using JCI cells, which are a carrier culture producing continuously high JCV titers. The results indicated that PARP-1 inhibitors, such as 3-aminobenzamide (3-AB), suppress JCV replication and propagation significantly in vitro, as judged by DNA replication assay, hemagglutination, and real-time PCR analysis. It has been also shown that 3-AB reduced PARP-1 activity in IMR-32 cells. According to the results of the MTT assay, the enzyme activity of 3-AB-treated cells was slightly lower than that of DMSO-treated cells. However, the significant suppression of JCV propagation is not related to the slight decrease in cell growth. To our knowledge, this is the first report that PARP-1 inhibitor suppresses the replication of JCV significantly in neuroblastoma cell lines via the reduction of PARP-1 activity. Thus, PARP-1 inhibitors also may be a novel therapeutic drug for PML.

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Section: Methodsmentioning

confidence: 99%

“…A DNA replication assay was carried out as described previously [Nukuzuma et al, 2012]. IMR‐32 cells were plated into poly‐ L ‐lysine‐coated 35‐mm dishes in 2 ml of DMEM containing with 10% FBS until they reached 70–80% confluency.…”

Section: Methodsmentioning

confidence: 99%

Suppressive effect of PARP‐1 inhibitor on JC virus replication in vitro

Nukuzuma¹,

Kameoka

Sugiura

et al. 2012

Journal of Medical Virology

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“…Cytotoxicity was measured by an MTT assay, as previously described (13). IMR-32 and JCI cells were plated in 96-well microtiter plates at a concentration of 5.0 Â 10 4 (topotecan) or 2.5 Â 10 4 (b-lapachone) cells/ well/100 mL medium 24 hr prior to addition of various concentrations of topotecan or b-lapachone.…”

Section: Quantification Of Cell Proliferationmentioning

confidence: 99%

“…DNA replication assay using RT-PCR IMR-32 cells were cultured in 6-well plates containing 2 mL complete growth medium until 70-80% confluency had been reached. JCV DNA transfection was performed as previously described (13). Briefly, 1.0 mg viral DNA (M1-IMRb) excised from a recombinant plasmid with EcoRI was introduced into cells using FuGENE 6 transfection reagent (Roche), according to the manufacturer's instructions.…”

Section: Quantification Of Cell Proliferationmentioning

confidence: 99%

Suppressive effect of topoisomerase inhibitors on JC polyomavirus propagation in human neuroblastoma cells

Nukuzuma¹,

Nakamichi

Kameoka

et al. 2016

Microbiology and Immunology

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JC polyomavirus (JCPyV) causes progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system, in immunocompromised patients. Because no drugs have been approved for treating PML, many antiviral agents are currently being investigated for this purpose. The inhibitory effects of the topoisomerase I inhibitors topotecan and β-lapachone were assessed by investigating viral replication, propagation and viral protein 1 (VP1) production in cultured cells. JCPyV replication was assayed using the human neuroblastoma cell line IMR-32 transfected with the JCPyV plasmid and RT- PCR combined with Dpn I treatment. Dpn I digests the input plasmid DNA containing methylated adenosine, but not newly replicated JCPyV DNA, in IMR-32 cells. It was found that JCPyV replicates less in IMR-32 cells treated with topotecan or β-lapachone than in untreated cells. Moreover, drug treatment of JCI cells, which are IMR-32 cells persistently infected with JCPyV, led to a reduction in the amount of JCPyV DNA and population of VP1-positive cells. These results demonstrate that topotecan and β-lapachone affects JCPyV propagation in human neuroblastoma cell lines, suggesting that topotecan and β-lapachone could potentially be used to treat PML.

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“…Recent studies have shown that HIV-1 viral proteins per se can act on oligodendrocytes and produce detrimental effects, which are independent of JCV [ 6 , 9 , 10 ]. HIV-1 viral proteins, including the envelope glycoprotein 120 (gp120), trans-activator of transcription (Tat), and negative regulatory factor (Nef), have been implicated in HIV-1-associated oligodendrocyte injury [ 9 , 11 , 12 , 13 , 14 ]. Among these viral proteins, Tat has consistently been detected in both infected and uninfected oligodendrocytes in the brains of AIDS patients [ 7 ], and exhibited a synergistic detrimental effect with JCV or with addictive drugs, such as morphine.…”

Section: Introductionmentioning

confidence: 99%

Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders

Liu

et al. 2016

Brain Sciences

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Oligodendrocytes wrap neuronal axons to form myelin, an insulating sheath which is essential for nervous impulse conduction along axons. Axonal myelination is highly regulated by neuronal and astrocytic signals and the maintenance of myelin sheaths is a very complex process. Oligodendrocyte damage can cause axonal demyelination and neuronal injury, leading to neurological disorders. Demyelination in the cerebrum may produce cognitive impairment in a variety of neurological disorders, including human immunodeficiency virus type one (HIV-1)-associated neurocognitive disorders (HAND). Although the combined antiretroviral therapy has markedly reduced the incidence of HIV-1-associated dementia, a severe form of HAND, milder forms of HAND remain prevalent even when the peripheral viral load is well controlled. HAND manifests as a subcortical dementia with damage in the brain white matter (e.g., corpus callosum), which consists of myelinated axonal fibers. How HIV-1 brain infection causes myelin injury and resultant white matter damage is an interesting area of current HIV research. In this review, we tentatively address recent progress on oligodendrocyte dysregulation and HAND pathogenesis.

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Exogenous human immunodeficiency virus‐1 protein, tat, enhances replication of JC virus efficiently in neuroblastoma cell lines

Cited by 9 publications

References 20 publications

Suppressive effect of PARP‐1 inhibitor on JC virus replication in vitro

Suppressive effect of PARP‐1 inhibitor on JC virus replication in vitro

Suppressive effect of topoisomerase inhibitors on JC polyomavirus propagation in human neuroblastoma cells

Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders

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