Persistent Infection of Rabies Virus (HEP-Flury Strain) in Human Neuroblastoma Cells Capable of Producing Interferon

Honda, Yoshikazu; Kawai, Akihiko; Matsumoto, Seiichi

doi:10.1099/0022-1317-66-5-957

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…Because PV and coxsackieviruses have different receptors, our results suggest that one of the early steps of the PV growth cycle-i.e., adsorption, penetration, decapsidation-is probably involved in the resistance to PV superinfection. In contrast to results reported for persistent rabiesvirus infection (31), the synthesis of a or f3 interferon was not detected in persistently infected IMR-32 and SK-N-MC cells, since less than 3 units/ml was found in cell supernatants (J. L. Virelizier, personal communication).…”

Section: S3 (Imrcontrasting

confidence: 46%

Persistent poliovirus infection of human neuroblastoma cells.

Colbère-Garapin

Christodoulou

Crainic

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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Two human neuroblastoma cell lines were persistently infected with poliovirus strains of all three serotypes. In persistently infected IMR-32 cells, which were studied in greatest detail, viral antigens were present in most cells, and over a 9-month period virions were found in the medium at high titers. Persistently infected cells were resistant to superinfection by Sabin 1, 2, and 3 poliovirus but sensitive to coxsackievirus B3. The viruses recovered from persistently infected cells were studied for conservation of epitopes, host cell specificity, and temperature resistance phenotype. The antigenic site 1 carried by the major capsid protein VP1 was modified on the persistent viruses of all three serotypes. This was confirmed for one virus by sequencing the corresponding genomic region in which two mutations were detected. The titers of persistent viruses were 1-3 log10 units higher on IMR-32 cells than on nonneuronal HEp-2 cells, while parental viruses had similar titers on both lines. When thermosensitive viruses were used to initiate the infection, the persistent viruses were found to be thermoresistant at 390C. Together the results indicate that the persistent infection correlated with the selection of highly mutated viral strains. Poliovirus-infected neuroblastoma cell lines thus constitute an in vitro model ofchronic viral infections, which are increasingly implicated in human neural diseases.Poliomyelitis paralyses are caused by poliovirus (PV)-induced necroses of motor neurons (1, 2). A late postpolio syndrome has been described: new focal motor neuron deterioration emerges after an average period of 30 years from initial infection (3, 4). One of the hypotheses proposed to account for this syndrome is a persistent viral infection (3, 4). Several members ofthe picornavirus family are effectively able to induce a persistent infection ofcells in vivo and in vitro (5-11). It is assumed that the selection of viral mutants, viral interference, and interferons play a role in this persistence (12,13). For PV, the viral cytolytic action was shown to be limited by the intercellular matrix (14). Cultures in which only a small fraction of cells were susceptible to PV have been described (15)(16)(17). In a more recent study, Kaplan et al. (18) isolated PV-infected HeLa cell lines blocked at different steps of the virus life cycle which underwent periodic crises with cytopathic effects (CPE).In cell lines of neuronal origin, PV-cell interactions have been studied only in one-step growth experiments during the first 8 hr post infection (p.i.) (19). We report here the establishment of a persistent PV infection of human neuroblastoma cells. Most cells harbored viral antigens and cultures produced virions for months at high titers in the absence of detectable CPE. Persistently infected cell lines and the resulting PV mutants are described.MATERIALS AND METHODS Materials. The Leon 37, vFG68 (20), LSc2ab (S1), P712 Ch 2ab (S2), and P3/Leon 12alb (S3) Sabin strains (21) of PV were used. Another enterovirus, coxsacki...

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Section: S3 (Imrcontrasting

confidence: 46%

Persistent poliovirus infection of human neuroblastoma cells.

Colbère-Garapin

Christodoulou

Crainic

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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“…Immediate induction of IFN may prevent the spread of reactivating virus within the nervous system by inhibiting release of viral particles and activating host defense mechanisms such as natural killer cells (22). Moreover, in another virus system, neuroblastoma cells expressing high levels of IFN-␤ support persistent rabies virus infections (25). This finding suggests that the IFN response may be involved in ensuring the viability of FIG.…”

Section: Fig 3 Confirmation Of Differential Displaymentioning

confidence: 99%

Use of Differential Display Reverse Transcription-PCR To Reveal Cellular Changes during Stimuli That Result in Herpes Simplex Virus Type 1 Reactivation from Latency: Upregulation of Immediate-Early Cellular Response Genes TIS7, Interferon, and Interferon Regulatory Factor-1

Tal‐Singer

Podrzucki

Lasner

et al. 1998

J Virol

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The detailed mechanism which governs the choice between herpes simplex virus (HSV) latency and reactivation remains to be elucidated. It is probable that altered expression of cellular factors in sensory neurons leads to induction of HSV gene expression resulting in reactivation. As an approach to identify novel cellular genes which are activated or repressed by stimuli that reactivate HSV from latency and hence may play a role in viral reactivation, RNA from explanted trigeminal ganglia (TG) was analyzed by differential display reverse transcription-PCR (DDRT-PCR). Nearly 50 cDNAs whose mRNA level was modified by the stress of explantation were isolated and sequenced. We present a listing of a spectrum of altered RNAs, including both known and unknown sequences. Five of those differentially displayed transcripts were identified as interferon-related murine TIS7 mRNA. These results were confirmed in both infected and uninfected ganglia by quantitative RNase protection assay and immunostaining. Alpha and beta interferons and interferon regulatory factor-1 (IRF-1) were also induced by explantation. In addition, we have identified sequences that correspond to IRF-1 consensus binding sites in both HSV type 1 origins of replication. Our findings suggest that physiological pathways that include these cellular factors may be involved in modulating HSV reactivation.

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Interactions of Rabies Virus and Host Cells

Tsiang

1988

Developments in Veterinary Virology

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Persistent Infection of Rabies Virus (HEP-Flury Strain) in Human Neuroblastoma Cells Capable of Producing Interferon

Cited by 4 publications

References 36 publications

Persistent poliovirus infection of human neuroblastoma cells.

Persistent poliovirus infection of human neuroblastoma cells.

Use of Differential Display Reverse Transcription-PCR To Reveal Cellular Changes during Stimuli That Result in Herpes Simplex Virus Type 1 Reactivation from Latency: Upregulation of Immediate-Early Cellular Response Genes TIS7, Interferon, and Interferon Regulatory Factor-1

Interactions of Rabies Virus and Host Cells

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