Further studies on an inhibitor of viral activity appearing in infected cell cultures and its role in chronic viral infections

Ho, Monto; Enders, John F.

doi:10.1016/0042-6822(59)90135-7

Cited by 139 publications

(54 citation statements)

References 8 publications

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“…In long-term persistence in BHK21 cells established using VSV virions and defective-interfering (DI) particles, Holland et al (1976) found that ts and small plaque mutants evolved which contributed to the stability of persistence. For many years a role for interferon in establishment and/or maintenance of persistent infections has also been proposed by several investigators working with influenza virus type A, NDV, mumps virus (Henle et al, 1959), poliovirus (Ho & Enders, 1959), vaccinia virus (Glasgow & Habel, 1962), Sindbis virus (Enzmann, 1973) and VSV (Nishiyama, 1977). Recently, Sekellick & Marcus (1978, 1979 have proposed that induction of interferon may occur by DI particles or by ts mutants, and that these dual factors may play a synchronous role in VSV persistence.…”

Section: Introductionmentioning

confidence: 99%

Chronic Production of Defective-interfering Particles by Hamster Embryo Cultures of Herpesvirus Persistently Infected and Oncogenically Transformed Cells

Dauenhauer

Robinson

O’Callaghan

1982

Journal of General Virology

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SUMMARYHighly passaged defective-interfering (DI) particle preparations of equine herpesvirus type 1 (EHV-1) were found to mediate the co-establishment of persistent infection and oncogenic transformation of permissive hamster embryo cells. Four cell lines, designated DI-1 to DI-4, were shown to possess biological properties typical of transformed cells and to induce the rapid formation of metastatic fibrosarcomas when injected into syngeneic LSH hamsters. Corresponding DI tumour cell lines, designated DI-1T to DI-4T, were found to be virus non-producing, to be transplantable in the hamster, and, like the four parent DI cell lines, to express EHV-1-coded antigens and to be resistant to superinfection with EHV-1 but not with a heterologous virus, vesicular stomatitis virus. All transformed cell lines, but not the tumour cell lines, contained a population of cells (2.6 to 9%) that continued to release infectious virus after 100 passages in culture. The production of interferon and selection of temperature-sensitive mutants did not appear to play a role in the maintenance of persistent infection. However, it was demonstrated that these persistently infected cells continued to release not only infectious virus but also DI particles after more than 2 years in culture. DI particles were shown to be present in released virus by: (i) detection of the defective virus DNA species (density 1-724 g/ml; standard EHV-1, density 1.716 g/ml) by CsCI analytical ultracentrifugation techniques; (ii) measurement of interference activity of virus released from DI-I to DI-4 cells against standard EHV-1 replication; (iii) the presence of the 35 megadalton BgllI fragment unique to the DI particle genome in DNA of released virus. These studies indicate that herpesvirus DI particles may function both in the initiation and maintenance of persistent infection and alter the cytocidal effects of infection to allow the establishment of oncogenic transformation and persistent infection.

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Section: Introductionmentioning

confidence: 99%

Chronic Production of Defective-interfering Particles by Hamster Embryo Cultures of Herpesvirus Persistently Infected and Oncogenically Transformed Cells

Dauenhauer

Robinson

O’Callaghan

1982

Journal of General Virology

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“…These include inhibition of cytopathic effect, plaque reduction and inhibition of virus yield (Glasgow et al, 1967;Lerner & Baily, 1976;Rasmussen & Farley, 1975). Although some of the early reports suggested that herpesviruses were not sensitive to IFN (Ho & Enders, 1959;Glasgow et al, 1967), more recent studies have indicated that virus yields are reduced in IFNtreated cells (Rasmussen & Farley, 1975). Nonetheless, relatively high concentrations of IFN were required for this effect as compared with other virus groups.…”

Section: Introductionmentioning

confidence: 99%

Inhibition by Interferon of Herpes Simplex Virus Thymidine Kinase and DNA Polymerase in Infected and Biochemically Transformed Cells

Panet

Falk

1983

Journal of General Virology

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SUMMARYThe induction of thymidine kinase (TK) and DNA polymerase was inhibited by interferon (IFN) in mouse L-cells infected with herpes simplex virus type 1 (HSV-1). The inhibitory activity of IFN at this early stage of HSV-1 replication was followed by a reduced virus yield and was dependent on the multiplicity of infection.The expression of a cloned thymidine kinase (tk) gene of HSV-1, in biochemically transformed L-cells (LTK+), was not affected by IFN. These same LTK + cells, however, developed an antiviral state since, upon HSV-1 infection, the induction of TK and DNA polymerase of the replicating virus was inhibited by IFN. Furthermore, IFN inhibited the transactivation of the HSV-1 tk gene in the biochemicaUy transformed LTK + cells, which followed infection by a virus mutant defective in the tk gene (HSV-1 TK-). This transactivation is dependent on expression of immediate-early HSV-1 s-genes. These results indicate that IFN inhibits HSV-I replication at an early step prior to DNA synthesis. In addition, IFN displays a differential effect on the HSV-1 thymidine kinase gene, either when part of the replicating virus or when expressed as a cellular gene in biochemically transformed cells.

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“…Members of the herpesvirus group have generally been regarded as being only moderately susceptible to the effects of interferon when compared with other viruses (5,8,14). It has also been reported that type 2 strains of herpes simplex virus (HSV) are more susceptible to the action of interferon and an interferon inducer than HSV type 1 isolates (8,9) and that another member of the herpesvirus group, cytomegalovirus (CMV), is more resistant to the effects of interferon than HSV (3).…”

mentioning

confidence: 99%

Treatment of a Murine Cytomegalovirus Infection with Exogenous Interferon, Polyinosinic-Polycytidylic Acid, and Polyinosinic-Polycytidylic Acid–Poly- l -Lysine Complex

Kern

Olsen

Overall

et al. 1978

Antimicrob Agents Chemother

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Further studies on an inhibitor of viral activity appearing in infected cell cultures and its role in chronic viral infections

Cited by 139 publications

References 8 publications

Chronic Production of Defective-interfering Particles by Hamster Embryo Cultures of Herpesvirus Persistently Infected and Oncogenically Transformed Cells

Chronic Production of Defective-interfering Particles by Hamster Embryo Cultures of Herpesvirus Persistently Infected and Oncogenically Transformed Cells

Inhibition by Interferon of Herpes Simplex Virus Thymidine Kinase and DNA Polymerase in Infected and Biochemically Transformed Cells

Treatment of a Murine Cytomegalovirus Infection with Exogenous Interferon, Polyinosinic-Polycytidylic Acid, and Polyinosinic-Polycytidylic Acid–Poly- l -Lysine Complex

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