Interferon production and response to exogenous interferon in two cell lines of mouse brain origin persistently infected with Sendai virus

Collins, Arlene R.; Flanagan, Thomas D.

doi:10.1007/bf01315630

Cited by 8 publications

(3 citation statements)

References 11 publications

(1 reference statement)

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“…These carrier cultures are often susceptible to crises in which most cells die due to extensive virus replication. Both interferons and defective interfering particles have been implicated in controlling the equilibrium (Collins & Flanagan, 1977). Other persistently infected cell cultures, which are probably more relevant to persistence in tissues, are characterized by infection of most, if not all of the cells.…”

Section: Introductionmentioning

confidence: 99%

Measles virus superinfection immunity and receptor redistribution in persistently infected NT2 cells

Ludlow

McQuaid

Cosby

et al. 2005

Journal of General Virology

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A recombinant measles virus (MV) expressing red fluorescent protein (MVDsRed1) was used to produce a persistently infected cell line (piNT2-MVDsRed1) from human neural precursor (NT2) cells. A similar cell line (piNT2-MVeGFP) was generated using a virus that expresses enhanced green fluorescent protein. Intracytoplasmic inclusions containing the viral nucleocapsid protein were evident in all cells and viral glycoproteins were present at the cell surface. Nevertheless, the cells did not release infectious virus nor did they fuse to generate syncytia. Uninfected NT2 cells express the MV receptor CD46 uniformly over their surface, whereas CD46 was present in cell surface aggregates in the piNT2 cells. There was no decrease in the overall amount of CD46 in piNT2 compared to NT2 cells. Cell-to-cell fusion was observed when piNT2 cells were overlaid onto confluent monolayers of MV receptor-positive cells, indicating that the viral glycoproteins were correctly folded and processed. Infectious virus was released from the underlying cells, indicating that persistence was not due to gross mutations in the virus genome. Persistently infected cells were superinfected with MV or canine distemper virus and cytopathic effects were not observed. However, mumps virus could readily infect the cells, indicating that superinfection immunity is not caused by general soluble antiviral factors. As MVeGFP and MVDsRed1 are antigenically indistinguishable but phenotypically distinct it was possible to use them to measure the degree of superinfection immunity in the absence of any cytopathic effect. Only small numbers of non-fusing green fluorescent piNT2-MVDsRed1 cells (1 : 300 000) were identified in which superinfecting MVeGFP entered, replicated and expressed its genes. INTRODUCTIONThe presence of measles virus (MV) in patients with subacute sclerosing panencephalitis (SSPE) provides a prime example of the long-term persistence of a human RNA virus. Individuals suffer a lethal condition in which the brain is heavily infected with MV containing a variety of mutations (Baczko et al., 1993). These variants are derived from the MV involved in the acute infection (Rima et al., 1997). The virus persists in an unknown site in the body for a period of two to 30 years (Modlin et al., 1977). In SSPE, the virus primarily infects neurones and oligodendrocytes in the central nervous system and months to years can pass between the onset of symptoms and death. Persistent MV infection has also been implicated in a number of other human diseases including autoimmune chronic hepatitis, Paget's disease, otosclerosis and Crohn's disease. In almost all cases the evidence for such claimed association has not been confirmed by other investigators (reviewed by Rima, 1999). Whilst in SSPE MV infection occurs primarily, though not exclusively, in non-dividing cells, infection of bone marrow precursor cells, for example osteoblasts and osteoclasts, has been implicated, though not confirmed, in diseases such as Paget's disease of bone and otosclerosis (Basle et ...

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Section: Introductionmentioning

confidence: 99%

Measles virus superinfection immunity and receptor redistribution in persistently infected NT2 cells

Ludlow

McQuaid

Cosby

et al. 2005

Journal of General Virology

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“…A variant of Sendal virus (Sendaias) was recovered from eggs inoculated with supernatant fluid from a persistently infected line of C 3I=[ mouse cells, MB/SenAs (2). The cells were derived from suckling mice infected with Sendais~ virus.…”

Section: Virusesmentioning

confidence: 99%

“…Antiserum to Sendal52 virus was prepared in rabbits and characterized as previously described (2). A guinea pig antiserum to parainfluenza type 1 (Sendal), NIH reference reagent, was used for hemolysis inhibition experiments.…”

Section: Antiserummentioning

confidence: 99%

Recovery of a Sendai virus variant with temperature-sensitive hemolytic activity from persistently infected cells from mouse brain

Collins

Flanagan

1978

Archives of Virology

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A persistently infected cell line designated MB/Senas was established by cultivation of mouse brain cells from four-day-old C3H mice infected intracerebrally at birth with 10(6) PFU of Sendai virus, strain 52. After 5 passages, 0.16 per cent of Sendai52 antiserum (containing two 50 per cent plaque reducing doses/ml of serum) was introduced into the culture medium. The addition of antiserum was accompanied by a rise in cell-associated viral antigen from a level of 5 per cent antigen positive cells to 100 per cent demonstrable by both intracellular and membrane immunofluorescence. A variant of Sendai52 virus, designated Sendaias, was recovered from MB/Senas by inoculation of supernatant medium into chick embryos. Infection of chick embryos at 37 degrees C was abortive. Fifty per cent or less of chick embryos infected at dilutions 10(-1) to 10(-9) yielded detectable virus. Hemagglutination (HA) was weak but could be improved by trypsinization of allantoic fluids. Neuraminidase (NA) activity was barely detectable. Hemolysis (HE) was absent. Propagation of Sendaias virus at 33 degrees C showed no change from weak HA and NA activities but HE activity was now apparent which was temperature sensitive. Mortality of infected chick embryos increased to 100 per cent. HE activity and lethality for chick embryos was thermolabile at 45 degrees C.

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The role of interferon in viral infections

Sonnenfeld

Merigan

1979

Springer Semin Immunopathol

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Interferon, a product of mammalian tissues, was originally described as an antiviral agent over twenty years ago. Only in the past few years has evidence started to accumulate that interferon actually played a role in vivo in natural virus infections.Initially, evidence was accumulated showing that interferon could inhibit the replication of many viruses in vitro. The interferon, through induction of a second antiviral protein, could inhibit in vitro viral transcription or translation. Later, indirect evidence for an effect of interferon on in vivo viral infections was obtained by showing that (a) a temporal relationship existed between the appearance of interferon in viral infections and the progress of the infection and (b) treatment of virally infected animals with exogenous interferon or interferon inducer often resulted in less severe infections.The most recent and direct evidence for a role for interferon in natural viral infections involves the use of an anti-interferon globulin. In several cases, injection of the anti-interferon globulin into animals infected with a wide variety of viruses resulted in a severely altered course of infection. These studies suggest that interferon is directly involved in the progress of viral infections. The involvement of the interferon in the viral infections could be a direct effect of the interferon on viral replication, or an interaction of the interferon with other host defenses, such as the immune system.

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Interferon production and response to exogenous interferon in two cell lines of mouse brain origin persistently infected with Sendai virus

Cited by 8 publications

References 11 publications

Measles virus superinfection immunity and receptor redistribution in persistently infected NT2 cells

Measles virus superinfection immunity and receptor redistribution in persistently infected NT2 cells

Recovery of a Sendai virus variant with temperature-sensitive hemolytic activity from persistently infected cells from mouse brain

The role of interferon in viral infections

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