Persistent infection of cultivated cells with lymphocytic choriomeningitis virus: Regulation of virus replication
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Superinfection
Viral Interference
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Superinfection
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Lymphocytic choriomeningitis (LCM) virus infection of the mouse is the best-studied model of persistent viral infection. In cell culture, persistent LCM virus infections are associated with the production of large quantities of defective interfering (DI) LCM virus. These defective interfering particles cannot replicate by themselves yet can interfere with the replication of the standard virus and prevent the cytolytic effect caused by the standard virus. It is important to determine the mechanism of interference and to establish whether the DI virus plays a role in vivo. Biological and biochemical properties of the standard and DI virus particles and also virus enzymes are compared. Antigenic analyses reveal that cells releasing only DI virus particles have less cell surface expression of viral antigens than cells releasing the standard virus. In the animal model, the DI virus is shown to have a protective effect against the pathogenesis of the LCM virus disease both in the mouse and in the rat.
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Viral Interference
Feline leukemia virus
Superinfection
Viral transformation
Feline immunodeficiency virus
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Mumps virus
Viral Interference
Multiplicity of infection
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Superinfection exclusion or homologous interference, a phenomenon in which a primary viral infection prevents a secondary infection with the same or closely related virus, has been observed commonly for viruses in various systems, including viruses of bacteria, plants, and animals. With plant viruses, homologous interference initially was used as a test of virus relatedness to define whether two virus isolates were "strains" of the same virus or represented different viruses, and subsequently purposeful infection with a mild isolate was implemented as a protective measure against isolates of the virus causing severe disease. In this study we examined superinfection exclusion of Citrus tristeza virus (CTV), a positive-sense RNA closterovirus. Thirteen naturally occurring isolates of CTV representing five different virus strains and a set of isolates originated from virus constructs engineered based on an infectious cDNA clone of T36 isolate of CTV, including hybrids containing sequences from different isolates, were examined for their ability to prevent superinfection by another isolate of the virus. We show that superinfection exclusion occurred only between isolates of the same strain and not between isolates of different strains. When isolates of the same strain were used for sequential plant inoculation, the primary infection provided complete exclusion of the challenge isolate, whereas isolates from heterologous strains appeared to have no effect on replication, movement or systemic infection by the challenge virus. Surprisingly, substitution of extended cognate sequences from isolates of the T68 or T30 strains into T36 did not confer the ability of resulting hybrid viruses to exclude superinfection by those donor strains. Overall, these results do not appear to be explained by mechanisms proposed previously for other viruses. Moreover, these observations bring an understanding of some previously unexplained fundamental features of CTV biology and, most importantly, build a foundation for the strategy of selecting mild isolates that would efficiently exclude severe virus isolates as a practical means to control CTV diseases.
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Closterovirus
Citrus tristeza virus
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A clone of cells derived from a continuous line of cat cells (CCC) spontaneously produced an RNA C-type virus (CCC virus) which did not have the group-specific antigen of the standard strains of feline leukemia viruses but did have that of the RD-114 virus. Single-hit infection of a virus yielding CCC cell with only the feline leukemia virus pseudotype of murine sarcoma virus [MSV(FeLV)] resulted in the release of a pseudotype of MSV coated with the CCC virus envelope. Host range, transmission of virus, helper functions, interference properties, and specific neutralization showed that the CCC and the RD-114 isolates as well as their respective MSV pseudotypes are closely similar if not identical. Parental, virus-negative cells frozen before the existence of RD-114 were chemically induced to yield CCC-like virus de novo. Infection of susceptible human cells with the chemically induced virus resulted in interference with the CCC virus pseudotype of MSV but not with the FeLV pseudotype of MSV.
Viral Interference
Helper virus
Feline leukemia virus
clone (Java method)
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Superinfection
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Arenavirus
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Viral Interference
Feline leukemia virus
Superinfection
Feline immunodeficiency virus
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More than 200 cells were cloned from populations of mammalian cells persistently infected with Japanese encephalitis virus. Only four cloned cultures contained cells that had viral antigen measurable by immunofluorescence and that released infectious virus, yet all clones harbored virus-specific RNA. Superinfection of cloned cells with wild-type Japanese encephalitis virus did not produce cytopathic effects, but resulted in production of viral antigen and infectious virus in formerly nonproducing clones. Cocultivation of nonproducer clone cells with normally permissive cells did not induce virus production, nor did treatment of nonproducer clones with various inhibitors of DNA, RNA, or protein synthesis. It is suggested that the cloning procedure may have selected for a particular subpopulation of cells and that defective virus is also involved in establishment and maintenance of persistent infection.
clone (Java method)
Viral transformation
Superinfection
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Helper virus
Permissiveness
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The biological properties and in vitro growth behavior of the Snyder-Theilen strain of feline sarcoma virus (ST-FSV) were determined. The virus replicated and induced cell transformation in feline embryo fibroblast cultures as well as in heterologous host cultures of human, canine, and porcine origin. Virus stocks were found to contain an excess of an associated, noncytopathogenic virus identical with the feline leukemia virus. Focus assays in feline embryo cultures gave “nondefective” “one-hit” titration patterns. The viral envelope characteristics established by viral neutralization and viral interference tests indicated that the ST-FSV is similar or identical with the Gardner-Arnstein strain of feline sarcoma virus and is a member of the subgroup B of the feline leukemia-sarcoma viruses.
Feline leukemia virus
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Heterologous
Viral transformation
Gammaretrovirus
Picornavirus
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