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An avian oncovirus mutant (SE 21Q1b) deficient in genomic RNA: biological and biochemical characterization

M Linial, E Medeiros, W S Hayward

    Cell
    |December 1, 1978
    PubMed

    Insights

    Researchers identified a Rous sarcoma virus mutant (SE 21Q1b) that fails to package its own RNA, instead packaging cellular RNA. This RNA packaging defect prevents viral replication and transformation, highlighting a critical step in retroviral assembly.

    Area of Science:

    • Virology
    • Molecular Biology
    • Genetics

    Background:

    • Avian retroviruses, such as Prague Rous Sarcoma Virus (PR-RSV-E), are crucial tools for studying cell transformation and viral replication.
    • Viral RNA packaging is a complex process essential for the assembly of infectious virions.
    • Understanding mutations affecting RNA packaging can elucidate the mechanisms of retroviral assembly and host-cell interactions.

    Purpose of the Study:

    • To characterize a novel nonconditional mutant of PR-RSV-E, designated SE 21Q1b, with distinct properties related to viral particle formation.
    • To investigate the molecular basis for the observed defect in RNA packaging and its impact on viral infectivity.
    • To explore the consequences of this packaging defect on viral gene expression and the potential for genetic rescue.

    Main Methods:

    • Isolation and continuous culture of a PR-RSV-E mutant (SE 21Q1b) from transformed quail cells.
    • Analysis of viral particle composition, including RNA content and protein components.
    • Infectivity assays to assess the transformation and replication potential of SE 21Q1b virions.
    • Superinfection experiments with other retroviruses to evaluate genetic rescue and packaging interference.

    Main Results:

    • SE 21Q1b virions are produced by continuously growing transformed quail cells but are unable to infect or replicate in other cells.
    • These virions contain cellular RNAs and 4S RNA instead of the genomic 39S RNA, indicating a failure in specific viral RNA packaging.
    • Viral proteins and RNA-dependent DNA polymerase within SE 21Q1b virions are functional, and viral RNAs are synthesized and translated in producer cells.
    • Superinfection allows packaging of superinfecting viral RNA but does not rescue SE 21Q1b genetic markers or correct the aberrant cellular RNA packaging.

    Conclusions:

    • SE 21Q1b represents an RNA packaging mutant of PR-RSV-E, characterized by the preferential packaging of cellular RNAs over viral genomic RNA.
    • The mutation likely involves a defect in a signal required for efficient genomic RNA packaging or an altered packaging factor with changed specificity.
    • This mutant provides a valuable model for studying the mechanisms of retroviral RNA selection and packaging, and the interplay between viral and cellular RNAs.

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