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Updated: Sep 2, 2026

MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
INTRACELLULAR FATE OF MENGO VIRUS RIBONUCLEIC ACID
Abstract:
Homma, M. (The Wistar Institute, Philadelphia, Pa.), and A. F. Graham. Intracellular fate of Mengo virus ribonucleic acid. J. Bacteriol. 89:64-73. 1965.-P(32)-labeled, purified preparations of Mengo virus adsorbed rapidly and irreversibly to L cells maintained in suspension cultures. At intervals after adsorption of labeled virus, the total ribonucleic acid (RNA) of infected cells was extracted by a phenol technique. Infectivity titrations on this RNA showed that it retained its full biological activity during the early part of the eclipse period. Sucrose gradient sedimentation analyses showed also that this RNA lost none of its structural integrity throughout the eclipse period. No evidence was found for a double-stranded structure involving parental RNA. When cells infected with P(32)-labeled virus were broken open during the first 7 hr after infection, no more than 20% of the parental RNA could be digested with ribonuclease. Electron microscopy indicated that only one particle in five of the purified viral populations was infectious. It is suggested that only one of five adsorbed virus particles was uncoated and that its RNA remained in the cell in an undegraded form during the eclipse period. The other adsorbed particles were not uncoated and took no part in the process of infection. The maximal transfer of parental RNA to progeny virus was 4.5%.
Insights
Mengo virus ribonucleic acid (RNA) remained intact and infectious within host cells during the early infection phase. Only a fraction of adsorbed virus particles successfully delivered their RNA for replication, suggesting a selective uncoating process.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Mengo virus infection involves the entry of viral ribonucleic acid (RNA) into host cells.
- Understanding the intracellular fate of viral RNA is crucial for comprehending viral replication cycles.
- The early stages of viral infection, including the eclipse period, are critical for establishing infection.
Purpose of the Study:
- To investigate the intracellular fate and biological activity of Mengo virus RNA after adsorption to host cells.
- To determine if parental viral RNA remains intact and functional during the early stages of infection.
- To explore the uncoating process and the role of parental RNA in Mengo virus infection.
Main Methods:
- Labeling purified Mengo virus with P(32) for tracking.
- Adsorption of labeled virus to L cells in suspension culture.
- Extraction of total cellular RNA using a phenol technique at various time points.
- Infectivity titrations to assess RNA biological activity.
- Sucrose gradient sedimentation to analyze RNA structural integrity.
- Ribonuclease digestion assays to evaluate RNA degradation.
- Electron microscopy to assess viral particle infectivity.
Main Results:
- P(32)-labeled Mengo virus adsorbed rapidly and irreversibly to L cells.
- Extracted RNA retained full biological activity and structural integrity throughout the early eclipse period.
- No evidence of a double-stranded structure involving parental RNA was found.
- Less than 20% of parental RNA was susceptible to ribonuclease digestion within 7 hours post-infection.
- Electron microscopy revealed only 20% of purified viral particles were infectious.
- A maximum of 4.5% of parental RNA was transferred to progeny virus.
Conclusions:
- Mengo virus RNA remains undegraded and biologically active within the host cell during the early eclipse period.
- A significant portion of adsorbed virus particles may not undergo uncoating, with only a fraction delivering functional RNA.
- The findings suggest a selective uncoating mechanism, where only infectious viral particles contribute their RNA to the infection process.
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