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ABSTRACT: The mechanism of blocked replication of human adenoviruses in monkey cells was examined. Previous experiments have placed the replicative block at the level of transcription of translation of adenovirus mRNA. Coinfection of the monkey cells with simian virus 40 enhances adenovirus replication in these cells. We compared the adenovirus mRNA transcribed during infection of permissive human cells and enhanced and unenhanced monkey cells. Adenovirus mRNA from enhanced monkey cells appeared to be identical to adenovirus mRNA from human cells. This indicated that simian virus 40 coinfection did not overcome the blocked replication by substituting for a missing adenovirus transcript. Comparison of adenovirus mRNA from enhanced and unenhanced monkey cell infection revealed two types of transcriptional discrepancies. There was a decrease in both the complexity and the relative abundance of several regions of the enhanced adenovirus mRNA. However, neigher of these transcriptional defects was sufficient to totally explain the difference in yield of infectious virus and viral protein seen in these two types of infection.
Journal of Virology 08/1978; 27(1):136-48. · 5.40 Impact Factor
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S G Baum
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ABSTRACT: Persisten infections of monkey cells have been established by using two serotypes of human adenovirus. The persistently infected cells show no morpho logical changes, but continue ot produce low titers of infectious adenovirus. The inapparent infection can, at any time, be converted to a cytolytic productive one by superinfection with simian virus 40. Persistence in this system does not appear to result from multiple rounds of lytic infection, nor is it mediated by production of defective interfering particles. The persistently infected cells do not possess the characteristics of oncogenic transformation. Results of these studies also whow that the nonpermissiveness of monkey cells to adenovirus replication can be partially overcome by infection at high multiplicity.
Journal of Virology 09/1977; 23(2):412-20. · 5.40 Impact Factor
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Cold Spring Harbor Symposia on Quantitative Biology 02/1975; 39 Pt 1:567-73.
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ABSTRACT: Events occurring during the abortive infection of monkey cells by human adenoviruses have been compared to those occurring during the complete replicative cycle which results from adenovirus and SV40 coinfection of these cells. Previous studies had indicated a block to replication at a posttranscriptional level. This paper describes the examination of two posttranscriptional events: attachment of polyadenylic acid sequences to adenovirus mRNA, and association of this mRNA with polyribosomes. Posttranscriptional addition of poly(A) sequences to mRNA appears to take place normally in the absence of SV40 coinfection. “Late” adenovirus mRNA, though synthesized in the nonpermissive infection, appears to be deficient in its association with polyribosomes. This finding is consistent with the previously described defect in late adenovirus protein synthesis in the unenhanced infection of monkey cells.
Virology 08/1974; 60(1):45-53. · 3.35 Impact Factor
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ABSTRACT: Adenovirus type 2 DNA synthesis, either in permissive human cells or nonpermissive monkey cells, becomes independent of protein synthesis after the appearance of progeny viral DNA. In the presence of cycloheximide, semiconservative replication and initiation of progeny molecules can occur.
Journal of Virology 05/1973; 11(4):544-51. · 5.40 Impact Factor
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ABSTRACT: The defect which prevents human adenovirus replication in monkey cells and the mechanism whereby this restriction is overcome by coinfection with simian virus 40 (SV40) have been studied. Adenovirus capsid proteins are not synthesized efficiently in monkey cells in the absence of SV40. Adenovirus "enhancement" by SV40 was found to be the product of increased efficiency of replication by a small percentage of cells. This enhancement effect apparently occurred only when SV40 and adenovirus infected the same cells. These findings suggest that the replicative block occurs prior to virion assembly, and an accompanying report seeks to locate the site of restriction more precisely at the post-transcriptional level.
Journal of Virology 09/1972; 10(2):211-9. · 5.40 Impact Factor
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ABSTRACT: The mechanism by which simian virus 40 converts the abortive adenovirus type 7 infection of monkey cells into an efficient lytic infection has been investigated. Analysis of ribonucleic acid (RNA) synthesis during unenhanced and enhanced infection of monkey cells has shown that adenovirus RNA synthesized in the abortive infection contains both "early" and "late" sequences. In hybridization competition experiments, early adenovirus RNA from human cells prevented the hybridization of only 20% of the adenovirus RNA transcribed in unenhanced infection. Further, the RNA from unenhanced cells was able to completely block the hybridization of RNA synthesized during enhanced infection. Finally, virus-associated RNA, which is a late RNA transcribed in lytic adenovirus infection, is also produced in the unenhanced infection. An accompanying paper describes a marked deficiency in adenoviral capsid protein synthesis in the unenhanced infection. We conclude that RNA sequences, which are sufficient to code for the synthesis and assembly of structural proteins of adenovirus, are transcribed but are not efficiently translated in the unenhanced adenovirus infection of monkey cells.
Journal of Virology 09/1972; 10(2):220-7. · 5.40 Impact Factor
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ABSTRACT: The DNA and protein components of the adenovirus 7-simian virus (SV)40 hybrid virus "E46(+)" have been investigated. The Ad.7-SV40 hybrid DNA genome could be distinguished from nonhybrid Ad. 7 genome on the basis of its molecular weight in an alkaline sucrose gradient. The hybrid genome could also be separated from nonhybrid adenovirus 2 DNA when purified transcapsidant adenovirus 2(+t7) (Ad.7-SV40 DNA within an Ad.2 capsid) was studied. The presence and amount of SV40 DNA in the hybrid virus genome was determined by DNA-RNA hybridization. The results presented suggest: (i) that about 10% of the particles in the E46(+) preparations contained SV40 DNA covalently linked to adenovirus DNA; (ii) that the hybrid virus genome has a molecular weight 10-12% lower than that of nonhybrid virus, consistent with a deletion of adenovirus DNA; and (iii) that the hybrid virus contained only 40-50% of a total SV40 genome. The protein components of the Ad.7-SV40 hybrid virus were examined by acrylamide gel electrophoresis in sodium dodecyl sulfate. No significant quantitative or qualitative differences between the proteins of hybrid and nonhybrid adenovirus were demonstrated.
Proceedings of the National Academy of Sciences 08/1971; 68(7):1525-9. · 9.68 Impact Factor
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Virology 03/1968; 34(2):373-6. · 3.35 Impact Factor
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Proceedings of the National Academy of Sciences 12/1966; 56(5):1509-15. · 9.68 Impact Factor
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Proceedings of the National Academy of Sciences 03/1966; 55(2):336-41. · 9.68 Impact Factor
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Proceedings of the National Academy of Sciences 01/1965; 52:1340-7. · 9.68 Impact Factor
