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At least 469 records · Page 26Linked to original sources
PubMed1991

Characterization of herpes simplex virus type 1 DNA during latent infection in mice.

Micrococcal nuclease digestion technique in combination with spot-blotting hybridization have been used for the characterization of latent Herpes simplex virus type 1 (HSV-1) DNA in mouse brainstems. Two kinds of samples were used i.e. undigested DNA from mouse brainstems and DNA after prolonged digestion (i.e. for 30 minutes) with micrococcal nuclease from the same source. Each sample contained 5 micrograms of DNA (concentration was measured after digestion with micrococcal nuclease and isolation of DNA). Two kinds of probes were used: -virus specific probe, -host cellular probe. In the performed experiments, we observed the increased susceptibility of latent HSV-1 DNA for micrococcal nuclease digestion, comparing it to host DNA, which may reflect differences in protection of latent viral DNA by nuclear proteins and also may be associated with existing limited transcription of HSV-1 genome during latency.

Animals↗
PubMed1982

Poliovirus-induced inhibition of host RNA synthesis studied in isolated HEp-2 cell nuclei.

Nuclei isolated from uninfected HEp-2 cells synthesized RNA for 60 to 90 min. The individual RNA polymerase activities were determined by alpha-amanitin differential inhibition and the RNA products characterized by electron microscope (EM) autoradiography and sucrose gradient centrifugation. In nuclei prepared from poliovirus-infected cells, the capacity to synthesize RNA in vitro decreased with time after infection. RNA polymerase II activity (hnRNA synthesis) was preferentially inhibited more than was the polymerase I activity (rRNA synthesis). Poliovirus-infected cytoplasm (S-30) inhibited in vitro RNA synthesis in uninfected nuclei by selectively affecting the polymerase II activity. Selective inhibition of hnRNA synthesis by the crude extracts could be monitored by EM autoradiography directly. Determinations of individual RNA polymerase activities by differential alpha-amanitin inhibition were done only after treatment of the infected cytoplasm with micrococcal nuclease to abolish virus RNA replication. Selective inhibition of hnRNA synthesis depended on preincubation of the nuclei together with the infected cytoplasm, indicating that inhibitory substances from the infected cytoplasm entered the nuclei. Isolated nuclei therefore provide a useful system for studying the nature of the inhibitor(s) and of host RNA synthesis inhibition by picornaviruses.

Cell Line↗
PubMed1986

Changes in the nucleoprotein complexes of a baculovirus DNA during infection.

The nature of the DNA-protein complexes assumed by Autographa californica nuclear polyhedrosis virus (AcNPV) DNA during infection of Spodoptera frugiperda cells was investigated by micrococcal nuclease digestion of infected nuclei. Both parental viral DNA and progeny viral DNA assumed a chromatin-like structure early in infection. By late times (24 hr) p.i., the viral DNA acquired a unique nucleoprotein structure. In addition to fragments of mononucleosome size (185 bp), two subnucleosomal bands of 120 and 90 bp were observed. The subnucleosomal bands contained exclusively viral DNA. No alteration in the nature of the host chromatin structure following AcNPV infection was observed. An examination of the basic chromatin-associated proteins revealed two major viral-induced proteins having molecular weights of 15K and 39K. The induction of the basic 15K protein between 10 and 24 hr p.i. coincided with the appearance of the altered nucleoprotein structure observed by 24 hr p.i. and the cessation of histone synthesis.

Animals↗
PubMed1985

The structure of adenovirus chromatin in infected cells.

The structure of adenovirus chromatin in infected cells was studied by micrococcal nuclease digestion and hybridization with virus-specific probes. In the early phase of infection (5 h) a significant proportion of viral molecules was organized like actively transcribed cellular chromatin. As expected for a transcriptionally active population of molecules, even at high multiplicity of infection the nucleosomal repeating pattern was less distinct than in a transformed cell which contained the corresponding but less active genomic region. The observed repeating pattern in infected cells was unlikely to be due to integrated molecules since less than 0.07% of input genomes became associated with cellular DNA. After the onset of viral DNA replication, the pool of viral chromatin organized like cellular chromatin rapidly increased. In addition, newly replicated molecules also maintained the cellular chromatin-like organization as measured by [3H]thymidine incorporation after the cessation of cellular DNA synthesis. These data suggest that newly replicated viral molecules are organized by histones into cell-like chromatin throughout the infection cycle. Coincident with the peak of viral DNA and core protein synthesis, and the decline of histone synthesis, the late, core-like non-repeating viral chromatin became dominant, increasingly obscuring the underlying repeating pattern. Experiments suggest that this late chromatin is destined for encapsidation, that the early chromatin persists and that viral core proteins do not displace histones on viral DNA. A model is proposed suggesting that transcription and type I replication occur on histone-condensed templates, while type II replication products late in infection are condensed by core proteins and are destined for encapsidation.

Adenoviruses, Human↗
PubMed1986

Adenoviral protein VII packages intracellular viral DNA throughout the early phase of infection.

The proteins associated with parental, adenoviral DNA in productively-infected HeLa cells have been examined both directly and indirectly. HeLa cells infected with 32P-labelled Ad2 were irradiated with u.v. light at various points in the infectious cycle. Following degradation of the DNA, nuclear proteins carrying cross-linked nucleotides, or oligonucleotides, were distinguished from virion phosphoproteins by the resistance of their 32P radioactivity to 1 M NaOH. The major core protein of the virion, protein VII, was found to be associated with viral DNA throughout infection, even when cells were infected at a multiplicity of 0.14. Micrococcal nuclease digestion of intranuclear viral DNA 4 h after infection liberated two nucleoprotein particles containing viral DNA, neither of which co-migrated with HeLa cell mononucleosomes. These results indicate that core protein VII remains associated with parental adenoviral DNA during productive infections. The observation that protein VII can be cross-linked to DNA in cells infected at very low multiplicity, together with the results of a comparison of proteins cross-linkable to viral DNA in cells infected by wild-type virus and a non-infectious mutant containing the precursor to protein VII, suggest that nucleoproteins comprising viral DNA and protein VII must be the templates for expression of pre-early and early viral genes.

Adenoviruses, Human↗
PubMed1983

Chromatin-like structure of adeno-associated virus DNA in infected cells.

Adeno-associated virus (AAV) is a single-stranded DNA virus which requires adenovirus as a helper for productive infection. We studied whether intracellular AAV DNA in KB cells was present in a chromatin-like structure by digesting infected cell nuclei with micrococcal nuclease. Virus DNA was detected by agarose gel electrophoresis followed by blotting and hybridization to nick-translated [32P]DNA probes. After coinfection with adenovirus, AAV DNA was present in nucleosome-like structures which were similar to cell nucleosomes and were double stranded as judged by insensitivity to S1 nuclease digestion. In the absence of adenovirus, intracellular AAV DNA also formed similar nucleosome-like structures which were also insensitive to S1 digestion and were formed in both the presence and absence of hydroxyurea. These latter structures probably formed on AAV duplexes created either by reassociation of infecting parental single-stranded DNA or by covalent integration into the cell genome rather than by de novo AAV DNA synthesis. These results have implications for the mechanism of AAV genome replication, transcription, and integration into the cell genome.

Cell Line↗