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Biomedical subjects

R D Barry

Publications and source records attributed to R D Barry.

At least 37 records · Page 2Linked to original sources
PubMed1983

Characterization of human parainfluenza viruses. I. The structural proteins of parainfluenza virus 2 and their synthesis in infected cells.

Two strains of human parainfluenza virus 2 (HPV2), P2 1972/6 and P2 1980, grow to high titre in MEK3 cells, and their structural proteins and virus-induced protein synthesis have been characterized by gel electrophoresis and immunoprecipitation. Purified viruses contain seven polypeptides, including cellular actin: L (175K mol. wt.), HN (72K to 74K), NP (66K to 67K), F1 (52K to 58K), P (49K), A (44.5K) and M (39K). Virus-induced polypeptide synthesis was first detected at 8 h post-infection with the appearance of NP; other major structural proteins were detected from 10 to 12 h after infection and onwards. The synthesis of both the structural glycoproteins was demonstrated, although proteolytic processing could not be detected. Reproducible differences in the gel migration of the HN, F1 and NP polypeptides were found in whole virus, in infected cells and cells subjected to immunoprecipitation. These differences may reflect genetic diversity within HPV2 and provide a means of probing the molecular epidemiology of these viruses.

Animals↗
PubMed1975

Characterization of the mRNA of influenza virus.

The kinetics of the appearance of influenza mRNA, the distribution of mRNA between free and membrane-associated polyribosomes, its poly(A) content, and the extent to which the genome was transcribed into mRNA early in infection were determined. Polyribosomes were prepared from influenza virus-infected cells labeled for 30-min periods at various times after infection with [3H]uridine. Most of the 3H-labeled RNA extracted from these polyribosomes sedimented as a heterogeneous 8S to 20S peak in sucrose gradients, and it was largely complementary to virion RNA. By the following criteria, the complementary RNA had properties normally ascribed to mRNA: (i) it labeled rapidly with [3H]uridine; (ii) after glutaraldelyde treatment, it banded with polyribosomes in CsCl density gradients; and (iii) it contained poly(A). In chick cells at 37 C, virus mRNA was first detectable at 45 min postinfection and reached its maximal rate of appearance at 2 to 2.5 h postinfection. The free and membrane-bound polyribosomes of infected cells were separated and were found to contain the same classes of mRNA. There was no absolute segregation of mRNA sequences into either polyribosome class although each probably contained distinct ratios of the different mRNA's. From 45 min postinfection onwards, both membrane-bound and free polysomal poly(A)-containing RNA contained sequences complementary to at least 80% of the genome RNA, whereas poly(A)-minus RNA contained sequences complementary to 90 to 100% of the genome. There was no evidence for the temporal control of transcription of influenza mRNA. At 31 C, when virus development was slowed relative to 37 C,complementary RNA first appeared at 1 h postinfection. At this time, total polysomal RNA contained sequences complementary to the whole genome.

Base Sequence↗
PubMed1970

The effects of UK2054 on the multiplication of influenza viruses.

The isoquinoline compound UK2054 prevents the uptake of influenza virus by susceptible cells. Pre-incubation of virus particles with 500 mug./ml. UK2054 at 37 degrees C. for 2 hr. does not reduce virus infectivity. Host cells vary in their responsiveness to the inhibitory effect of UK2054; virus multiplication is inhibited in chick allantoic cells by lower concentrations than those required to inhibit virus growth in chick embryo fibroblasts. The effectiveness of UK2054 is reduced by the presence of serum.It is concluded that inhibition of influenza virus multiplication by UK2054 might result from interaction of the inhibitor with both virus and cells. Any direct combination between inhibitor and virus is completely reversible.

Animals↗
PubMed1970

Ribonucleic acid polymerase induced in cells infected with Sendai virus.

A ribonucleic acid (RNA)-dependent RNA polymerase was induced in chick embryo fibroblast cells after infection with Sendai virus (parainfluenza 1 virus). The enzyme was associated with the microsomal fraction of infected cells and reached maximum detectable activity at 18 hr after virus infection. The activity of the enzyme in vitro was dependent on the presence of added magnesium ions and all four nucleoside triphosphates and was not inhibited by actinomycin D. The RNA synthesized by the enzyme in vitro was sensitive to ribonuclease and consisted of a complex mixture of RNA species including 34S, 24S, and 18S components. Similar RNA components were detected in the microsomal fraction of Sendai virus-infected cells by labeling with (3)H-uridine from 17 to 18 hr postinfection in the presence of actinomycin D. Of the RNA synthesized by Sendai virus-induced RNA polymerase in vitro, 98% became insensitive to ribonuclease after annealing with RNA extracted from purified Sendai virus particles.

Animals↗