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T Barrett

Publications and source records attributed to T Barrett.

At least 181 records · Page 10Linked to original sources

AIDS myths.

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Acquired Immunodeficiency Syndrome↗

Comparison of messenger RNAs induced in cells infected with each member of the morbillivirus group.

Virus-specific mRNAs radiolabelled with [32P]orthophosphate in the presence of actinomycin D were extracted from the cytoplasm of Vero cells infected with each of the known morbilliviruses: measles virus, canine distemper virus, rinderpest virus, and peste des petits ruminants virus. When analysed on denaturing agarose-formaldehyde gels the major RNA species from all viruses in the group were identical, except for canine distemper virus where one of the virus-specific mRNAs (mRNA 5), which probably codes for the virus haemagglutinin (S.E.H. Russell, D. K. Clarke, E. M. Hoey, B. K. Rima, S. J. Martin, J. Gen. Virol. 66, 433-441 (1985], was significantly smaller than the corresponding mRNA induced by the other viruses. Plasmid DNA containing a virus-specific insert, representing greater than 98% of the gene derived from the P-protein mRNA of canine distemper virus, showed significant cross-hybridisation with all the other members of the morbillivirus group.

Animals↗

Nucleotide sequence of the entire protein coding region of canine distemper virus polymerase-associated (P) protein mRNA.

The entire coding region of the polymerase-associated (P) protein gene of canine distemper virus has been sequenced. A single cDNA clone which represents 98% of the mRNA encoding this protein was used to determine the nucleotide sequence. The sequence predicts a major protein of 507 amino acids and a molecular weight of 54 936. There is also a second, overlapping, open reading frame with a start signal 21 bases downstream of the first AUG which could code for a protein of 174 amino acids with a predicted molecular weight of 20 292. This arrangement of the genome for the P protein of canine distemper virus is exactly analogous to that published recently for the P gene of measles virus (Bellini, W.J. et al., 1985, J. Virol. 53, 908-919). When the sequences are aligned at the first AUG, considerable homology is seen at both the nucleotide and protein sequence level.

Amino Acid Sequence↗

Epidemiologic and laboratory investigation of an outbreak of Campylobacter enteritis associated with raw milk.

An outbreak of gastroenteritis occurred in March-April 1981, in Wichita, Kansas, and involved more than 250 persons who drank raw milk from a single local dairy. Campylobacter jejuni was recovered from 60 of 116 (52%) persons in households that had one or more ill family members. A cohort study of families that belonged to a food cooperative that purchased raw milk from the implicated dairy showed a significant association between illness and having drunk raw milk. Thirty-nine of 55 (71%) persons who drank raw milk became ill compared with four of 36 (11%) persons who did not drink raw milk (p less than 0.01, t test, accounting for clustering). Peak (convalescent) antibody titers to C. jejuni, determined by indirect immunofluorescence, in 20 raw-milk drinkers showed a geometric mean of 1:27 in contrast to geometric mean titer of 1:6 in 10 well persons from the cohort who did not drink raw milk (p less than 0.002, t test). C. jejuni was recovered from 21 of 34 (66%) raw-milk drinkers, versus none of 26 people who did not drink raw milk (p less than 0.001, Fisher's exact test, one tailed). C. jejuni of the same serotype was isolated from the case-patients and from rectal swabs of cows in the dairy. These findings indicate that raw milk contaminated by Campylobacter was the vehicle for this outbreak.

Animals↗

Molecular cloning of the nucleoprotein gene of canine distemper virus.

Messenger RNAs labelled in vivo in Vero cells infected with canine distemper virus were analysed by electrophoresis on 1.5% agarose gels containing 2 M-formaldehyde. Seven virus-specific RNA bands could be distinguished which were not sensitive to actinomycin D treatment and were confined to the polyadenylated RNA fraction. The most abundant virus-specific mRNA species had a molecular weight of 0.52 X 10(6) and its coding capacity was consistent with it being the mRNA for the most abundant virus-specific protein, the nucleoprotein. Polyadenylated RNA of this size class was purified by electrophoresis on a polyacrylamide gel and cloned into the PstI site of plasmid pBR322. A virus-specific clone obtained, clone 224, was then used to select messenger RNA from infected cells. The messenger RNA selected had a molecular weight of 0.52 X 10(6) and directed the synthesis of only the virus-specific nucleoprotein when used to stimulate a wheat germ cell-free system.

Animals↗

Viruses in the etiology of atherosclerosis.

To examine the possible role of viruses in the etiology of atherosclerosis, we searched for the presence of viral genomes in arterial tissues by in situ hybridization. Because chickens infected with Marek disease virus, a herpesvirus, develop atherosclerotic lesions after infection, we looked for the presence of herpesvirus or parts thereof in human artery wall tissue, particularly in individuals with evidence of atherosclerosis. Herpesvirus probes were used on specimens of aortic wall removed from patients undergoing coronary bypass surgery. Evidence for the presence of herpes simplex viral mRNA was obtained in 13 specimens. Some of the specimens positive for herpes simplex virus appear to represent early stages in atherogenesis. Evidence for the presence of cytomegalovirus or Epstein-Barr viral genome was not observed in any of the specimens examined. We have also shown that herpes simplex virus can infect human fetal smooth muscle cells in culture. There are several ways in which viruses could operate in the pathogenesis of atherosclerosis: They could induce proliferation of artery wall intimal smooth muscle cells via injury or by genomic alterations leading to clonal expansion of intimal smooth muscle cell populations. We suggest that expression of at least a part of the herpesvirus genome in arterial smooth muscle cells may in some cases be instrumental in initiating or maintaining this enhanced cell proliferation. Furthermore, viral agents could explain other puzzling features in the occurrence of atherosclerosis and the attendant heart disease and strokes.

Animals↗

Traveler's diarrhea at sea: two multi-pathogen outbreaks caused by food eaten on shore visits.

In 1976 and 1981, two outbreaks of gastrointestinal illness aboard cruise ships occurred within 24 hours following onshore visits to Haiti and Mexico, respectively. Three hundred eighty-six of 600 (64 per cent) and 98 of 260 (38 per cent) passengers became ill following luncheons in Port-au-Prince, Haiti, and Cozumel, Mexico. No increase in illness was observed among those passengers who did not attend the onshore luncheons. In both outbreaks, unrefrigerated seafood dishes served at outdoor buffets were epidemiologically incriminated as the vehicles of transmission. Several species of Vibrion, Salmonella, and toxigenic Escherichia coli were recovered from stool specimens of ill passengers in both outbreaks. In addition, invasive Escherichia coli and Shigella were isolated from stool specimens of ill passengers who ate at the Haitian buffet. Previous investigations of outbreaks of gastrointestinal illness aboard cruise ships have implicated exposures on board as the source and have involved only a single pathogen.

Diarrhea↗

Campylobacter enteritis associated with contaminated water.

Approximately 3000 people in Bennington, Vermont, 19% of the population, had a diarrheal illness during the first and second weeks of June 1978. Persons affected reported abdominal cramps (86%), diarrhea (82%), malaise (73%), and headache (47%). The mean duration of illness was 4.6 days. The illness was associated with drinking unboiled water from the town water system. Investigation showed that the entire water system was probably contaminated and the source of contamination was the main unfiltered water source. Bolles Brook. Campylobacter fetus subspecies jejuni was cultured from 15 of 42 rectal swabs obtained from persons who had been ill, but not from swabs obtained from 23 persons who served as controls. No environmental samples of water and no specimens from wild or domestic animals were positive for Campylobacter. This appears to be the first waterborne outbreak of gastroenteritis associated with C. fetus subspecies jejuni.

Adult↗

Non-O group 1 Vibrio cholerae gastroenteritis associated with eating raw oysters.

A cluster of five cases of non-O group 1 (non-O1) V. cholerae gastroenteritis occurred in one Florida locality during November 1979. Clinical findings included nausea, vomiting, and abdominal cramping in all affected persons; two had bloody diarrhea. All five persons gave a history of eating raw oysters within four days of onset of illness. A case-control study statistically associated the eating of raw oysters with development of illness (p = 0.0008); this finding was confirmed by a retrospective cohort study of patients hospitalized for diarrhea (p = 0.0001). Non-O1 V. cholerae organisms were isolated from oysters and water samples taken from areas where ill persons had obtained their oysters. In at least one instance the same serotype was isolated from a patient's stool specimen and from the water where the patient had obtained oysters. Non-O1 V. cholerae infection must be considered in the differential diagnosis of shellfish-associated gastroenteritis.

Adult↗

Influence of the host cell on influenza virus replication.

The replication of influenza virus is characterized by a unique dependence upon host cell nuclear function. In contrast to all other negative strand RNA viruses, transcription from host cellular DNA is a prerequisite for the synthesis of virus-specific messenger RNA; new DNA synthesis is not required. We have analysed the distribution of each of the nine virus-specified proteins between the nucleus and cytoplasm of virus-infected cells, and find that in addition of the NP and the NS1 proteins, two of the three P proteins show preferential migration into the nucleus. This subgroup of virus proteins may be involved in the early transcription of the viral genome which probably occurs in the nucleus. In non-permissive cell lines and in cells whose DNA function has been impaired by treatment with ultraviolet light, N-acetoxyacetaminofluorene or low doses of actinomycin D, production of some late virus proteins is inhibited. The specific host function required for this switch to late protein synthesis is unknown but in the cells treated with actinomycin D an abnormal accumulation of virus-specific mRNA occurs in the nucleus. In all cases studied, synthesis of new vRNA ceases when production of these late proteins has been blocked.

Animals↗

Influenza virus-specific RNA and protein syntheses in cells infected with temperature-sensitive mutants defective in the genome segment encoding nonstructural proteins.

Virus-specific protein and RNA syntheses have been analyzed in chicken embryo fibroblast cells infected with two group IV temperature-sensitive (ts) mutants of influenza A (fowl plague) virus in which the ts lesion maps in RNA segment 8 (J. W. Almond, D. McGeoch, and R. D. Barry, Virology 92:416-427, 1979), known to code to code for two nonstructural proteins, NS1 and NS2. Both mutants induced the synthesis of similar amounts of all the early virus-specific proteins (P1, P2, P3, NP, and NS1) at temperatures that were either permissive (34 degrees C) or nonpermissive (40.5 degrees C) for replication. However, the synthesis of M protein, which normally accumulates late in infection, was greatly reduced in ts mutant-infected cells at 40.5 degrees C compared to 34 degrees C. The NS2 protein was not detected at either temperature in cells infected with one mutant (mN3), and was detected only at the permissive temperature in cells infected with mutant ts47. There was no overall reduction in polyadenylated (A+) complementary RNA, which functions as mRNA, in cells infected with these mutants at 40.5 degrees C compared to 34 degrees C, nor was there any evidence of selective accumulation of this type of RNA within the nucleus at the nonpermissive temperature. No significant differences in ts mutant virion RNA transcriptase activity were detected by assays in vitro at 31 and 40.5 degrees C compared to wild-type virus. Virus-specific non-polyadenylated (A-) complementary RNA, which is believed to act as the template for new virion RNA production, accumulated normally in cells at both 34 and 40.5 degrees C, but at 40.5 degrees C accumulation of new virion RNA was reduced by greater than 90% when compared to accumulation at 34 degrees C.

Animals↗

Splicing in vitro?

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Base Sequence↗

The smallest genome RNA segment of influenza virus contains two genes that may overlap.

The genome of influenza virus consists of eight segments of single-stranded RNA, each of which encodes a different polypeptide. In addition to the eight recognized gene products, the virus specifies a distinct smaller nonstructural polypeptide (NS2), which is translated from a separate species of virus-specific mRNA. The location on the virus genome of the gene encoding this polypeptide was investigated by hybridization of the NS2 mRNA with isolated subgenomic RNA species, and by correlation of the inheritance of a strain-specific NS2 with inheritance of particular genome RNA segments during recombination between two different virus strains. The genetic information for NS2 was found to reside in the smallest genome RNA segment of the virion, which also encodes the NS1 polypeptide. Considering the sizes of the molecules involved, it is likely that the coding sequences for the two polypeptides overlap.

Genes, Viral↗