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Biomedical subjects

R W Darlington

Publications and source records attributed to R W Darlington.

At least 19 recordsLinked to original sources
PubMed1981

Serologic and molecular comparisons of several equine herpesvirus type 1 strains.

The molecular and serologic relatedness of 2 recent respiratory tract isolates of equine herpesvirus type 1, designated T1 and T2, were compared with the Army 183, Kentucky-A hamster-adapted (KyA-ha), and L-M cell-adapted (KyA-LM) strains. Electrophoresis in polyacrylamide gels revealed differences in virion structural proteins among 4 purified strains. Seven envelope glycoproteins (molecular weight of 93,000, 65,000, 62,000, 60,000, 36,000, 20,000, and 18,000) corresponding to virion proteins 13, 16, 17, 18, 23, 25, and 26a, respectively, found in both the Army 183 and KyA-ha strains had slightly different molecular weight counterparts in both the T1 and T2 isolates, which had identical structural protein profiles. virion protein 19 (58,000 daltons), a nonglycosylated protein, was present in reduced amounts in the respiratory tract isolates, whereas virion protein 8a (200,000 daltons) was absent. Virion protein 8a, an envelope glycoprotein, was only present in the KyA-ha strain. The T1 and T2 isolates were not neutralized by equine herpesvirus type 2 antiserum and revealed little cross-neutralizatio with the Army 183 and KyA-ha strains in plaque-reduction neutralization tests. Restriction endonuclease cleavage maps of viral DNA revealed a similar, but not identical, number and size of DNA fragments between T1 and T2 isolates. Likewise, DNa profiles of Army 183, KyA-ha, and KyA-LM were also similar to each other, but vastly different from the respiratory tract isolates.

Animals↗
PubMed1980

Rotavirus infection in foals.

Fecal samples from 86 foals with diarrhea were examined by electron microscopy during a 2.5 year period. Of these, 26 (30%) were positive for rotavirus. All of the cases were found in epizootic areas. The disease was produced in an experimental foal by inoculation via stomach tube of a bacteria-free fecal filtrate containing rotavirus. Examination of postmortem tissues from the duodenum and jejunum of 2 naturally infected foals and an experimentally infected foal revealed replicating virus in the intestinal epithelial cells. A limited survey of complement-fixing antibody to rotavirus in horses from Kentucky, Virginia, and France indicated that all horses had antibody to the virus. The sole exception was 1 foal from which blood samples were collected prior to suckling. These results were presumptive evidence that rotavirus is a major cause of diarrhea in foals, and the presence of antibody in horses from diverse areas is evidence for the ubiquitousness of this infection.

Animals↗
PubMed1979

Variable infection of Vero cells and homologous interference after co-cultivation with HeLa cells with persistent defective infection by Edmonston measles virus.

The HeLa subline K11A-HG-1 (line of HeLa cells persistently infected with Edomonston measles virus but containing little or no transmissible infectious virus) was co-cultivated with Vero cells. Focal syncytia were formed containing measles antigen and accumulations of nucleocapsid-like structures with no detectable production of transmissible infectious virus or positive hemadsorption. The infection aborted between 2 and 3 weeks after preparation of co-cultures. Upon subculture of co-cultures, occasionally complete infections (progressive syncytial degeneration, hemadsorption, and production of transmissible infectious virus) appeared. A linear dose response curve for nontransmissible infection was obtained along with evidence that measles antigen had to be present on the surface of K11A-HG-1 cells for their infectivity for Vero cells. The basis for initiation of Vero cell infection by living K11A-HG-1 cells, but not by nonviable intact K11A-HG-1 cells killed by a virus-preserving technique, nor by disrupted K11A-HG-1 cells, is, at present, a matter of speculation. However, several lines of evidence were obtained which suggested that subsequent development of delayed variable transmissible Vero cell infection occurred because of a type of viral interference, including the presence of an inhibitor in K11A-HG-1 cultures, the bulk of which was cell-associated.

Antigens, Surface↗
PubMed1975

Evaluation of topical polyinosinic acid-polycytidylic acid in treatment of localized herpes zoster in children with cancer: a randomized, double-blind controlled study.

Twenty-four children with cancer and localized herpes zoster were randomized to receive either topical polyinosinic acid-polycytidylic acid [poly(I:C)] or a saline placebo. Solutions containing 1.0 or 2.5 mg of drug per ml were applied to the lesions every 3 h, seven times a day for 7 consecutive days. Serial, standardized color photographs were used to evaluate the progression of lesions and maximum percentage of dermatome involvement. In patients receiving poly(I:C), the median days of new lesions after therapy was 2.0 days as opposed to 3.5 days in placebo-treated patients. This difference was not statistically significant. Moreover, the total median days of lesions and percentage of dermatome involvement were similar in both groups, as were complications. Neither the concentration nor the total dose of drug was related to the outcome of infection. We conclude that topical poly(I:C), as used in this study, was of no benefit in treatment of localized herpes zoster.

Administration, Topical↗
PubMed1974

The presence of the Lucké herpesvirus genome in induced tadpole tumors and its oncogenicity: Koch-Henle postulates fulfilled.

Herpesvirus extracted from a naturally occurring frog renal carcinoma (Lucké tumor) induced virus-free Lucké tumors in developing frogs. Herpesvirus recovered from an induced tumor after incubation at low temperature of tumor fragments cultured in vitro was oncogenic when injected into developing frog embryos. With the exception of the "pure culture" requirement, this experiment fulfills Koch-Henle postulates for the identification of the causative agent of the Lucké tumor.

Adenocarcinoma↗
PubMed1972

Sendai virus-induced transcriptase from infected cells: polypeptides in the transcriptive complex.

A Sendai virus-induced transcriptase-template complex was isolated from the cytoplasm of infected cells by combined sedimentation and isopycnic centrifugation. This transcriptive complex banded at 1.27 g/cm(3) in D(2)O-sucrose gradients. It contained two polypeptides, the viral nucleocapsid structure unit (molecular weight, 60,000) and the largest virion polypeptide (molecular weight, 75,000). The buoyant density, chemical composition, and electron microscopic appearance of the transcriptive complex indicate a structure like that of viral nucleocapsids.

Animals↗
PubMed1971

Channel catfish virus: a new herpesvirus of ictalurid fish.

Channel catfish virus was studied in ictalurid fish cell culture, the only system of fish, amphibian, avian, and mammalian cells found to be susceptible. Channel catfish virus infection resulted in intranuclear inclusions and extensive syncytium formation. Replication occurred from 10 to 33 C, but not higher. Best growth was from 25 to 33 C, and the amount of virus released nearly equalled the amount which remained cell-associated. The virus was labile to lipid solvents, and indirect determinations with labeled precursors and a metabolic inhibitor showed evidence of deoxyribonucleic acid. Electron microscopy showed progeny virus, about 100 nm in diameter, in various stages of development in cell nuclei by 4 hr. Present also were nuclear masses of exceptionally electron-dense lamellar material, with a unit dimension of 10 to 15 nm. Virus was enveloped at the nuclear membrane and in cytoplasmic vacuoles, resulting in virions having a diameter of 175 to 200 nm. Negative staining demonstrated icosehedral symmetry and 162 capsomeres. Our data indicate that channel catfish virus is a herpesvirus.

Animals↗
PubMed1969

Disruption of myxoviruses with Tween 20 and isolation of biologically active hemagglutinin and neuraminidase subunits.

Myxoviruses were disrupted with Tween 20 at high pH, and the major surface antigens were separated in biologically active form. The neuraminidase had a sedimentation coefficient of 10.8S, and the hemagglutinin had a sedimentation coefficient of 8.1S. Electron microscopic examination of negatively stained preparations revealed structures identical in size and morphology to the neuraminidase and hemagglutinin subunits described by others. Inhibition of neuraminidase activity by antibody to the hemagglutinin which occurred with intact viruses (probably for "steric" reasons) did not occur after the viruses were disrupted with Tween 20. Serological assays for neuraminidase were possible in the presence of the mild surfactant, whereas serological assays for hemagglutinin were possible after removal of the reagent. Disruption of myxoviruses with Tween 20 therefore provides a method for the independent study of these antigens during antigenic drift.

Animals↗
PubMed1968

Herpesvirus envelopment.

The growth and envelopment processes of three representative herpesviruses, equine abortion, pseudorabies, and herpes simplex, were examined in baby hamster kidney (BHK 21/13) cells by bioassay (plaque-forming units) and electron microscopy. The envelopment process was identical for all three viruses. After assembly in the nucleus, the nucleocapsid acquired an envelope by budding from the inner nuclear membrane. This membrane was reduplicated as the enveloped particle was released so that the budding process did not result in disruption of the continuity of the nuclear membrane. That portion of the nuclear membrane which comprised the viral envelope was appreciably thicker than the remainder of the membrane and exhibited numerous projections on its surface. Once enveloped, the viral particles were seen in vesicles and vacuoles in the cell cytoplasm. These appeared to open at the cytoplasmic membrane, releasing the virus from the cell. There was no detectable difference in the size or appearance of enveloped particles in intra- or extracellular locations.

Animals↗
PubMed1968

Isolation and properties of Newcastle disease virus nucleocapsid.

Deoxycholate (DOC) disrupted virions of Newcastle disease virus (NDV), releasing viral nucleocapsids. The nucleocapsids sedimented at about 200S in sucrose gradients and measured from 1.3 to 1.4 mu long by electron microscopy. NDV nucleo-capsids were resistant to pancreatic ribonuclease. These nucleocapsids contained all the 50S ribonucleic acid (RNA) in NDV virions, while virus-associated RNA sedimenting at less than 50S was external to the virions.

Bile Acids and Salts↗