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Biomedical subjects

J S Guy

Publications and source records attributed to J S Guy.

At least 19 recordsLinked to original sources

Reactivation of latent pseudorabies virus infection in vaccinated commercial sows.

Pseudorabies virus (PRV) was isolated from 9 of 44 PRV-vaccinated seropositive sows on 5 of 11 farms. Although serum-neutralization antibody titers were 1:16 to 1:256, 28 virus isolates were obtained from tonsil, nasal, or buccal swab samples from 9 sows given 2 ml of dexamethasone/kg of body weight IM for 5 days. Pseudorabies virus was isolated from 6 of 20 sows (3 of 5 farms) given a killed-virus vaccination. Virus was obtained from 3 of 24 sows (2 of 6 farms) given modified-live virus and killed-virus vaccination. Evaluation of the 9 PRV with 5 restriction endonucleases revealed 4 PRV existing genotypes. The 9 isolated types of PRV appeared to be indistinguishable by Kpn I and BamHI restriction endonuclease analysis; however, when analyzed with Sal I, HinfI, and Pst I, isolates 7 (farm D), 8 (farm C), and 9 (farm B) had numerous differences. Isolates 1, 2, 3, and 4 (farm F) and 5 and 6 (farm G) appeared to be the same genotype when further analyzed with Pst I, HinfI, and Sal I.

Animals

Discovery of noninfectious viral genes complementary to Marek's disease herpes virus in quail susceptible to cholesterol-induced atherosclerosis.

Japanese quail genetically selected on the basis of atherosclerosis susceptibility were tested for infection by Marek's disease herpesvirus (MDV). Viral DNA was detected in the atherosclerotic aortas of susceptible (SUS) quail by the technique of DNA hybridization. Southern blot analysis demonstrated that restriction mapping of aortic DNA was specific and different from that of MDV. Screening of quail embryos by dot-blot hybridization detected that MDV DNA existed in 100% of SUS quail tested. Resistant (RES) quail were a mixed population, with 16% of embryos resembling the SUS group. Functional MDV was not found by a number of methods including virus isolation, serological test, and exposure of sentinel chicks to SUS quail. These results suggest that the SUS quail possess a portion of the MDV genome in the germline, and the viral genes have been coselected by their susceptibility to cholesterol-induced atherosclerosis.

Animals

Experimental ocular herpesvirus infection in the cat. Sites of virus replication, clinical features and effects of corticosteroid administration.

Experimentally induced ocular feline herpesvirus 1 (FHV-1) infection was studied in 30 specific pathogen-free cats. In ten cats, the ability of five field isolates of FHV-1 to replicate in the epithelium and substantia propria of cornea and conjunctiva was demonstrated by histochemical techniques. Feline herpesvirus 1 was found to preferentially infect and induce necrosis of conjunctival epithelium. Although significant histologic lesions were not induced, all FHV-1 strains were observed to replicate in corneal epithelium; minimal viral antigen was detected in the corneal stroma. The course and clinical features of ocular FHV-1 infection were then studied over a period of 60 days in two groups of ten cats: in one group, infection was preceded by administration of subconjunctival betamethasone. In each of these groups, a distinct clinical syndrome developed. In cats not receiving corticosteroids, a course of epithelial keratitis, characterized by the formation of punctate and dendritic epithelial lesions, persisted for up to 24 days postinfection. In the corticosteroid treated group, a chronic (greater than 60 days) stromal keratitis developed, characterized by geographic epithelial ulceration, interstitial edema and deep vascularization. Other complications observed in corticosteroid-treated animals included decreased tear production, calcific-band keratopathy and a unique stromal disorder of cats termed corneal sequestration. The results of this study indicate that while epithelial keratitis may occur during primary infection, stromal keratitis does not, unless immune responsiveness to FHV-1 is concomitantly suppressed. This feature is similar to naturally occurring HSV-1 keratitis of humans, but contrasts to other animal model systems in which stromal keratitis predictably occurs during primary infection. Study of this animal model, therefore, may allow unique insights into the events preceding the establishment of stromal keratitis.

Animals

In vitro susceptibility of feline herpesvirus-1 to vidarabine, idoxuridine, trifluridine, acyclovir, or bromovinyldeoxyuridine.

In vitro activities of 9-[( 2-hydroxyethoxy] methyl) guanine (acyclovir), (E)-5-(2-bromovinyl)-2'deoxyuridine, 9-beta-D-arabinofuranosyladenine (vidarabine), 5-iodo-2'-deoxyuridine (idoxuridine), and 5-trifluoromethyl-2'-deoxyuridine (trifluridine) were studied against 6 strains of feline herpesvirus-1. A significant difference was not detected among viral strains in their susceptibility to these compounds (P = 0.442). The relative potency of these compounds was trifluridine much greater than idoxuridine greater than vidarabine greater than bromovinyldeoxyuridine much greater than acyclovir. Concentrations of trifluridine and idoxuridine (0.67 and 6.8 microM, respectively) required to reduce plaque numbers by 50%, compared with that of controls, were significantly lower (P less than 0.001) than were those of other compounds.

Acyclovir

Bovine coronavirus genome.

The tissue culture-adapted strain (Mebus) of the bovine coronavirus was grown to titers of greater than 10(7) 50% tissue culture infective doses per ml in secondary bovine embryo kidney cells, and the RNA was isotopically labeled with [3H]uridine. The RNA was extracted from purified virus and was found to have the following properties. (i) It consisted primarily of a homogeneous large-molecular-weight species which comigrated electrophoretically with vesicular stomatitis viral RNA and therefore had an apparent molecular weight of 3.8 X 10(6). (ii) It remained as a 3.8 x 10(6)-molecular-weight molecule after heat denaturation when rapidly harvested virus was examined. (iii) It was 80% susceptible to pancreatic RNase A digestion in high (0.3 M) NaCl, and the 20% resistant fraction was 4S to 7S in size. (iv) It was polyadenylated to the extent that 40 and 60% of the native RNA bound to polyuridylic acid-Sepharose and oligodeoxythymidylic acid-cellulose, respectively, under conditions of high (0.5 M) NaCl.

Animals

Increased virulence of modified-live infectious laryngotracheitis vaccine virus following bird-to-bird passage.

Modified-live (ML) infectious laryngotracheitis (ILT) vaccine viruses, both tissue-culture-origin (TCO) and chicken-embryo-origin (CEO), were passaged 20 times in specific-pathogen-free chickens. After serial bird-to-bird passage, increased virulence was observed for CEO virus but not TCO virus. Increased mortality and increased severity and duration of respiratory disease were observed in chickens inoculated with chicken-passaged CEO viruses; only mild respiratory disease (no mortality) occurred in chickens inoculated with chicken-passaged TCO viruses. These findings suggest that ML ILT vaccine viruses may increase in virulence after bird-to-bird passage.

Animals

Partial characterization of a turkey enterovirus-like virus.

Small round viruses, 18 to 24 nm in diameter, were detected by electron microscopy in droppings of young turkeys with enteritis. The virus was propagated in embryonated turkey eggs and tentatively identified as an enterovirus based on size, intracytoplasmic morphogenesis, buoyant density of 1.33 g/ml in CsCl, and a single-stranded RNA genome of approximately 7.5 kb. It was distinguished from avian encephalomyelitis virus by cross-immunofluorescence. These results identify an enterovirus-like virus as a possible etiologic agent of enteric disease of young turkeys. However, its role in this disease remains to be established.

Animals

Virulence of infectious laryngotracheitis viruses: comparison of modified-live vaccine viruses and North Carolina field isolates.

Virulence of six modified-live (ML) infectious laryngotracheitis (ILT) vaccine viruses was compared with that of 11 field isolates (indistinguishable from vaccine viruses by DNA restriction endonuclease analyses) by intratracheal exposure of 4-week-old, specific-pathogen-free chickens. Virulence of ILT viruses was based on an intratracheal pathogenicity index, mortality, and tracheal lesions. Intratracheal pathogenicity indices for ML vaccine viruses ranged from 0.0 to 0.14, while those for field isolates were 0.20 to 0.82. Mortality was a consistent clinical feature of field isolates; all produced mortality, with seven of the 11 isolates causing two or more deaths per inoculation group. In contrast, only one of six ML vaccine viruses produced mortality (one death per inoculation group). In general, tracheal lesions were more severe in chickens inoculated with field isolates and were produced more consistently than in chickens inoculated with vaccine viruses. These studies indicate that virulence of ILT field isolates was greater than that of ML vaccine viruses. Together with previous restriction endonuclease analyses, these findings suggest the possibility that field isolates originated from ML vaccine viruses through reversion to parental-type virulence.

Animals

Restriction endonuclease analysis of infectious laryngotracheitis viruses: comparison of modified-live vaccine viruses and North Carolina field isolates.

Six modified-live (ML) infectious laryngotracheitis (ILT) vaccine viruses, three reference strains, and 18 field isolates were compared by restriction endonuclease analysis of their DNA. Viral DNA digestion patterns were established for vaccine viruses using restriction endonucleases PstI, BamHI, KpnI, and HindIII. Using these enzymes, five of six ML vaccine viruses had identical restriction endonuclease cleavage patterns. Vaccine viruses had distinct patterns compared with ILT virus reference strains Illinois-N71851, Cover, and NVSL. Restriction endonuclease cleavage patterns of 18 field isolates of ILT virus, obtained from ILT outbreaks in North Carolina, were indistinguishable from vaccine viruses. These results suggest a possible role of vaccine or vaccine-like viruses in recent ILT outbreaks.

Animals