Human conjunctivitis due to the Newcastle-disease virus of fowls.
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[Further research on the antigenic structure of Newcastle disease virus].
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Animals↗
Virus susceptibility of mouse hemopoietic cells in vitro: inhibition of granulocyte-macrophage precursor cells by Newcastle disease virus.
Normal mouse bone marrow cells were exposed to encephalomyocarditis virus (EMC), reovirus type 3 (REO3), influenza virus (FLU), and Newcastle disease virus (NDV) then assayed for granulocyte-macrophage precursor cells by the technique of colony formation in agar. Exposure to EMC, REO3, and FLU caused a slight but variable loss of colony-forming potential, whereas exposure to NDV caused a very marked loss. NDV acted directly on the cells, not indirectly through release of colony-inhibiting factors or destruction of colony-stimulating factor. Experiments with NDV inactivated by heat, ether, or ultraviolet irradiation indicated that colony inhibition was associated with fully infective virus, even though some of the inactivated preparations had retained full hemagglutinin, neuraminidase, or hemolytic activity.
Animals↗
Newcastle disease virus--some properties of Australian strains.
Seventeen Australian strains of Newcastle disease virus were tested for their biological properties: mean death time, heat stability of the hemagglutinin and infectivity of the virus at 56 C, the elution time of virus from chicken erythrocytes, and the ability to hemagglutinate equine red blood cells. The strains differed considerably in their reactions. All had mean-death-time indices of 112 or greater, indicating that all were lentogenic. Strains were identified that had heat-labile and -stable hemagglutinin and infectivity, slow and fast elution, and variable ability to agglutinate equine erythrocytes. The significance of the results is discussed in terms of their usefulness in identifying exotic strains of the virus.
Animals↗
The fate of glutamate in different brain regions of the chick during Newcastle disease virus infection.
Alterations in the glutamate metabolism during Newcastle disease virus (NDV) infection were studied in different brain regions of chick. The glutamate dehydrogenase, the glutamine synthetase, the glutamic acid decarboxylase activities were decreased and the glutamine content was decreased in all brain regions of chick after 24 hr. and 72 hr. of NDV infection. The results obtained in the present study reveal that the glutamate metabolism and its conversion to GABA were operated in low profile during NDV infection.
Animals↗
Pathogenicity of two strains of Newcastle disease virus in the grey-breasted helmet guinea fowl.
Thirty-five 6-week-old guinea fowl keets, seronegative for maternal antibodies to Newcastle disease virus, were infected with Herts strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (IM) or intranasally (IN). Clinical signs were first noticed four days post infection (PI) in the group infected IM but five days PI in the group infected IN with Herts strain of Newcastle disease virus. These clinical signs were similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Herts strain. The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets. The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets. Neither gross or microscopic lesions were observed in keets that had received the Kumarov strain.
Animals↗
Fractionation of Newcastle disease virus by chromatography on diethylaminoethyl cellulose.
Wilson, Dwight E. (Rensselaer Polytechnic Institute, Troy, N.Y.). Fractionation of Newcastle disease virus by chromatography on diethylaminoethyl cellulose. J. Bacteriol. 84:295-301. 1962.-The L. Kansas and NK strains of Newcastle disease virus were chromatographed on diethylaminoethyl (DEAE) cellulose ion-exchange columns. L. Kansas virus eluted from DEAE columns showed one peak of hemagglutinating and infective particles. Two peaks of hemagglutinins and one peak of infective particles were observed when the NK strain was chromatographed, indicating that the stock virus contained a noninfectious hemagglutinating component. Treatment of the noninfectious particles with Genetron 113 resulted in an increase in the ratio of infective to hemagglutinating particles. The Genetron-treated noninfectious particles were also eluted from the DEAE column at a higher salt concentration than the untreated noninfectious particles. The results indicate that the Genetron treatment removes inhibitors of infectivity bound to the noninfectious virus particle.
Animals↗
Onset of protective immunity in chicks after vaccination with a recombinant herpesvirus of turkeys vaccine expressing Newcastle disease virus fusion and hemagglutinin-neuraminidase antigens.
The onset of protective immunity from lethal Newcastle disease virus (NDV) challenge of chicks was determined after vaccination with a recombinant herpes virus of turkeys (HVT) expressing the fusion and hemagglutinin-neuraminidase proteins of NDV. One-day-old specific-pathogen-free chicks devoid of maternal antibodies to NDV were vaccinated with 130 to 3300 plaque forming units of HVT (depending on the trial) and then challenged at 4, 7, 10, and 14 days postvaccination (DPV) with a neurotropic velogenic strain of NDV (GB Texas). The recombinant vaccine afforded 0%, 35-75%, 85%, and 94-100% protection when the vaccinated birds were challenged at 4, 7, 10, and 14 DPV, respectively. In all trials, challenge caused 100% mortality in unvaccinated control chicks. Newcastle disease virus was reisolated from the lung, liver, spleen, and brain of birds dying in all trials regardless of vaccine dosage or time of challenge, except when challenge occurred at 14 DPV.
Animals↗
Neurochemical and neuroendocrine responses to Newcastle disease virus administration in mice.
Mice injected intraperitoneally with Newcastle disease virus (NDV) responded with increased plasma concentrations of ACTH and corticosterone and increased hypothalamic concentrations of the tryptophan and of the norepinephrine catabolite, 3-methoxy,4-hydroxyphenylethyleneglycol (MHPG) and the serotonin catabolite, 5-hydroxyindoleacetic acid (5-HIAA). Two different strains of NDV, a lentogenic and a mesogenic one, elicited dose-dependent effects in these responses. Both strains elicited near maximal responses at doses around 1000 hemagglutination units. The maximal effects on ACTH, corticosterone and MHPG occurred around 2 h, but the effects on tryptophan and 5-HIAA were greatest at 8 h. Similar responses in plasma corticosterone, and cerebral tryptophan and 5-HIAA were observed following i.p. injection of polyinosinic-polycytidylic acid, but MHPG was not altered. The cyclo-oxygenase inhibitor, indomethacin, had little effect on the NDV-induced increases in plasma corticosterone and ACTH, and hypothalamic indolamines, but essentially ablated the MHPG response. The effect of NDV on plasma corticosterone, like that of endotoxin (LPS), was prevented by hypophysectomy, suggesting that the pituitary was required for these responses. These endocrine and neurochemical responses to NDV resemble those to interleukin-1 (IL-1) and LPS. Therefore we tested mice pretreated with the IL-1-receptor antagonist. This treatment prevented the neurochemical and plasma ACTH and corticosterone responses to IL-1, but did not alter those to LPS, and prevented the endocrine and neurochemical responses to NDV in approximately half of the animals. Thus IL-1 may be a mediator of the responses to NDV, but additional factors may also be involved.
Animals↗
Quantification of cell fusion by twenty-one strains of Newcastle disease virus using flow microfluorometry.
The cell-fusing ability of Newcastle disease virus (NDV) was quantified using flow microfluorometry (FMF). The rate of polykaryocyte formation, fusion dependence on multiplicity of infection, and cell fusion differences for 21 NDV strains were measured using this technique. No correlation was found between the virulence of a virus strain and its cell fusion index calculated from the FMF data.
Cell Fusion↗
Genome replication of Newcastle disease virus: involvement of the rule-of-six.
We examined replication of Newcastle disease virus (NDV) by using minigenomes consisting of the 3' leader and 5' trailer regions of NDV flanking a reporter gene encoding secreted placental alkaline phosphatase (SEAP). Negative-sense minigenome RNA was generated from transfected plasmid DNA by means of in vivo transcription. Subsequent replication of minigenome RNA was determined either after infection with NDV helpervirus or after contransfection with helperplasmids that expressed the essential viral replication proteins NP, P, and L. In both systems, efficient replication of minigenome RNA was observed only if the genome size was a multiple of six nucleotides. Hence, in these systems, replication of NDV minigenome RNA's is strictly dependent on the rule-of-six. When the supernatant from helpervirus-infected, transfected cells was used to infect fresh monolayers, efficient transfer of SEAP activity by virus-like particles was observed only if the size of the minigenome RNA obeyed the rule-of-six. However, after several serial passages, we also observed efficient transfer of SEAP activity by virus-like particles derived from minigenome RNA's that did not obey the rule-of-six. Evidence was obtained which indicated that successful replication of these minigenomes was not due to a change in genome size.
3' Untranslated Regions↗
Virus distribution and histopathologic changes in organs of chickens inoculated with Newcastle disease virus (avian paramyxovirus-1) isolated from racing pigeons.
The virus distribution and histopathologic changes in organs of 1-week-old chickens inoculated with three representative isolates of Newcastle disease virus isolated from racing pigeons in Japan were examined. All three isolates were recovered from various organs, including brain, for several days, but not from the blood. Results were highly correlated with their high intracerebral pathogenicity indices (ICPI), in spite of their long mean death time of minimum lethal dose (MDT/MLD).
Animals↗
[Persistence of Newcastle disease virus in mouse cells].
The course of persistent infection in Newcastle disease virus (NDV)-infected mouse L cells (LNDV) was analysed. The production of infectious intra- and extracellular virus was markedly reduced (less than 10(1) PFU/ml), 30% of the cells produced virus-specific antigen. Analysis of the synthesis of 3H-nucleocapsid RNA in the LNDV system revealed predominance of low molecular weight RNAs. Virus-specific sequences were shown to be present in fraction of DNA extracted by Hirt's method. Only the "supernatant" Hirt's fraction was infectious. The possibility of the presence of virus-specific sequences in free unintegrated form is discussed.
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Pathotyping of Newcastle disease viruses by RT-PCR and restriction enzyme analysis.
The technique of RT-PCR and restriction enzyme analysis was standardized to detect and differentiate Newcastle disease viruses. Digestion of RT-PCR-amplified, F gene sequences encoding for the cleavage activation sites of fusion protein with restriction enzymes AluI, BglI, HaeIII, HinfI, HhaI, RsaI, StyI and TaqI was carried out in order to characterize Newcastle disease viruses of varying pathogenicity. Restriction enzyme digestion of the amplicons by BglI and HhaI could group eight viruses, both field isolates and known vaccine strains, into lentogenic, mesogenic and velogenic pathotypes. By employing this technique directly on a clinical sample, Newcastle disease virus of the lentogenic pathotype could be detected.
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An assessment of the Australian V4 strain of Newcastle disease virus as a vaccine by spray, aerosol and drinking water administration.
An Australian strain of Newcastle disease virus, was evaluated for used as a vaccine following its administration by drinking water, aerosol and spray to chickens at 1 and 21 days of age. Haemagglutination inhibition antibody was produced and persisted for 11 weeks. Aerosol vaccination induced higher levels of haemagglutination inhibition antibody than the other methods of vaccination. No respiratory disease was observed following vaccination. Chickens vaccinated by aerosol and spray were fully protected when challenged at 5, 7 and 11 weeks of age with virulent Newcastle disease virus. Mortality of 10 to 30 per cent was observed in chickens vaccinated by drinking water and intranasally following challenge.
Administration, Intranasal↗
Virus isolation from tracheal explant cultures and oropharyngeal swabs in attempts to detect persistent Newcastle disease virus infections in chickens.
Three-to-seven-week-old broiler-type chickens were inoculated with Newcastle disease virus (NDV) by eye-drop (ED) or intratracheally (IT), and virus isolation was attempted from oropharyngeal (oral) swabs and medium harvested from tracheal explant cultures (TEC). The TEC were maintained in screw-capped tissue-culture flasks for at least 1 month, and medium harvested at regular feeding times was assayed for NDV and NDV antibody. The earliest and latest sample times were 3 and 21 days after NDV inoculation. The three experiments done were: Expt. 1, infection of nonvaccinates with NDV strain La Sota; Expt. 2, infection of NDV vaccinates and nonvaccinates with NDV strain Largo; and Expt. 3, infection of NDV vaccinates and nonvaccinates with NDV wild-type strain Kansas-Manhattan (KM) and two temperature-sensitive (ts) clones derived by J. S. Youngner from the KM strain. All experiments yielded similar results. On day 3 postinoculation (PI), most chickens were shedding virus recoverable by oral swabs and detectable in harvests from TEC prepared on that day. On day 7 PI, there was a sharp reduction in the frequency of virus-positive oral swabs, but there was no decline in the frequency of virus-positive TEC. On day 14 PI or later, all oral swabs and TEC were virus-negative, except for one chicken in Expt. 3 that was oral-swab-positive. There was no evidence of NDV persistence in the TEC of oral-swab-negative chickens on or after day 14 PI. The results of these experiments are in contrast with previous reports of the detection of latent NDV by virus isolation from harvests of TEC prepared 18 or more days PI. The ts clones of strain KM used in Expt. 3 induced a markedly poorer antibody response and were shed for a shorter time than the KM parental virus.
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RNA sequence and transcriptional properties of the 3' end of the Newcastle disease virus genome.
The 3' end of the genomic RNA of Newcastle disease virus (NDV) has been sequenced and the leader RNA defined. Using hybridization to a 3'-end-labeled genome, leader RNA species from in vitro transcription reactions and from infected cell extracts were found to be 47 and 53 nucleotides long. In addition, the start site of the 3'-proximal mRNA was determined by sequence analysis of in vitro [beta-82P]GTP-labeled transcription products. The genomic sequence extending beyond the leader region demonstrated an open reading frame for at least 42 amino acids and probably represents the amino terminus of the nucleocapsid protein (NP). The terminal 8 nucleotides of the NDV genome were identical to those of measles virus and Sendai virus while the sequence of the distal half of the leader region was more similar to that of vesicular stomatitis virus. These data argue for strong evolutionary relatedness between the paramyxovirus and rhabdovirus groups.
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Relationship between the ribonucleic acid synthesizing capacity of ultraviolet-irradiated Newcastle disease virus and its ability to induce interferon.
Ultraviolet (UV)-irradiated Newcastle disease virus which has lost its infectivity but has the capacity to induce interferon also has the capacity to induce ribonucleic acid (RNA) synthesis both in vitro and early in infection in vivo. With large doses of UV irradiation, RNA-synthesizing capacity and interferon-inducing capacity are lost in parallel. Limited amounts of base-paired RNA associated with a transcriptive intermediate are involved in this RNA synthesis. These findings suggest the possibility that the single-stranded RNA of the UV-irradiated virus induces interferon by serving as a template for the synthesis of base-paired RNA. UV irradiation of the virus breaks down viral RNA but at a rate which is too slow to be a major cause of the loss of RNA-synthesizing capacity. Evidence is presented which suggests that less of the template RNA of the UV-irradiated virus is copied and that the product which is synthesized is smaller than that synthesized by nonirradiated virus.
Animals↗