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PubMed1985

Antibodies to Newcastle disease virus in various human diseases.

Sera of patients with infectious mononucleosis (IM) and various other diseases were studied for agglutinins against Newcastle disease virus (NDV)-modified human group O red blood cells (NDVO) and antibodies to the NDV preparations. In agreement with previous studies, the NDVO antibodies are found in a wide variety of diseases in addition to IM, including Japanese IM-like syndrome (22%), syphilis (24%), lepromatous leprosy (30%), systemic lupus erythematosus (29%), multiple sclerosis (18%) and cancer (17%); these antibodies were also found in patients with renal allografts (29%). It was also noted that the Victoria (VIC), Roakin and Herts strains, but not B1 strain of NDV are active in the NDVO agglutination, and VIC and Roakin strains, but not B1 strain in the immunodiffusion. Immunodiffusion and enzyme immunoassay with various preparations of the VIC strain revealed that the major antigen(s) of the virus under study is carried by the hemagglutinin-neuraminidase (H-N) glycoproteins. The H-N molecule was also shown to be able to modify human erythrocytes for the agglutination by the pathologic sera.

ABO Blood-Group System↗
PubMed1987

Differences in virus-induced polypeptides in cells infected by cytopathic and noncytopathic biotypes of bovine virus diarrhea-mucosal disease virus.

Two biotypes of bovine viral diarrhea-mucosal disease virus are present in nature: one that induces cytopathology in infected bovine cells and the other that infects cells without overt cytopathology. Infections with both types of virus yield similar amounts of infectious progeny virus. Field and laboratory isolates of both biotypes of bovine viral diarrhea (BVD) virus were analyzed by radioimmunoprecipitation and polyacrylamide gel electrophoresis of infected cell extracts. The noncytopathic biotype BVD (NCB-BVD) virus isolates can be differentiated from cytopathic biotype BVD (CB-BVD) isolates on the basis of peculiar polypeptide profiles they induce in the infected cell. The most abundant polypeptide in CB-BVD infected cells is the 80K polypeptide. NCB-BVD virus-infected cells lack the 80K polypeptide and induce a predominant 118K polypeptide. D-[2-3H]Mannose labeling of cells infected with NCB-BVD indicated that at least three polypeptides are N-glycosylated: 75K, 56K-58K, and 48K. In addition the sizes and ratios of the glycoproteins induced by all virus isolates showed a marked variation. We present evidence indicating that there is remarkable heterogeneity among the field viral isolates of BVD and this methodology is of potential value for molecular epidemiology studies.

Animals↗
PubMedDate not supplied

Response to several avian respiratory viruses as affected by infectious bursal disease virus.

After being inoculated with the infectious bursal disease virus (IBDV) at one day of age, specific-pathogen-free chickens were inoculated with either Newcastle disease virus (NDV), infectious bronchitis virus (IBV), or infectious laryngotracheitis virus (ILTV). Their immunity was challenged 2-3 weeks later with homologous virus, and antibody titers were determined for ILTV and IBV. Several studies were made to determine the effects of IBDV on the development of persistent or chronic virus infections. Chickens susceptible to IBDV were exposed to IBDV at one day and inoculated at two weeks of age with either NDV, IBV, or ILTV. Two, three, four, and five weeks postinoculation with the respiratory viruses, tracheal swabbings were collected for virus isolations. The birds were challenged with homologous virus at five weeks postinoculation. The results show that early (1-day) infections with IBDV affect the response of young birds to several avian respiratory viruses, as indicated by lowered resistance to challenge and humoral antibody levels for birds inoculated with ILTV and NDV. Birds infected with IBV and IBDV withstood IBV challenge but were much more prone to persistent infections than were birds not exposed to IBDV. High death rates and decreased weights in all IBDV-inoculated groups demonstrated the damaging effects of early IBDV infection.

Animals↗
PubMed1999

Antigenic profile of African horse sickness virus serotype 4 VP5 and identification of a neutralizing epitope shared with bluetongue virus and epizootic hemorrhagic disease virus.

African horse sickness virus (AHSV) causes a fatal disease in horses. The virus capsid is composed of a double protein layer, the outermost of which is formed by two proteins: VP2 and VP5. VP2 is known to determine the serotype of the virus and to contain the neutralizing epitopes. The biological function of VP5, the other component of the capsid, is unknown. In this report, AHSV VP5, expressed in insect cells alone or together with VP2, was able to induce AHSV-specific neutralizing antibodies. Moreover, two VP5-specific monoclonal antibodies (MAbs) that were able to neutralize the virus in a plaque reduction assay were generated. To dissect the antigenic structure of AHSV VP5, the protein was cloned in Escherichia coli using the pET3 system. The immunoreactivity of both MAbs, and horse and rabbit polyclonal antisera, with 17 overlapping fragments from VP5 was analyzed. The most immunodominant region was found in the N-terminal 330 residues of VP5, defining two antigenic regions, I (residues 151-200) and II (residues 83-120). The epitopes were further defined by PEPSCAN analysis with 12mer peptides, which determined eight antigenic sites in the N-terminal half of the molecule. Neutralizing epitopes were defined at positions 85-92 (PDPLSPGE) for MAb 10AE12 and at 179-185 (EEDLRTR) for MAb 10AC6. Epitope 10AE12 is highly conserved between the different orbiviruses. MAb 10AE12 was able to recognize bluetongue virus VP5 and epizootic hemorrhagic disease virus VP5 by several techniques. These data will be especially useful for vaccine development and diagnostic purposes.

African Horse Sickness Virus↗
PubMed1987

Fusion of erythrocytes by Newcastle disease virus.

Newcastle disease virus-induced fusion of chick embryo (CE) and chicken erythrocytes has been studied at the ph range between 5.5 and 8.0. The highest degree of fusion of CE erythrocytes was observed at pH 5.5, whereas the chicken erythrocytes fused at pH 5.5-6.0 only. Freezing and thawing of low-haemolytic virus preparation increased its erythrocyte fusion activity. Ammonium chloride did not cause a statistically significant effect on the multiplication of virus preparations expressing different haemolysis and erythrocyte fusion activity.

Animals↗
PubMed1978

In vitro comparison of foot-and-mouth disease virus subtype variants causing disease in vaccinated cattle.

Foot-and-mouth disease virus isolates of types O, A and SAT 2, from diseased animals in herds routinely vaccinated twice a year were compared antigenically with the vaccine strains in the complement-fixation, neutralization and radial immunodiffusion tests. It was found that strains which had readily infected vaccinated cattle had R values against the vaccine strain in the complementfixation and radial immunodiffusion tests of 30 or less, while strains causing primary outbreaks with little spread had R values of 30-40. Threefold differences in humoral neutralizing antibody concentration between the field variant and the vaccine strain in sera from vaccinated animals were likely to be significant in terms of protection.

Animals↗
PubMed1989

Immunodetection of bluetongue virus and epizoötic hemorrhagic disease virus in Culicoides variipennis (Diptera: Ceratopogonidae).

The avidin-biotin complex immunoperoxidase system has been used with nitrocellulose membranes to detect bluetongue virus serotypes 10 (BTV-10) and 11 (BTV-11) and epizootic hemorrhagic disease virus (EHDV) serotype 1 (EHDV-1) in individual specimens of Culicoides variipennis (Coquillett). The cross reactivity between BTV-10 and BTV-11 indicates that polyclonal antisera cannot be used to distinguish between flies infected with BTV-10 and BTV-11; however, the procedure can be used to discriminate flies infected with BTV-10 or BTV-11 from flies infected with EHDV-1. Because the test is rapid and sensitive and does not require expensive equipment, it could be used in the field to determine the relative numbers of flies infected with BTV or EHDV.

Animals↗
PubMed2004

Using epidemiological information to develop effective integrated virus disease management strategies.

Virus diseases cause serious losses in yield and quality of cultivated plants worldwide. These losses and the resulting financial damage can be limited by controlling epidemics using measures that minimise virus infection sources or suppress virus spread. For each combination of virus, cultivated plant and production system, there is an 'economic threshold' above which the financial damage is sufficient to justify using such measures. However, individual measures used alone may bring only small benefits and they may become ineffective, especially over the long term. When diverse control measures that act in different ways are combined and used together, their effects are complementary resulting in far more effective overall control. Such experiences have led to the development of integrated management concepts for virus diseases that combine available host resistance, cultural, chemical and biological control measures. Selecting the ideal mix of measures for each pathosystem and production situation requires detailed knowledge of the epidemiology of the causal virus and the mode of action of each individual control measure so that diverse responses can be devised to meet the unique features of each of the different scenarios considered. The strategies developed must be robust and necessitate minimal extra expense, labour demands and disruption to standard practices. Examples of how epidemiological information can be used to develop effective integrated disease management (IDM) strategies for diverse situations are described. They involve circumstances where virus transmission from plant-to-plant occurs in four different ways: by contact, non-persistently or persistently by insect vectors, and by root-infecting fungi. The examples are: Subterranean clover mottle virus (SCMoV) (contact-transmitted) and Bean yellow mosaic virus (BYMV) (non-persistently aphid-transmitted) in annually self-regenerating clover pasture; three seed-borne viruses (all non-persistently aphid-transmitted) plots of pasture legume improvement programmes; Tomato spotted wilt virus (TSWV) (persistently thrips-transmitted) in vegetables in seedling nurseries, protected cropping or field systems; and lettuce big-vein disease (fungus-transmitted) in lettuce in seedling nursery, hydroponic, infested field or uninfested field situations. By describing the kinds of approaches required, this article is intended to help future research and extension programmes devise integrated disease management strategies that not only function effectively to diminish the losses caused by economically important plant virus diseases but also fulfill the requirement of being environmentally and socially responsible.

Animals↗
PubMed1995

Induction of protection against Borna disease by inoculation with high-dose-attenuated Borna disease virus.

Borna disease is a chronic neurological disease caused by an enveloped negative-strand RNA virus (BDV). Experimental disease can be reproduced in rats with brain homogenates derived from infected animals or with virus derived from infected cells in culture. The virus replicates in cultured cells without evidence of cytopathic effect or production of significant levels of cell-free virus. Borna disease is caused by an immunopathological response to viral infection of neural cells. To further investigate the pathogenesis of Borna disease, rats were inoculated with different doses of BDV attenuated by culture in MDCK cells. Low doses of attenuated BDV (10(2)-10(4) TCID50) resulted in typical clinical disease and severe encephalitis; however, the lag period between inoculation and disease was considerably longer than that with virulent BDV. In contrast, animals inoculated with a high dose of attenuated BDV (10(5)-10(6) TCID50) did not develop clinical disease, although a mild encephalitic response was present that did not progress beyond the mild encephalitis. Animals inoculated with a high dose of BDV developed high titers of anti-BDV antibody and were protected against virulent challenge. Protection was correlated with the rapid induction of an immune response in the animals and the lack of any biologically detectable virus in the CNS.

Animals↗
PubMed1986

Genotypic and phenotypic variation of biotypes coexisting in the Hickman strain of Newcastle disease virus.

Many Newcastle disease virus strains are composed of several biotypes which coexist in the wild and in laboratory cultures. We have studied some of the phenotypic and genotypic properties of 6 virus clones from the coexisting biotypes of the Hickman strain of Newcastle disease virus. These clones were readily distinguishable from the parent virus strain and from each other by their RNA fingerprints. Fingerprints of the most virulent clones (Hi/LC, Hi/MC, and Hi/LR) contained 61% to 77% of the oligoribonucleotides present in the fingerprint of the Hickman parent strain. None of the clones killed chickens as rapidly as did the parent strain, although some clones killed embryonating eggs as rapidly as did the parent strain.

Genotype↗
PubMed1997

[Borna disease virus. An etiological agent in neuropsychiatric diseases?].

Borna disease virus has long been recognized as a cause of sporadic cases and epidemics of meningoencephalomyelitis in horses and sheep in southern parts of Germany. however, sero-epidemiological surveillances indicate that Borna disease virus has a global distribution in horses, without the recognition of clinical manifestations associated with the infection, in other parts of the world. During the past five years evidence has been presented suggesting that humans also can become infected with this virus or a closely related virus. A significantly increased sero-prevalence is seen in patient populations with a variety of neuropsychiatric and behavioral disorders, suggesting that Borna disease virus or a closely related virus may play an etiological role in some of these diseases. A review of the literature is given.

Animals↗
PubMed1990

Cutaneous histopathologic findings in 'antiphospholipid syndrome'. Correlation with disease, including human immunodeficiency virus disease.

The term antiphospholipid syndrome is used to characterize a complex of clinical and pathologic findings mediated by a group of antibodies formed against a family of antiphospholipids. These antiphospholipid antibodies were originally found in patients with lupus erythematosus in whom the partial thromboplastin time was prolonged and in patients with other autoimmune diseases; subsequently, they have been observed in association with a variety of other conditions, including infections, reactions to drugs, malignant neoplasms, human immunodeficiency virus disease, and as an isolated finding. In recent years, there has been some clarification of the significance of the various tests for antiphospholipid antibodies, including the lupus anticoagulant test and the anticardiolipin antibody tests, in predicting the antiphospholipid syndrome. The mechanism of disease, however, has not been well defined. The most common cutaneous lesion seen in seven patients with lupus anticoagulant and anticardiolipin antibody who have the antiphospholipid syndrome was ulceration due to thrombosis of dermal veins and arteries. Often there is a reactive vascular proliferation around the thrombosed vessels. The presence of primary thrombosis of both veins and arteries in thrombotic disorders is unusual and may provide insight into the mechanism of thrombosis in antiphospholipid syndrome.

AIDS-Related Complex↗
PubMed1989

Antigenic relationship among strains of ibaraki virus and epizootic haemorrhagic disease virus studied with monoclonal antibodies.

Twelve monoclonal antibodies against ibaraki virus (IbV) were established and preliminarily characterised by indirect immunoperoxidase (IIP), haemagglutination inhibition (HI) and neutralisation (NT) tests. Five antibodies reacted in the IIP test with all IbV and epizootic haemorrhagic disease virus (EHDV) strains tested, and five antibodies reacted with IbV and Alberta strain (serotype 2) but not with New Jersey strain (serotype 1) of EHDV. Two of 12 antibodies showed both HI and NT activities. Viral proteins with molecular weights of about 24,000 daltons (24KD) and 78KD were determined by two monoclonal antibodies in Western blot analysis. One of two antibodies with the ability of both HI and NT recognised a viral protein with a molecular weight of about 78KD.

Animals↗
PubMed2007

Morphometric analysis of the retina from horses infected with the Borna disease virus.

Borna disease (BD) is a fatal disorder of horses, often characterized by blindness. Although degeneration of retinal neurons has been demonstrated in a rat model, there are controversial data concerning whether a similar degeneration occurs in the retina of infected horses. To investigate whether BD may cause degeneration of photoreceptors and possibly of other neuronal cells at least at later stages of the disease, we performed a detailed quantitative morphologic study of retinal tissue from Borna-diseased horses. BD was diagnosed by detection of pathognomonic Joest-Degen inclusion bodies in the postmortem brains. Paraffin sections of paraformaldehyde-fixed retinae were used for histologic and immunohistochemical stainings. Numbers of neurons and Müller glial cells were counted, and neuron-to-Müller cell ratios were calculated. Among tissues from 9 horses with BD, we found retinae with strongly altered histologic appearance as well as retinae with only minor changes. The neuron-to-Müller cell ratio for the whole retina was significantly smaller in diseased animals (8.5 +/- 0.4; P < .01) as compared with controls (17.6 +/- 0.8). It can be concluded that BD in horses causes alterations of the retinal histology of a variable degree. The study provides new data about the pathogenesis of BD concerning the retina and demonstrates that a loss of photoreceptors may explain the observed blindness in infected horses.

Animals↗
PubMed2002

The immunopathogenesis of Borna disease virus infection.

Borna disease virus (BDV) infection represents an excellent model system to study immunopathological mechanisms based on a T cell-mediated immune reaction in the central nervous system. The single-stranded RNA Borna disease virus, a member of Bornaviridae in the order of Mononegavirale, lacks cytopathogenicity both in vitro and in vivo. After experimental infection BDV causes a persistent infection of the central nervous system and induces Borna disease, an immune-mediated encephalomyelitis. The infiltrating immune cells have been characterized as CD4-positive, CD8-positive T-cells, macrophages and B cells. CD8-positive T cells represent the effector cell population exhibiting antigen specificity for the nucleoprotein.

Animals↗
PubMed1992

A ten-year follow-up on stage II malignant melanoma patients treated postsurgically with Newcastle disease virus oncolysate.

Newcastle disease virus oncolysate was examined as an adjunctive immunotherapeutic agent in the postsurgical management of 83 cases of Stage II malignant melanoma. At this time, all the patients have been under observation for at least 10 years, and over 60% are alive and free of recurrent disease. Older studies in the United States report postsurgical survival figures for Stage II cases of 5-15%. More contemporary studies indicate a 33% survival at 10 years. The unusual disease-free survival periods in the present study, including exceptional survivals in 21 patients with head and neck disease and six cases with cerebral metastases, suggest a unique role for the administration of Newcastle disease virus oncolysate in the management of Stage II malignant melanoma patients.

Adult↗