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At least 19 recordsLinked to original sources

PubMed1992

Pathogenicity of feline leukemia virus is commonly associated with variant viruses.

Many of the serious diseases resulting from feline leukemia virus (FeLV) infection are associated with the generation of novel variant viruses. The prototype FeLV-A virus is highly stable and circulates in the cat population without apparent antigenic change. However, recombination with cellular oncogenes produces viruses which cause leukemia or other malignant diseases. Other recombinants within the env genes of FeLV-A and endogenous FeLV are recognized as belonging to a second subgroup, FeLV-B, the presence of which is correlated with an increased risk of infection with FeLV and a higher incidence of leukemia. Mutants of FeLV which affect the env gene are phenotypically of a third subgroup, FeLV-C, and have a close association with erythroid aplasia. None of these viruses, apart from FeLV-B, is transmitted further in nature. Therefore the generation of these novel viruses and the production of disease is an inadvertent consequence of FeLV infection.

Anemia↗

PubMed1992

Genetic mechanisms of antigenic variation in infectious bursal disease virus: analysis of a naturally occurring variant virus.

The major immunogenic protein VP2 from a pathogenic field isolate (variant A virus) of infectious bursal disease virus (IBDV) was cloned and sequenced to examine antigenic variations. The VP2 open reading frame consists of 1509 nucleotides and codes for a 503 amino acid protein. Overall, the VP2 amino acid sequence of the variant A virus shares 98.6% identity with VP2 genes from other published IBDV strains. However, within the central region of VP2 (amino acids 222-334) lies a highly divergent area that we have termed the variable domain. Relative to five other IBDV isolates, a total of six amino acid changes occur within the variable domain of the variant A virus. At positions 284-288, a substitution of isoleucine to threonine, a decrease in the number of Chou and Fasman beta turns, and a switch from a hydrophilic to a hydrophobic region are found only in the variant A virus. Together these changes predict a decrease in antigenicity as determined by calculation of potential antigenic sites. This suggests that only minor changes within VP2 contributed to the emergence of a variant virus that can cause disease in immunized birds.

Amino Acid Sequence↗

PubMed1979

Role of virus variants and cells in maintenance of persistent infection by measles virus.

Hamster embryo fibroblasts persistently infected with a derivative of the Schwarz vaccine strain of measles virus spontaneously released virus particles with an average buoyant density considerably lower than that of the parental virus. The released virus contained all of the measles virus structural proteins and interfered with replication of standard virus. All of the virus structural proteins were associated with a membrane-free cytoplasmic extract from the persistently infected cells. Membrane-free cytoplasmic extracts prepared from Vero cells lytically infected with Schwarz strain measles contained little or no virus envelope structural protein. Maintenance of persistent infection may involve both the presence of virus variants and a defect in the ability of the infected cell to replicate the virus efficiently.

Animals↗

PubMed1992

Chronic hepatitis B virus infection in an anti-HBc-nonreactive blood donor: variant virus or defective immune response?

Viral sequence and host immune response were investigated in an unusual, asymptomatic chronic hepatitis B virus carrier (human leukocyte antigen type A24, Bw61, Bw62, Bw6, DRw11, DRw52, DQw7) who was consistently nonreactive for antibody to HBc and had a normal ALT level over a 5-yr study period. The precore and core region DNA sequences of virus isolated from his serum had seven silent mutations that resulted in no changes in the amino acid sequence of the adr HBsAg subtype. He had no abnormalities in the number of peripheral blood T or B cells and no HBcAg-specific suppressor T cells. His lymphocytes proliferated in vitro in response to phytohemagglutinin, pokeweed mitogen, Staphylococcus aureus and tetanus toxoid but not to recombinant HBcAg. Unlike other HBsAg carriers and hepatitis B virus-immune individuals, his monocytes did not ingest beads coated with HBcAg. Failure to produce antibody to HBc was not due to an hepatitis B virus variant but to a selective immune system defect in this asymptomatic HBsAg carrier.

Amino Acid Sequence↗

PubMed1990

Viral escape by selection of cytotoxic T cell-resistant virus variants in vivo.

Viruses persist in an immune population, as in the case of influenza, or in an individual, as postulated for human immunodeficiency virus, when they are able to escape existent neutralizing antibody responses by changing their antigens. It is now shown that viruses can in principle escape the immunosurveillance of virus-specific cytotoxic T cells by mutations that alter the relevant T-cell epitope.

Amino Acid Sequence↗

PubMed1991

In vitro and in vivo replication capacity of the precore region defective hepatitis B virus variants.

Although the precore region defective hepatitis B virus variants have been implicated in chronic liver disease and fulminant hepatitis, our knowledge on the molecular biology of these variants is still limited. Using an in vitro transfection assay, we confirmed the replication competent but HBeAg-negative nature of the major variants containing a TAG stop codon in the distal precore region associated with one or two point mutations. Transfection of the two-point-mutated variant into a chimpanzee induced serological responses including anti-HBc and anti-HBs. Interestingly, anti-HBe response was found in the absence of HBeAg antigenemia, suggesting that anti-HBe can be stimulated by degraded HBc. Using the rabbit reticulocyte system the possible effect of the different precore region mutations on the expression of HBcAg from precore- and core-mRNAs was also studied.

Animals↗

PubMed1978

Characterization of a Sinbis virus variant with altered host range.

A variant of Sindbis virus which is much more infectious for mouse cells than the standard virus has been examined for biochemical properties which might be responsible for this biological difference. The variant has a much enhanced ability to adsorb to mouse plasmacytoma (MOPC 315) cells, but when these cells were pretreated with heparin, they were able to adsorb the standard virus almost as well as the variant. This suggested that there was a surface charge difference between variant and standard virus. Differential elution of the viruses from hydroxyapatite and the results of isoelectric focusing of the virion glycoproteins substantiate this interpretation. Both viral glycoproteins E1 and E2 from the variant were more negatively charged than those of the standard virus but we were unable to find changes in tryptic peptides of the variant. Differences were found in stability of the two virus strains to heat and proteolytic enzymes.

Adsorption↗

PubMedDate not supplied

[Biological properties of tick-borne encephalitis virus variants isolated by transfection].

Variants of tick-borne encephalitis virus (TBA) isolated by inoculation of pig embryo kidney cell cultures (SPEV) with infectious DNA from chronically infected HEp-2-Soph cells produced cytopathic effect in SPEV cell cultures. In suckling mice inoculated intracerebrally they induced inapparent infection. Titers of TBE virus variants in SPEV cell cultures treated with DEAE-dextran increased considerably. As a result of filtration a variant was obtained replicating in SPEV cell cultures without any CPE. The cytopathic effect developed only when SPEV cells were treated with DEAE dextran. This variant is assumed to consist of two subpopulations 1 of which produces the cytopathic effect in DEAE-dextran-untreated SPEV cells while the other needs DEAE-dextran treatment of cells for its CPE manifestation.

Animals↗

PubMed1992

Encephalomyocarditis (EMC) virus-induced myocarditis by different virus variants and mouse strains.

The mode of occurrence of encephalomyocarditis (EMC) virus-induced myocarditis in mice was pathologically and virologically investigated using 2 virus variants (highly diabetogenic EMC-D and non-diabetogenic EMC-B) and 2 mouse strains (diabetes-susceptible BALB/c and diabetes-resistant C57BL/6). Mice were inoculated with 10(5) PFU/head of the virus intraperitoneally and observed up to 7 days post inoculation (7DPI). As compared with EMC-B-infected BALB/c and EMC-D-infected C57BL/6 mice, EMC-D-infected BALB/c mice developed marked myocarditis and exhibited a heart virus titer of more than 100 times above that of the others after 4DPI. Electron microscopically, small aggregations of virus-like particles, with 20-25 nm in diameter, were found in the cytoplasm of degenerated cardiomyocytes showing mitochondrial and myofibrillar degeneration in EMC-D-infected BALB/c mice.

Animals↗

PubMed1979

Characterization of two Chikungunya virus variants.

The stability of virulence and plaque size of two variants of Chikungunya virus (genus Alphavirus) were examined. Mouse pathogenicity did not coincide with infective virus levels in the brain. An increase in the average survival times of mice receiving a lethal dose of the variant which allowed prolonged survival at high doses and harvested late after infection was observed. Studies in Vero cells suggested that the number of infective virus particles produced per cell was lower with the small plaque variant, though these cells were selective for this clone. On the other hand suckling mice or antisera favoured a more virulent large plaque variant.

Animals↗

PubMed1975

Isolation of a Sindbis virus variant by passage on mouse plasmacytoma cells.

A variant of Sindbis virus has been isolated by growing a stock of virus, previously passaged on chicken embryo cells, in mouse plasmacytoma (MOPC 315) cells in suspension culture. An indirect immunofluorescence test and infective center assay showed that only a small fraction of cells could be infected by the stock wild-type virus, but that the population of virus accumulating after a few passages on the mouse cells had host-range properties distinct from the stock virus. The mouse-passaged virus retained its virulence for the original host and back-passaging of this virus on chicken cells did not change its newly acquired properties. Thus, this variant appears to be a genetically distinct form of Sindbis that adsorbs to and grows much better than the stock virus on several types of mouse cells including cultures of mouse macrophages.

Animals↗

PubMed1991

Antigenic and genetic variation in cytopathic hepatitis A virus variants arising during persistent infection: evidence for genetic recombination.

Variants of hepatitis A virus (pHM175 virus) recovered from persistently infected green monkey kidney (BS-C-1) cells induced a cytopathic effect during serial passage in BS-C-1 or fetal rhesus kidney (FRhK-4) cells. Epitope-specific radioimmunofocus assays showed that this virus comprised two virion populations, one with altered antigenicity including neutralization resistance to monoclonal antibody K24F2, and the other with normal antigenic characteristics. Replication of the antigenic variant was favored over that of virus with the normal antigenic phenotype during persistent infection, while virus with the normal antigenic phenotype was selected during serial passage. Viruses of each type were clonally isolated; both were cytopathic in cell cultures and displayed a rapid replication phenotype when compared with the noncytopathic passage 16 (p16) HM175 virus which was used to establish the original persistent infection. The two cytopathic virus clones contained 31 and 34 nucleotide changes from the sequence of p16 HM175. Both shared a common 5' sequence (bases 30 to 1677), as well as sequence identity in the P2-P3 region (bases 3249 to 5303 and 6462 to 6781) and 3' terminus (bases 7272 to 7478). VP3, VP1, and 3Cpro contained different mutations in the two virus clones, with amino acid substitutions at residues 70 of VP3 and 197 and 276 of VP1 of the antigenic variant. These capsid mutations did not affect virion thermal stability. A comparison of the nearly complete genomic sequences of three clonally isolated cytopathic variants was suggestive of genetic recombination between these viruses during persistent infection and indicated that mutations in both 5' and 3' nontranslated regions and in the nonstructural proteins 2A, 2B, 2C, 3A, and 3Dpol may be related to the cytopathic phenotype.

Animals↗

PubMed1991

T-cell receptor and T-cell-resistant virus variants.

Analysis of the T-cell receptor has revealed the molecular basis of antigen recognition by T cells specific for viral antigens. Studies using T-cell receptor transgenic mice have provided evidence for clonal deletion of virus-specific T cells in persistently infected hosts and for selection of T-cell-resistant virus variants in vivo.

Animals↗

PubMed1976

Studies on a measles virus variant inducing persistent infections in cultured cells.I. Isolation and characterization of plaque purified virus clones.

Attempts were made to characterized by a plaque assay two variants of the Edmonston strain of measles virus and to obtain plaque purified virus populations. The UP non-cytocidal variant, in all the examined cell systems, mainly produced small but also large plaques; the DP cytocidal variant always large plaques. Three clones, UP-SP4, UP-LP4 and DP-LP4, were derived by plaque purfication respectively of the UP small plaque, UP large plaque and DP large plaque forming particles. The virus populations of the clones could be distinguished by some other biological and physical characters: cytopathic effect in roller tube cultures, growth potential in HeLa cells, thermal stability at 45 degrees C, stability of the properties during serial passages at different input multiplicity. The hypothesis was supported that the typical properties of the UP and DP variants are host-independent and genetically controlled viral markers.

Animals↗

PubMed1991

Sequence variations in the envelope protein of the hepatitis C virus: comparison with partial cDNA sequence of a new variant virus obtained by the polymerase chain reaction.

It has been reported that the envelope region located at the 3' portion of the structural protein coding region is one of the most variable regions at both nucleotide and amino acid sequence levels in the hepatitis C virus (HCV) genome. We cloned HCV cDNA fragments of an envelope protein coding region (HCVNK), which were derived from serum of a Japanese patient with hepatocellular carcinoma and were amplified by polymerase chain reaction. After determining the nucleotide sequence, deduced amino acid sequence of the envelope protein region was compared with those of six HCV strains already published (HCJ1, HCVUS, HCJ4, HCVJH, HCVJ and HCVBK). Homology analysis among the strains revealed that the seven strains were classified into two subtypes; a US subtype (HCJ1 and HCVUS) and a Japanese subtype (HCJ4, HCVJH, HCVJ, HCVBK and HCVNK), since percentage homologies between two subtypes (70.3-77.3%) were significantly lower than those within each subtype (83.9-93.5%). Detailed analysis of the amino acid sequences also indicates that the region at aa246-aa258, tentatively named intersubtype variable region-1, may distinguish the US subtype from the Japanese subtype.

Amino Acid Sequence↗

PubMed1977

Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression.

Infection of adult C57BL/6 mice with variants of the radiation leukemia virus resulted in variable leukemia incidence. One variant, designated D-RadLV, induced lymphatic leukemia in 0 to 25% of mice after virus inoculation directly into the thymus of young adult mice. The leukemia incidence could be increased to 80 to 100% by host exposure to x-rays. The second variant, A-RadLV, induced lymphatic leukemia in 80 to 100% of similarly inoculated mice without the need for additional radiation treatment. Adult mice were inoculated with D-radLV or A-RadLV. Both variants reduced the immune response to sheep erythrocytes whereas only D-RadLV had an immunosuppressive effect after immunization with a thymus-independent immunogen polyvinyl-pyrrolidone (PVP). Results of transfer experiments indicated that the immunosuppressive effects were expressed at the immunocompetent cell level. Thymus-derived cells were affected by A-RadLV since their immunocompetent function was impaired, whereas D-RadLV affected the marrow cell population of immunocytes. Exposure of D-RadLV-inoculated mice to x-rays induced functional impairment of both thymus and marrow cells. Since the radiation leukemia virus induces "T" lymphatic leukemia it could be proposed that the initial tropism of the virus to thymocytes would lead to high leukemia induction potential, whereas virus tropism to bone marrow cells would yield a low leukemia incidence. The coleukemogenic effect of x-rays could perhaps be related with its capacity to alter and introduce a change in virus-lymphoid cells interaction.

Animals↗

PubMed1992

Basis of neurovirulence of avirulent rabies virus variant Av01 with stereotaxic brain inoculation in mice.

Av01 is a variant of the challenge virus standard strain of fixed rabies virus that was selected with a neutralizing anti-glycoprotein monoclonal antibody, and has a single amino acid change in the glycoprotein. It is avirulent after both intracerebral and peripheral routes of inoculation in adult mice. In this study, Av01 was found to be neurovirulent with stereotaxic brain inoculation in either the striatum or cerebellum of adult mice. Mice that had been inoculated simultaneously with Av01 by the intracerebral and intrastriatal routes recovered. More infectious virus was present in the brains of mice inoculated intrastriatally than intracerebrally, and more neurons contained rabies virus antigen. However, the topographical distribution of infected neurons was similar with both routes. Serum neutralizing antibodies against rabies virus were produced later and in smaller quantities after intrastriatal inoculation. Av01 is probably neurovirulent after stereotaxic brain inoculation because this route produces both a direct site of viral entry into the central nervous system and a low level of immune stimulation.

Animals↗

PubMedDate not supplied

[Determination of antibody specificity to a new influenza B virus variant by means of the immunoadsorption test].

Immunoadsorption test was used for determination of the strainspecificity of antibody to a new antigenic variant of influenza B virus (B/Hong Kong/5/72 and B/Yamagata/1/73) in human sera collected in April, 1973--March, 1974. The new strains were shown to be circulating in Moscow City only late in February and in March 1974. The experimental data show the immunoadsorption test to give more definite ideas not only on the qualitative differences between strains but also on the specificity of the immunologic response.

Adsorption↗