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At least 1,207 records · Page 67Linked to original sources
PubMed2002

Helicobacter pylori SabA adhesin in persistent infection and chronic inflammation.

Helicobacter pylori adherence in the human gastric mucosa involves specific bacterial adhesins and cognate host receptors. Here, we identify sialyl-dimeric-Lewis x glycosphingolipid as a receptor for H. pylori and show that H. pylori infection induced formation of sialyl-Lewis x antigens in gastric epithelium in humans and in a Rhesus monkey. The corresponding sialic acid-binding adhesin (SabA) was isolated with the "retagging" method, and the underlying sabA gene (JHP662/HP0725) was identified. The ability of many H. pylori strains to adhere to sialylated glycoconjugates expressed during chronic inflammation might thus contribute to virulence and the extraordinary chronicity of H. pylori infection.

Adhesins, Bacterial↗
PubMed1979

Persistent infection of a human lymphoblastoid cell line with equine herpesvirus 1.

Infection of a human lymphoblastoid cell line (Jijoye line derived from a Burkitt lymphoma which contains Epstein-Barr virus) with equine herpesvirus 1, maintained and observed for 53 days, was characterized by the continuous production of infectious extracellular and intracellular virus. Maximum virus production correlated with active cell multiplication. Less than 15% of the cells possessed viral capsid antigen at any one time. Five percent of the cells in the Jijoye line possess Epstein-Barr viral capsid antigen; 80% of the Epstein-Barr viral caspid-containing cells also contained equine herpesvirus 1 antigen as detected by double staining. The interaction of equine herpesvirus 1 and lymphoblastoid cells provides a useful in vitro model which may help clarify the mechanism for herpesvirus latency.

Antigen-Antibody Reactions↗
PubMed1979

Reactivation of polyoma virus in kidneys of persistently infected mice during pregnancy.

Female mice infected at birth with 10(7) 50% tissue culture infective doses of polyoma virus were mated when at least 6 weeks old. Polyoma was not detected in any tissues of 27 female mice before mating except for trace amounts in the kidneys of 2 mice, but late in gestation polyoma virus could be found in the kidneys of 21 of 38 mice with titers of 10(3.7) to 10(6.2) 50% tissue culture infective doses per gram of kidney. The virus was not detected in the brain, salivary gland, lung, liver, spleen, ovaries, placenta, or fetuses during gestation. Nonpregnant females were injected with female sex hormones over a period of 17 days, and polyoma was then detected in kidneys of 4 of 18 mice. Treatment of cultures of mouse embryo fibroblasts with either sexhormones or a glucocorticosteroid resulted in approximately a threefold increase in the rate of infection of cells with polyoma virus.

Animals↗
PubMed1980

Immune responses of goats persistently infected with caprine arthritis-encephalitis virus.

Eight cesarean-derived goat kids were inoculated with caprine arthritis-encephalitis virus (CAEV), and proliferative responses of their peripheral blood mononuclear cells to mitogens and CAEV antigen were monitored for 9 months. Antibody specific for CAEV was measured by an enzyme-linked immunosorbent assay. Five cesarean-derived noninfected goats were tested simultaneously. Significant differences between the infected and control mononuclear cell proliferation reactions to CAEV began 14 days post-inoculation and continued in a fluctuant manner until 134 days post-inoculation. The magnitude of the proliferative reaction steadily increased in infected goats until the end of the experiment at 271 days post-inoculation. Responses to mitogens were not significantly different between infected and control goats. Virus-inoculated goats produced CAEV-specific antibody that reached a maximum level between 49 and 77 days post-inoculation and then declined to lower levels through 271 days post-inoculation. The virus-inoculated goats developed mild but characteristic clinical evidence of caprine arthritis-encephalitis, and CAEV was reisolated from four goats at 286 days post-inoculation. The five control goats developed neither an anti-CAEV immune response nor clinical disease, and CAEV could not be reisolated from them.

Animals↗
PubMed1980

Anti-deoxyribonucleic acid antibody associated with persistent infection of mink with Aleutian disease virus.

Anti-deoxyribonucleic acid (DNA) antibody was quantitated in sera from mink infected with Aleutian disease virus (ADV). During the course of the disease after experimental infection, the amount of anti-DNA antibody increased 60% initially, but then decreased to an intermediate level when measured 2.5 months later. The percentage of serum immunoglobulin, however, steadily increased over 3.5-fold during this period, resulting in the characteristic gammopathy. Correlation between the level of anti-DNA antibody and hypergammaglobulinemia was demonstrated with sera from chronically infected mink. Competition experiments and use of labeled nucleic acids indicated that the immunoactivity was more specific for double-stranded DNA than single-stranded DNA or ribonucleic acid. Anti-DNA antibody was found in purified immunoglobulin from chronically infected mink. Differences in avidity of antibody to DNA among antisera that had the same equivalence point were found. Avidity of antibody for DNA increased during the course of the disease.

Aleutian Mink Disease↗
PubMed1983

Immune rabbit sera do not recognize antigenic variants of caprine arthritis-encephalitis virus isolated during persistent infection.

Isolates of caprine arthritis-encephalitis virus recovered 12 to 18 months after infection of goats were tested for neutralization by using rabbit antisera directed to the original inoculum virus. Only slight differences in neutralization kinetics between the long-term isolates and the original virus were detected, indicating that heterologous rabbit antisera do not detect antigenic variation of the neutralizing epitopes of caprine arthritis-encephalitis virus.

Animal Diseases↗
PubMed1999

Typing of bovine viral diarrhea viruses directly from blood of persistently infected cattle by multiplex PCR.

A nested multiplex PCR was developed for genotyping of bovine viral diarrhea viruses (BVDVs). The assay could detect as little as 3 50% tissue culture infective doses of BVDV per ml and typed 42 out of 42 cell culture isolates. BVDV was also successfully typed, with or without RNA extraction, from all 27 whole-blood samples examined from 22 carriers or probable carriers and 5 experimentally infected cattle.

Animals↗
PubMed1976

Induction of measles virus hemagglutinin in a persistently infected, nonvirogenic line of cells (BGM/MV).

BGM/MV cells carry measles virus antigens and nucleocapsid-like structures in their cytoplasm. There is no infectious virus demonstrable, and measles virus-induced cell surface changes detectable by hemadsorption (HAD) are absent. Treatment of cells with actinomycin D or cycloheximide or enucleation of cells with cytochalasin B induced surface changes in that the cells became HAD positive. 6-Azauridine treatment of cells did not inhibit the induction of HAD, suggesting that RNA synthesis was not required. Cycloheximide treatment of cells induced by enucleation inhibited the development of HAD, suggesting a requirement for protein synthesis.

Animals↗
PubMed1984

Structure and genetic complexity of the genomes of herpesvirus defective-interfering particles associated with oncogenic transformation and persistent infection.

The complexity and structural organization of defective-interfering (DI) particle DNA of equine herpesvirus type 1 (EHV-1) have been elucidated by using restriction enzyme and Southern blot hybridization analyses. DI particles were generated by serial high-multiplicity passage of EHV-1 in L-M cells, and total viral DNA was extracted from virus purified from supernatants of these serial passages. EHV-1 DI particle DNA was quantitatively separated from standard (STD) DNA by several cycles of CsCl isopycnic banding in a vertical rotor. Restriction endonuclease digestion profiles of pure DI DNA were completely different from the mapped patterns observed for EHV-1 STD DNA. Digestion of pure defective DNA with restriction enzymes (Bg/II, EcoRI, and XbaI), for which there are few or no cleavage sites within the S (short) region of the EHV-1 STD genome, yielded high-molecular-weight supermolar DNA bands, suggesting that a large subgenomic repeat unit was present in defective DNA. DNA blot hybridization analysis with the Bg/II supermolar fragment of defective DNA, intact DI particle genomic DNA, and EHV-1 STD DNA restriction enzyme fragments as 32P-labeled probes indicated that the EHV-1 DI particle genome originates predominately from the STD DNA S region (0.77 to 1.00 map units) and to a lesser extent from the left terminus of the unique long (UL) region (0.00 to 0.05 map units). None of the EHV-1 DNA sequences associated to date with EHV-1 oncogenesis (0.32 to 0.38 map units; O'Callaghan et al. in B. Roizman [ed.], Herpesviruses, in press; Robinson et al., Cell 32:204-219, 1983, and Proc. Natl. Acad. Sci., U.S.A., 78:6684-6688, 1981) were detected in the DI particle DNA. The importance of these data with regard to DNA replication of DI particles and the role of DI particles in one model system of EHV-1 oncogenic transformation are discussed.

Animals↗
PubMed1987

Course and extent of variation of equine infectious anemia virus during parallel persistent infections.

Comparisons of peptide and oligonucleotide maps of glycoproteins and RNA from nine isolates of equine infectious anemia virus (EIAV) that were generated during parallel infections of two Shetland ponies revealed that each isolate was structurally unique. Each EIAV isolate contained a unique subset of variant peptides, oligonucleotides, or both, indicating that structural variation in EIAV is a random and noncumulative process and that a large spectrum of possible EIAV variants can be generated in infected animals.

Animals↗
PubMed1991

Atypical dissemination of the highly neurotropic Borna disease virus during persistent infection in cyclosporine A-treated, immunosuppressed rats.

In adult rats infected with Borna disease virus, the virus was found exclusively in the brain, whereas in cyclosporine A-treated rats, infectious virus was also detected in peripheral nerve fibers and, unexpectedly, in adjacent organ-specific cells. In contrast to untreated virus-infected rats, no major histocompatibility complex class II expression was found in the brain of cyclosporine A-treated animals.

Animals↗