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PubMed2006

An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection.

Helicobacter pylori persistently colonizes about half the human population and contributes to the development of peptic ulcer disease and gastric cancer. This organism has evolved means to structurally alter its surface characteristics to evade innate and adaptive immune responses. H. pylori produces LPS O-antigen units that can be posttranslationally fucosylated to generate Lewis antigens, structures also found on human epithelial cells. We demonstrate an extensive diversity of Lewis x and Lewis y expression in LPS O-antigen units, occurring over time and in different regions of the human stomach. Lewis expression patterns were correlated with the on/off status of the three fucosyltransferases (FucT), FutA, FutB, and FutC, which are regulated via slipped-strand mispairing in intragenic polyC tract regions of the corresponding genes. The alpha1,3-FucT, FutA and FutB, each contain a C-terminal heptad repeat region, consisting of a variable number of DD/NLRV/INY tandem repeats. Variations in the number of heptad repeats correlated to the sizes of O-antigen polymers to become decorated by fucose residues. Our data support a molecular ruler mechanism for how H. pylori varies its LPS fucosylation pattern, where one heptad repeat in the enzyme corresponds to one N-acetyl-beta-lactosamine unit in the O-antigen polysaccharide.

Amino Acid Sequence↗
PubMed1999

Phylogenetic characterization of a highly attenuated strain of equine arteritis virus from the semen of a persistently infected standardbred stallion.

An avirulent, novel variant of equine arteritis virus (EAV; CA95G) was isolated from the semen of a persistently infected Standardbred stallion. The CA95G virus caused subclinical infection and seroconversion in susceptible horses, and virus was isolated only once from blood and nasal secretions collected from 6 experimentally infected horses. Sequence analysis of genes encoding the known EAV structural proteins shows that this highly attenuated strain of EAV is genetically similar to virulent field strains of EAV and, in particular, to a strain of EAV that was isolated during an outbreak of equine viral arteritis in western Canada in 1986. Not only is the carrier stallion the critical natural reservoir of EAV, but genetic diversity of the virus is generated in the course of persistent infection of carrier stallions. The subtle genetic changes that facilitate and maintain persistent EAV infection of the stallion's reproductive tract likely influence phenotypic properties of the virus such as virulence.

Animals↗
PubMed1997

Resistance to infection with mouse hepatitis virus (MHV) in the cell clones derived from persistently infected DBT cells with the JHM strain of MHV.

PiD-10 and piD-11 cells that have been established from persistently infected DBT cells with the JHM strain of MHV (JHMV) were resistant to infection with JHMV. There was no significant difference in the amount of adsorbed virus among piD-10, piD-11 and DBT cells. When an expression of mRNA of the MHV receptor in piD-10 and piD-11 cells was analyzed by the RT-PCR method, no significant difference was observed in the intensities of the amplified products among piD-10, piD-11 and DBT cells. Treatment of virus-adsorbed cells with PEG, which induces fusion of the cellular membrane with the viral envelop, causes entry of virus particles into cells. There was no significant difference in the yields of virus between PEG-treated and PEG-untreated cells. The titers of infectious virus internalized into piD-10 and piD-11 cells were the same as those in DBT cells. When piD-10 and piD-11 cells were fused with PEG and infected with JHMV, the yields of infectious virion particles from the fused cells between piD-10 and piD-11 cells were significantly lower than those from the fused cells between DBT and piD-10 or piD-11 cells. The present study showed that resistance of piD-10 and piD-11 cells to JHMV infection is not due to an inhibition of JHMV entry into the cells.

Animals↗
PubMed1993

Detection of unintegrated human immunodeficiency virus type 1 DNA in persistently infected CD8+ cells.

The presence of unintegrated viral DNA has been reported in cells persistently infected by lentiviruses, including human immunodeficiency virus type 1 (HIV-1). We confirm that CD8+ cells can be productively and persistently infected by HIV-1 for up to 4 months, as determined by secretion of viral core antigen p24 into the extracellular medium and by indirect immunofluorescence. The expression of the external viral glycoprotein gp120 at the surface of these cells was demonstrated by two-colour flow cytometry. Progeny virions recovered from CD8+ cells were infectious in CD4+ T cells. Despite an absence of significant cytopathology, these chronically infected CD8+ cells were shown to harbour unintegrated HIV-1 DNA, as detected by quantitative PCR. Both linear and circular forms of the extrachromosomal viral genome were present in infected CD8+ cells, as early as 3 weeks before a peak in viral replication. These findings provide evidence that the presence of unintegrated viral DNA during lentiviral infection may not always correlate with c.p.e.

Base Sequence↗
PubMed1988

Lifelong persistent infection of hamster brain by human adenovirus type 6.

To establish an experimental persistent infection of the brain with human adenoviruses, adenovirus type 6 (ad 6) was inoculated intracerebrally into young adult hamsters. Hamsters appeared languid for a few days after inoculation, but recovered rapidly. By cocultivation of tissue fragments with HeLa cells, ad 6 was always recovered from the brains of hamsters throughout their lives, as long as 29 months, indicating the establishment of a lifelong persistent infection. Except for the first few days after inoculation, however, attempts to recover virus by inoculation of tissue extracts onto HeLa cells or by cultivation of tissue fragments alone were unsuccessful.

Adenoviruses, Human↗
PubMed1997

A hypothalamic neuronal cell line persistently infected with scrapie prions exhibits apoptosis.

Neuronal death and vacuolation are characteristics of the CNS degeneration found in prion diseases. Relatively few cultured cell lines have been identified that can be persistently infected with scrapie prions, and none of these cells show cytopathologic changes reminiscent of prion neuropathology. The differentiated neuronal cell line GT1, established from gonadotropin hormone releasing-hormone neurons immortalized by genetically targeted tumorigenesis in transgenic mice (P. L. Mellon, JJ. Windle, P. C. Goldsmith, C. A. Padula, J. L. Roberts, and R. I. Weiner, Neuron 5:1-10, 1990), was examined for its ability to support prion formation. We found that GT1 cells could be persistently infected with mouse RML prions and that conditioned medium from infected cells could transfer prions to uninfected cells. In many but not all experiments, a subpopulation of cells showed reduced viability, morphological signs of neurodegeneration and vacuolation, and features of apoptosis. Subclones of GT1 cells that were stably transfected with the trk4 gene encoding the high-affinity nerve growth factor (NGF) receptor (GT1-trk) could also be persistently infected. NGF increased the viability of the scrapie-infected GT1-trk cells and reduced the morphological and biochemical signs of vacuolation and apoptosis. GT1 cells represent a novel system for studying the molecular mechanisms underlying prion infectivity and subsequent neurodegenerative changes.

Animals↗
PubMed1981

[Persistent infections induced by viral agents in animals].

Several studies have been conducted on persistent infections induced by viruses which are usually lytic for the infected cells. At the onset of these infections at least four mechanisms seem to be involved, i.e., the defective interfering (DI) viral particles, the temperature-sensitive (ts) mutants, the interferon or the presence in the culture of integrated DNA proviral copies of RNA viruses. Actually these systems are very complex and their evolution could depend on several factors such as the type of virus, the growth temperature of the culture or the kind of culture. Beside the systems that have been discussed here there may be other still unknown factors which might be involved in persistent infections, both in vitro and in vivo. The discovery of these factors could eventually represent a realistic basis for a better understanding of the pathogenesis of slow virus diseases and also would offer the possibility to study the long-term reactions of the organism when subjected to vaccination with ts mutants.

Animals↗
PubMed1985

Effect of measles virus antibodies on a measles SSPE virus persistently infected C6 rat glioma cell line.

Maintenance of measles (SSPE-Lec) virus persistently infected C6 rat glioma cells in medium containing polyclonal measles antiserum resulted in the loss of detectable expression of all measles virus proteins. Removal of these cells from antiserum, however, led to a re-expression of virus proteins and the production of infectious virus. Cloning of antibody-modulated non-expressing cells in the presence of antiserum showed that re-expression of virus proteins was not due to an incomplete curing process following the addition of antiserum, as a large number of non-expressing cell clones developed the capacity to express measles virus antigen at different periods after removal of antiserum. Irradiation of persistently infected cells to give a non-growing culture showed that modulation was not mediated by a selection and outgrowth of a small percentage of non-expressing cells originally present in the culture. Antibody directed against C6 membrane proteins did not lead to modulation and it was also shown that only monoclonal antibodies with neutralizing activity could affect intracellular antigen expression. Immunoglobulin Fab fragments with neutralizing activity also had modulating activity. Although all modulated cell clones were more susceptible to homologous virus infection than control C6 cells, it was not possible to rescue any defective measles virus which may have been maintained in the culture.

Animals↗
PubMed1993

Estimation of herd incidence of infection with bovine virus diarrhoea virus (BVDV) in herds previously without animals persistently infected with BVDV.

On a previous occasion, all animals in 9 herds had been bled for bovine virus diarrhoea virus (BVDV) and antibodies. No animals persistently infected (PI) with BVDV were detected. Three years later 10 animals in each herd were tested again. By this time 60 out of 90 previously seronegative animals had seroconverted. Seroconversions had occurred in 8 of the 9 herds corresponding to a incidence risk of herd infection of 0.52 per year. The incidence risk of seroconversions in individual animals was 0.31. Examination of young stock for antibodies and determination of antibody titer in bulk milk were good indicators for ongoing infections in the herds. The number of herd infections seemed to be higher than could be explained from purchase of PI animals.

Animals↗
PubMed1993

Simian immunodeficiency virus mutants resistant to serum neutralization arise during persistent infection of rhesus monkeys.

We previously described the pattern of sequence variation in gp120 following persistent infection of rhesus monkeys with the pathogenic simian immunodeficiency virus SIVmac239 molecular clone (D.P.W. Burns and R.C. Desrosiers, J. Virol. 65:1843, 1991). Sequence changes were confined largely to five variable regions (V1 to V5), four of which correspond to human immunodeficiency virus type 1 (HIV-1) gp120 variable regions. Remarkably, 182 of 186 nucleotide substitutions that were documented in these variable regions resulted in amino acid changes. This is an extremely nonrandom pattern, which suggests selective pressure driving amino acid changes in discrete variable domains. In the present study, we investigated whether neutralizing-antibody responses are one selective force responsible at least in part for the observed pattern of sequence variation. Variant env sequences called 1-12 and 8-22 obtained 69 and 93 weeks after infection of a rhesus monkey with cloned SIVmac239 were recombined into the parental SIVmac239 genome, and variant viruses were generated by transfection of cultured cells with cloned DNA. The 1-12 and 8-22 recombinants differ from the parental SIVmac239 at 18 amino acid positions in gp120 and at 5 and 10 amino acid positions, respectively, in gp41. Sequential sera from the monkey infected with cloned SIVmac239 from which the 1-12 and 8-22 variants were isolated showed much higher neutralizing antibody titers to cloned SIVmac239 than to the cloned 1-12 and 8-22 variants. For example, at 55 weeks postinfection the neutralizing antibody titer against SIVmac239 was 640 while those to the variant viruses were 40 and less than 20. Two other rhesus monkeys infected with cloned SIVmac239 showed a similar pattern. Rhesus monkeys were also experimentally infected with the cloned variants so that the type-specific nature of the neutralizing antibody responses could be verified. Indeed, each of these monkeys showed neutralizing-antibody responses of much higher titer to the homologous variant used for infection. These experiments unambiguously demonstrate that SIV mutants resistant to serum neutralization arise during the course of persistent infection of rhesus monkeys.

Amino Acid Sequence↗
PubMed2004

In vivo analysis of the 3' untranslated region of GB virus B after in vitro mutagenesis of an infectious cDNA clone: persistent infection in a transfected tamarin.

GB virus B (GBV-B), the virus most closely related to hepatitis C virus (HCV), infects tamarins and causes acute hepatitis. The 3' untranslated region (UTR) of an infectious GBV-B clone (pGBB) has a proximal short sequence followed by a poly(U) tract and a 3' terminal sequence. Our investigators previously demonstrated that the 3' terminal sequence was critical for in vivo infectivity. Here, we tested the effect of deleting the short sequence and/or the poly(U) tract from pGBB; infectivity of each mutant was tested by intrahepatic transfection of two tamarins with transcribed RNA. A mutant lacking both regions was not viable. However, mutants lacking either the short sequence or the poly(U) tract were viable. All four tamarins had a wild-type-like acute infection and developed acute hepatitis. Whereas we found that five tamarins transfected with the wild-type clone pGBB had acute resolving infection, one tamarin transfected with the poly(U) deletion mutant became persistently infected. This animal had viremia and hepatitis until its death at week 90. The genomes recovered at weeks 2, 7, 15, 20, 60, and 90 lacked the poly(U) stretch. Eight amino acid changes were identified at week 90. One change, in the putative p7 protein, was dominant at week 15. Thus, persistence of GBV-B, like persistence of HCV, was associated with the emergence of virus variants. Four tamarins inoculated with serum collected at weeks 2 and 90 from the tamarin with persistent infection had an acute resolving infection. Nonetheless, the demonstration that GBV-B can persist in tamarins strengthens its relevance as a surrogate model for the study of HCV.

3' Untranslated Regions↗
PubMed1980

Oncogenic transformation by by equine herpesviruses. II. Coestablishment of persistent infection and oncogenic transformation of hamster embryo cells by equine herpesvirus type 1 preparations enriched for defective interfering particles.

Infection of permissive hamster embryo cells with virus preparations enriched for defective interfering (DI) particles of equine herpesvirus type 1 (EHV-1) resulted in persistent infection and oncogenic transformation. Six cell lines, designated DI-5 to -10, exhibited biological properties (immortality, increased saturation density, growth in soft agar, etc.) inherent to transformed cells, but 2 to 18% of the total cells in these cell lines were shown to release virus as judged by electron microscope studies and infectious center assays. The released virus was shown to be standard EHV-1 and not to contain DI particles as determined by density measurements of the viral DNA in the analytical ultracentrifuge and by interference assays using the released virus. Tumorigenicity studies revealed that inoculation of these persistently infected cells into newborn LSH inbred hamsters resulted in a lethal, fulminating hepatitis, whereas inoculation into older immunocompetent hamsters (+4 weeks) led to the development of metastatic fibrous sarcomas. Tumor cell lines (DI-5T to -10T) established from these sarcomas were shown to be transplantable and virus nonproducers. Hybridization analyses of cellular DNAs from DI transformed and tumor cell lines using 32P-labeled genomic EHV-1 DNA as probes indicated that the whole virus genome was detectable in multiple copies (23 to 45) in the transformed cells and that DNA sequences representing only 43.5 to 56.6% of the virus genome were present in amounts of 2 to 4 copies per cell in the DI tumor cells. Expression of these viral DNA sequences as demonstrated by the detection of virus-neutralizing antibodies, 50% neutralizing dose titers ranging from 1:50 to 1:1,000, in the sera of animals inoculated with either the virus-producing transformed cells or the virus-nonproducing tumor cells. Further, EHV-1-specific proteins were detected in the membrane and the perinuclear region of bothDI transformed and tumor cells by indirect immunofluorescent assays using antisera against EHV-1 structural antigens, EHV-1 nonstructural antigens, or preparations of EHV-1 DI particles. The roles of DI particles in mediating persistent infection and cellular transformation are discussed.

Animals↗
PubMed1992

Antigenic change in feline calicivirus during persistent infection.

To determine if antigenic variation occurred during persistent infection of cats with feline caliciviruses (FCV), nine persistent (progeny) isolates from nine different carrier cats were compared antigenically to the original infecting parent strain, FCV 255, by two-way cross-neutralization tests with rabbit antisera. Five of the nine progeny viruses isolated 35 to 169 days after initial infection were antigenically different from the parent strain. These five isolates represented four distinct antigenic phenotypes. The emergence of four distinctly different antigenic variants from a single parent strain indicates that FCV, like many other RNA viruses, exhibits considerable antigenic heterogeneity during replication in its natural host, and supports the hypothesis that antigenic variation contributes to chronic FCV infection.

Animals↗
PubMed1986

Persistent infection of rat insulinoma cells with Coxsackie B4 virus. Brief report.

Plaque purified Coxsackie B4 virus (CB4) caused a persistent infection of rat insulinoma (RIN) cells which lasted for the 70 day observation period. Infectious virus was produced and no cytopathic effect was observed. Indirect immunofluorescence and infectious center assays demonstrated that a majority of RIN cells were infected. Defective interfering particles were not demonstrated. Despite persistent infection, insulin synthesis by RIN cells was not altered.

Adenoma, Islet Cell↗
PubMed2006

The small colony variant (SCV) concept -- the role of staphylococcal SCVs in persistent infections.

The recovery of small colony variants (SCVs) from clinical specimens was first described at the beginning of the last century. However, not until the past decade was an association of these variants with chronic, recurrent, and persistent infections such as chronic osteomyelitis and persistent skin and softtissue infection described. Since then, a number of reports and prospective studies have supported a pathogenic role for SCVs in disease. Biochemical and other characteristics of SCVs have suggested a link between electron-transport defective SCV strains and persistent infections, however, the strains examined were genetically undefined SCVs. Therefore, a stable mutant in electron transport was generated by interrupting one of the hemin biosynthetic genes, hemB, in Staphylococcus aureus. This mutant showed characteristics typical of clinical SCVs such as slow growth, decreased pigment formation, low coagulase activity, reduced hemolytic activity, and resistance to aminoglycosides. Furthermore, the mutant was able to persist within cultured endothelial cells due to decreased a-toxin production. It was suggested that the intracellular location of this subpopulation might shield the variants from host defenses and antibiotics, thus providing one explanation for the difficulty in removing SCVs from host tissues. Therefore, a defect in the electron-transport system allows S. aureus SCVs to resist aminoglycosides and persist intracellularly. Because of their fastidious growth characteristics, they are easily missed or misidentified in the clinical laboratory. Therefore, when an infection persists for weeks or months or fails to respond to antimicrobial therapy, clinicians as well as laboratory personnel should consider further efforts to search for this staphylococcal subpopulation.

Animals↗
PubMed2006

Fetal protection following exposure to calves persistently infected with bovine viral diarrhea virus type 2 sixteen months after primary vaccination of the dams.

This study demonstrated that the bovine viral diarrhea virus (BVDV; types 1 and 2) fractions of a multivalent vaccine protected pregnant heifers and their fetuses at 149 to 217 days of gestation against exposure to calves persistently infected with BVDV type 2a. Eighty percent (eight of 10) of the control heifers were viremic at least 1 day following challenge, whereas all (20 of 20) BVDV-vaccinated heifers were virus isolation-negative on all postchallenge assessment days. Ninety percent (nine of 10) of the calves born to control heifers but only 5% (one of 20) of calves born to BVDV-vaccinated heifers seroconverted to BVDV type 2 before ingesting colostrum. One calf born to a control heifer was persistently infected. No calves from BVDV-vaccinated heifers were persistently infected.

Animals↗
PubMed1988

Stability of vaccinia virus DNA during persistent infections: accumulation of left-end deletions and of tandem repeats at both ends of the viral genome and prevention by interferon.

The stability of the large vaccinia virus genome (122 MDa) has been studied in long-term cultures of persistently infected Friend erythroleukemia (FEL) cells. Deletions of about 8 MDa at the left terminus of vaccinia DNA are generated at early passages, and are maintained even after 2 years of continuous cell passages. The generation of deletions is followed by a stable accumulation of tandem repeats up to 6 MDa at the left end and up to 2 MDa at the right end of vaccinia DNA. Neither translocations nor rearrangements of DNA are observed during persistent infection. A recombinational mechanism within the tandem repeats or a mechanism similar to that described for adenovirus might explain the reiteration of tandem repeats at both ends. Significantly, in persistently infected cultures continuously treated with interferon (IFN) both the deletion and the large accumulation of tandem repeats were completely blocked. We suggest that reiteration of tandem repeats at the termini of vaccinia DNA might provide signals for more efficient virus multiplication in FEL cells.

Animals↗
PubMed1994

Flock house virus: a simple model for studying persistent infection in cultured Drosophila cells.

Flock house virus (FHV), isolated from twenty Drosophila melanogaster cell lines, persistently infected with the virus, were examined during successive serial passages by plaque assay and sequence analysis. No phenotypic or genotypic changes in the virus were observed during the establishment of persistent infection, suggesting that it was a cellular modification that led to the first step in establishing the persistent state. Once this state was initiated, the virus was relieved of the need for a functional coat protein to propagate itself and mutations began to accumulate selectively in RNA2, the gene for the coat protein. These changes were manifested by a gradual drift to a smaller plaque population. The replicase activity, coded by RNA1, remained unaltered.

Animals↗