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PubMed1978

Persistent infections with "runde" virus in cell cultures and suckling mice.

A morphologically intact, persistently infected BHK 21/c13 cell culture was established by serial trypsinization and reseeding of cells infected with approximately one baby mouse LD50/cell. The extracellular virus infectivity dropped more than 3 log10 units from the 1st to the 4th passage, and was then unaltered up to passage 20. In 2-week-old mice but not in baby mice, a chronic disease with virus persistence up to 150 days was produced after intracerebral infection with moderate virus doses. The humoral immune response of the animals seemed to be adequate by the methods employed. Development of defective interfering virus particles was indicated by the von Magnus phenomenon in BHK 21/c13 cultures infected with serially passed, undiluted virus samples. Intracerebral infection of baby mice with such samples resulted in transient paresis and motion disturbances instead of the usually fatal encephalitis. Specific virus antigens but no infectious virus could be recovered from such animals.

Animals↗
PubMed1997

Viral persistent infection affects both transcriptional and posttranscriptional regulation of neuron-specific molecule GAP43.

Recently, we reported that in vitro and in vivo persistent infection of neurons by lymphocytic choriomeningitis virus (LCMV) downregulated GAP43 expression, a protein involved in neuronal plasticity associated with learning and memory. Here, we investigated the transcriptional and posttranscriptional events involved. Persistent LCMV infection of PC12 cells (PC12Pi) caused reduced levels of GAP43 steady-state mRNA when compared to uninfected PC12 cells. In addition, an increase in the steady-state levels of GAP43 mRNA observed in PC12 cells in response to nerve growth factor (NGF) was abrogated in PC12Pi cells. Nuclear run-on analysis revealed that the rate of GAP43 transcription was reduced threefold in PC12Pi cells compared to uninfected PC12 cells. Moreover, analysis of the half-life of GAP43 mRNA indicated that NGF-mediated stabilization of GAP43 transcripts was significantly diminished in PC12Pi cells. Treatment of PC12Pi cells with basic fibroblast growth factor, dibutyryl cyclic AMP, and 12-o-tetradecanoyl-phorbol-13-acetate, a potent activator of protein kinase C, did not increase the GAP43 mRNA steady-state level, suggesting that LCMV infection interferes with a step downstream from protein kinases A and C in the NGF signal transduction pathway.

Animals↗
PubMed2003

Characterisation of a pestivirus isolated from persistently infected mousedeer ( Tragulus javanicus).

Serum samples from the male Mousedeer A and the mother, father and sister of A were tested for bovine virus diarrhoea viruses (BVDV) by isolation, and for BVDV antibodies by blocking ELISA and homologous neutralisation test. Further, RNA was extracted and tested by RT-PCR protocol analysing the 5'-untranslated region and the E2 gene of pestivirus. The RT-PCR products were subsequently sequenced. Mousedeer A was positive in virus isolation on three occasions (days 1, 19 and 40) and by RT-PCR. The sister and mother of Mousedeer A were also found virus positive by isolation and RT-PCR. Mousedeer A, its sister and its mother, all had an antibody neutralisation titer below 10. The father of A was virus negative but was positive in the blocking antibody ELISA and had a high neutralisation antibody titer. The repeated detection of BVDV in Mousedeer A, the high amount of virus in serum, the lack of antibodies and the virus positive family members documented that the mousedeer were persistently infected with a pestivirus. The father of A probably had an acute infection resulting in antibodies to pestivirus and viral clearance. Sequence analysis and phylogenetic analysis revealed that the mousedeer pestivirus was closely related to BVDV Type 1f. The existences of persistently infected animals in non-domestic species have great implications for BVDV eradication campaigns in cattle.

5' Untranslated Regions↗
PubMed2002

Equine infectious anemia virus envelope evolution in vivo during persistent infection progressively increases resistance to in vitro serum antibody neutralization as a dominant phenotype.

Equine infectious anemia virus (EIAV) infection of horses is characterized by well-defined waves of viremia associated with the sequential evolution of distinct viral populations displaying extensive envelope gp90 variation; however, a correlation of in vivo envelope evolution with in vitro serum neutralization phenotype remains undefined. Therefore, the goal of the present study was to utilize a previously defined panel of natural variant EIAV envelope isolates from sequential febrile episodes to characterize the effects of envelope variation during persistent infection on viral neutralization phenotypes and to define the determinants of EIAV envelope neutralization specificity. To assess the neutralization phenotypes of the sequential EIAV envelope variants, we determined the sensitivity of five variant envelopes to neutralization by a longitudinal panel of immune serum from the source infected pony. The results indicated that the evolution of the EIAV envelope sequences observed during sequential febrile episodes produced an increasingly neutralization-resistant phenotype. To further define the envelope determinants of EIAV neutralization specificity, we examined the neutralization properties of a panel of chimeric envelope constructs derived from reciprocal envelope domain exchanges between selected neutralization-sensitive and neutralization-resistant envelope variants. These results indicated that the EIAV gp90 V3 and V4 domains individually conferred serum neutralization resistance while other envelope segments in addition to V3 and V4 were evidently required for conferring total serum neutralization sensitivity. These data clearly demonstrate for the first time the influence of sequential gp90 variation during persistent infection in increasing envelope neutralization resistance, identify the gp90 V3 and V4 domains as the principal determinants of antibody neutralization resistance, and indicate distinct complex cooperative envelope domain interactions in defining sensitivity to serum antibody neutralization.

Amino Acid Sequence↗
PubMedDate not supplied

Spontaneous shift of an HSV type 1 productive, persistently infected macrophage-like culture to a non-productive culture.

A herpes simplex virus type 1 (HSV1) productive, persistently infected murine macrophage-like culture was obtained by infection at low multiplicity (0.001). Persistent cultures were characterized by spontaneously ceasing to produce infectious viruses after initial HSV1 production. A similar pattern of virus production was observed in cultures obtained by reinfection of the persistent macrophages with the original virus. Nonetheless, in persistent and reinfected cultures (17/18) which did not produce infectious viruses, viral proteins were detected by immunoblot, although their molecular weight, number and pattern differed among the cultures.

Animals↗
PubMed1984

Clearance of feline leukemia virus from persistently infected pet cats treated by extracorporeal immunoadsorption is correlated with an enhanced antibody response to FeLV gp 70.

Six persistently feline leukemia virus (FeLV)-infected pet cats were treated by extracorporeal immunoadsorption with Staphylococcus aureus Cowan I (SAC) to remove circulating immune complexes and immunoglobulin G (IgG) from plasma. In three of these cats, the FeLV infection was eliminated, whereas in the other three cats the infection persisted. The amounts of peripheral blood leukocyte (PBL)-associated FeLV, soluble FeLV envelope glycoprotein (gp70) antigens in serum, and FeLV-gp70-specific antibodies were determined in all six cats at different times during treatment. In all of the cats, there were fluctuations in the amounts of FeLV-positive PBL and of serum antigen related to FeLV gp70. The one serologic parameter that always correlated with complete clearance of FeLV in the responder cats was the development of free antibodies to gp70. These results suggest that extracorporeal immunoadsorption treatment stimulates an existing low level antibody response to FeLV in some cats, and that these antibodies mediate the clearance of FeLV. The results also suggest that determination of antibody titer to FeLV is of value in predicting the outcome of extracorporeal immunoadsorption treatments as well as when treatment may be terminated.

Animals↗
PubMed2004

The N-terminal region of the murine coronavirus spike glycoprotein is associated with the extended host range of viruses from persistently infected murine cells.

Although murine coronaviruses naturally infect only mice, several virus variants derived from persistently infected murine cell cultures have an extended host range. The mouse hepatitis virus (MHV) variant MHV/BHK can infect hamster, rat, cat, dog, monkey, and human cell lines but not the swine testis (ST) porcine cell line (J. H. Schickli, B. D. Zelus, D. E. Wentworth, S. G. Sawicki, and K. V. Holmes, J. Virol. 71:9499-9507, 1997). The spike (S) gene of MHV/BHK had 63 point mutations and a 21-bp insert that encoded 56 amino acid substitutions and a 7-amino-acid insert compared to the parental MHV strain A59. Recombinant viruses between MHV-A59 and MHV/BHK were selected in hamster cells. All of the recombinants retained 21 amino acid substitutions and a 7-amino-acid insert found in the N-terminal region of S of MHV/BHK, suggesting that these residues were responsible for the extended host range of MHV/BHK. Flow cytometry showed that MHV-A59 bound only to cells that expressed the murine glycoprotein receptor CEACAM1a. In contrast, MHV/BHK and a recombinant virus, k6c, with the 21 amino acid substitutions and 7-amino-acid insert in S bound to hamster (BHK) and ST cells as well as murine cells. Thus, 21 amino acid substitutions and a 7-amino-acid insert in the N-terminal region of the S glycoprotein of MHV/BHK confer the ability to bind and in some cases infect cells of nonmurine species.

Animals↗
PubMed1990

Detection of bovine viral diarrhea virus genome in leukocytes from persistently infected cattle by RNA-cDNA hybridization.

A bovine viral diarrhea virus (BVDV) cDNA library was constructed. One cloned complementary DNA sequence was used as a probe to detect BVDV RNA by hybridization in infected cell cultures and in mononuclear leukocytes from persistently infected cattle by dot blot and in situ hybridization. The cDNA probe hybridized with all cytopathic and noncytopathic BVDV isolates tested. The hybridization results were consistent with results obtained using conventional subculturing and immunofluorescent staining methods and by inoculation of seronegative test cattle.

Animals↗
PubMed1993

SV40 DNA extracted from persistently infected Vero cells using miniprep columns for plasmids.

A recombinant pAT153 plasmid carrying the whole simian virus 40 (SV40) genome in the form of two consecutive Pst I restriction fragments was rapidly isolated using a commercially available minipreps DNA purification system. This rapid and simple method was used to extract SV40 DNA from infected Vero monkey cells. Viral DNA replication in persistently infected SVP-1 monkey cells was also conveniently followed over a period of 8 d by agarose gel electrophoresis and molecular hybridization using minipreps and the recombinant plasmid (pLCB104) as a probe. Unsatisfactory results were obtained, however, when herpes simplex virus DNA was tentatively extracted from infected Vero cells with the above method. Only covalently closed circular DNA molecules, with two strands unable to separate fully under denaturing conditions, were apparently retained after rapid neutralization by the silicone-based minipreps DNA purification resin.

Animals↗
PubMed2006

Genetic complexity of EHV-1 defective interfering particles and identification of novel IR4/UL5 hybrid proteins produced during persistent infection.

This study examined the genetic complexity of three equine herpesvirus 1 (EHV-1) defective interfering particles (DIP) and found the DIP genomes to range from 5.9 kbp to 7.3 kbp in total size. Each DIP contains an identical 5' end ( approximately 1.9 kb) that harbors UL3 and UL4 genes that are 100% identical to those of the infectious virus. DIP2 and DIP3 contain a previously described unique IR4/UL5 (EICP22/EICP27) hybrid gene (Hyb1.0). The DIP1 genome, however, appears to be generated from a different recombination event which results in the formation of a new distinct hybrid ORF. The new ORF (Hyb2.0) is comprised of 684 bp from the 5' end of IR4 fused to 45 bp from the 3' terminus of UL5. In contrast to Hyb1.0, the UL5 sequences present in Hyb2.0 are not in-frame. Thus, the Hyb2.0 protein is comprised of 228 residues from IR4 linked to a sequence of 15 amino acids that result from a frameshifted reading of UL5 sequences. Western blot analysis confirmed that the Hyb2.0 ORF is expressed during persistent infection to produce a family of proteins that migrate at 36-42 kDa. Fluorescence microscopy revealed that both Hyb proteins display diffuse cytoplasmic localization patterns dissimilar to the nuclear localization patterns of both IR4 and UL5. Neither Hyb protein, however, disrupts the nuclear entry of the EHV-1 immediate-early, IR4, or UL5 proteins or cellular TATA box binding protein (TBP) previously shown to interact with both IR4 or UL5 in productive infection. DIP genomic segments ( approximately 3.5-5.0 kbp) downstream of the 100% conserved origin of replication are highly variable among the three DIP genomes and contain large areas of repetitive sequences. The possibility that the non-coding sequences play a role in viral interference and/or persistent infection remains to be determined.

Amino Acid Sequence↗
PubMed1990

Hepatitis B viruses with precore region defects prevail in persistently infected hosts along with seroconversion to the antibody against e antigen.

The C gene of hepatitis B virus (HBV) codes for a nucleocapsid protein made of 183 amino acid residues and is preceded in phase by the precore (pre-C) region, encoding 29 residues. The pre-C-region product is required for the synthesis and secretion of hepatitis B e antigen (HBeAg), which is made of the C-terminal 10 amino acid residues of the pre-C-region product and the N-terminal 149 residues of the C-gene product. HBV mutants with pre-C-region defects prevailed in the circulation of three asymptomatic carriers as they seroconverted from HBeAg to the corresponding antibody (anti-HBe), and these mutants finally replaced nondefective HBV. HBV DNA clones were propagated from sera of an additional 15 carriers with anti-HBe and sequenced for the pre-C region. Essentially all HBV DNA clones (56 of 57 [98%]) revealed mutations that prohibited the translation of a functional pre-C-region product. A point mutation from G to A at nucleotide 83, converting Trp-28 (TGG) to a stop codon (TAG), was by far the commonest and was observed in HBV DNA clones from 16 (89%) of 18 carriers seropositive for anti-HBe. In addition, there were point mutations involving ATG codon to abort the translation initiation of the pre-C region, as well as deletion and insertion to induce frameshifts. Such mutations leading to pre-C-region defects were rarely observed in persistently infected individuals positive for HBeAg or in patients with type B acute hepatitis after they had seroconverted to anti-HBe. These results would indicate a selection of pre-C-defective mutants in persistently infected hosts, along with seroconversion to anti-HBe, by immune elimination of hepatocytes harboring nondefective HBV with the expression of HBeAg.

Amino Acid Sequence↗
PubMed1991

When Epstein-Barr virus persistently infects B-cell lines, it frequently integrates.

In this study we used Gardella gel analysis of intact DNA, Southern blotting of digested DNA, and fluorescence in situ hybridization to provide complementary and unequivocal information on the state of the Epstein-Barr virus (EBV) genome in persistently infected cells. The fluorescence in situ hybridization technique allowed us to directly visualize both integrated and episomal EBV DNA at the single-cell level. We show here that circularization of the EBV genome is rarely detected upon infecting activated normal B cells. The virus can persist upon infection of a different proliferating B-cell target, EBV-negative Burkitt's lymphoma tumor cell lines. Analysis of 16 such lines reveal again, that the virus infrequently persists as covalently closed episomes; rather, the virus preferentially persists by integrating into the host DNA (10 of 16 clones). The integrated virus is linear and usually intact, although 3 of 10 isolates have deletions from the left-hand end including the latent origin of replication. At the level of our analysis, no obvious relationship was seen between the integration sites. These studies provide, for the first time, a reproducible in vitro model system to study integration by EBV.

B-Lymphocytes↗
PubMed1984

In vitro propagation of canine distemper virus: establishment of persistent infection in Vero cells.

Primary cultures of bovine fibroblast (BF) and canine brain cells, persistently infected with virulent R252-canine distemper virus (CDV), were cocultured with African green monkey (Vero) cells. Transfer of persistent CDV from BF to Vero cells varied inversely with the in vitro passage level (age) of the CDV-infected BF cells. Successful transfer of CDV to Vero cells was signaled by the transient appearance of viral syncytia, rapid spread of viral antigen to all Vero cells in the culture, and by recovery of cell-free Vero-infectious virus in culture fluids. With time, viral cytopathic effects in Vero cells containing CDV disappeared, and the infected lines could not be distinguished from noninfected control Vero cells, except by immunoassay for viral antigen.

Animals↗
PubMed1977

Persistent infection of BHK21/WI-2 cells with rubella virus and characterization of rubella variants.

Persistently infected cell lines of BHK21/WI-2 cells have been established by infection with the wild type rubella virus strain M-33. These cell lines, BHK-MP1 and BHK-MP2, showed immunity-like resistance to superinfection with M-33 virus at both 34 degrees and 39.5 degrees C. They also showed intrinsic interference with the replication of Newcastle Disease Virus at 34 degrees C but not at 39.5 degrees C. They released a small number of infectious virus particles which were temperature sensitive variants, being able to form plaques at 34 degrees C, but not at 39.5 degrees C on BHK21/WI-2 and on its derivative, BSR. When BHK-MP1 cells were cultured at 34 degrees C in growth medium containing 10--20 microgram/ml of 5-bromodeoxyuridine (BudR) there was a 5- to 10-fold increase in infectious virus in the medium as compared with the untreated controls. Mitomycin C (0.5 microgram/ml) treatment for 7 hours likewise stimulated the release of virus from these cells. The enhancement of viral release by BudR was completely blocked by pretreatment with actinomycin D (5 microgram/ml) for 3 hours prior to BudR treatment. Since the variant can be induced by these prophage inducers and inhibited by actinomycin D it is suggested that the viral genome is converted to a DNA provirus which is analogous to the lysogenic state of bacteriophage.

Animals↗
PubMed1981

Measles virus: evolution of a persistent infection in BGM cells.

An African green monkey kidney cell line (BGM) persistently infected with measles virus (BGM/Hallé cells) has been studied during 3 years in culture. The early cell passages were characterized by slow growing cultures producing high yields of infections virus (10(6)--10(7) PFU/ml). These cells were gradually replaced by a population of cells multiplying at a similar rate as non-infected cells. During this evolution, the virus released from the cells changed from a large plaque variant, to a small plaque and eventually unlysed foci. Despite greater than or equal to 95 per cent of the cells being infected, the virus yield fell to the limits of detection. [35S]-methionine labelling of BGM/Hallé cultures at the 20th and 140th passage showed that in both cases all the measles virus structural proteins were synthesized. There were no changes in the apparent molecular sizes of the viral proteins during passage. Cell surface [125I]-labelling of BGM/Hallé cells indicates that viral envelope antigens are inserted into the membrane despite the diminution in virus yield. Several cell proteins not labelled in non-infected BGM cells are also labelled. These proteins could also be [125I]-labelled in clones of BGM/Hallé cells with had been "cured" of virus. Chase experiments of [125I]-pre-labelled BGM/Hallé cultures showed the radiolabelled antigen to be incorporated into virus particles. Non-infections virus particles released from the cells contained the same polypeptides as those released from a lytic infection.

Animals↗
PubMed2001

Persistent infection is a rare sequel following infection of pigs with swine vesicular disease virus.

Nine isolates from pigs persistently infected with a recent Italian isolate of swine vesicular disease (SVD) virus, ITL/9/93, were collected sequentially over 121 days and were characterized antigenically and biochemically. There was an accumulation of amino acid (aa) substitutions in the capsid proteins throughout the carrier state that could be correlated with alterations in antigenicity in virus isolates collected late stage in infection. The aa substitutions detected mainly occurred in VPI and antigenic changes were detected in late isolates both at antigenic site 1, resulting in loss of binding of Mab 4GO7, and at a closely located site which has not yet been named, recognized by Mab C29. In further experiments groups of pigs were exposed to a range of SVD viruses, but no virus was isolated beyond 16 days post infection (dpi) nor viral RNA detected beyond 42 dpi. Attempts to transfer infection to sentinel pigs introduced some time after initial infection of the original pigs were largely unsuccessful. The carrier state was established in only one out of five experimental infections of pigs with SVD virus and can therefore be considered a rare sequel toinfection with SVD virus and is of limited significance in the epidemiology of the disease.

Amino Acid Sequence↗
PubMed1991

Evidence for immune-mediated destruction as mechanism for LCMV-induced anemia in persistently infected mice.

A docile substrain of lymphocytic choriomeningitis virus (LCMV) causes a persistent infection in adult C3HeB mice and induces a severe anemia, which, unlike the viremia, eventually resolves. Measurements of red blood cell (RBC) survival rates demonstrated an increased rate of RBC clearance in these animals, indicating a hemolytic process for the anemia. Normal clearance rates of RBCs from infected mice transfused into control mice suggested that there was not an intrinsic defect in these cells. It also appeared that RBC destruction was immune-mediated, as cyclophosphamide treatments prevented the onset of anemia in infected mice, whereas adoptive transfer (AT) of immune splenocytes into immunocompromised mice reestablished the condition. The AT experiments also demonstrated that the onset of anemia correlated with the functional state of the immune cells. In addition, opsonization of RBCs was demonstrated by macrophage phagocytosis, and the appearance of opsonized RBCs corresponded with the course of the anemia. These findings support a hypothesis of RBC opsonization and subsequent phagocytosis by macrophages of the reticuloendothelial system as the mechanism for RBC destruction in LCMV-induced hemolytic anemia.

Anemia, Hemolytic, Autoimmune↗