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PubMed1991

Numerous transitions in human parainfluenza virus 3 RNA recovered from persistently infected cells.

The nucleotide sequences at the 3'-termini of human parainfluenza virus 3 (HPIV3) genomic RNAs recovered from two lines of persistently infected LLC-MK2 cells were determined following PCR amplification. After 29 months of persistence the 3'-end of the HPIV3 genome was found to be highly mutated. Interestingly, the only types of nucleotide changes observed were U to C and A to G transitions. Both U to C and A to G transitions were present on individual RNA molecules. The data indicate that biased hypermutational activity leading to U To C and A to G mutations operates in cultured cells during persistent HPIV3 infections.

Base Sequence↗
PubMed2000

B cells are required for the induction of intestinal inflammatory lesions in TCRalpha-deficient mice persistently infected with Cryptosporidium parvum.

Mice with targeted disruptions in the T-cell receptor alpha gene (TCRalpha-/-) spontaneously develop inflammatory intestinal lesions with extensive B-cell lamina propria infiltrates. Cryptosporidium parvum infection accelerates intestinal lesion formation in TCRalpha-/- mice. In the present study, TCRalpha-/- mice were crossed with JH-/- (B-cell-deficient) mice and challenged with C. parvum to determine if B cells are required for intestinal lesion development. TCRalpha-/- x JH-/- mice challenged with C. parvum, either as neonates or adults, became persistently infected, whereas TCRalpha-/+ x JH-/+ heterozygote control mice cleared the parasite. Cryptosporidium parvum colonization of TCRalpha-/- x JH-/- mice was heaviest in the distal ileum, with fewer parasites detected in the cecum and distal colon. Despite persistent infection, TCRalpha-/- x JH-/- mice did not develop inflammatory or hyperplastic intestinal lesions as detected in C. parvum-infected TCRalpha-/- mice. These findings demonstrate that B cells are a necessary component for the development of inflammatory intestinal lesions of C. parvum-infected TCRalpha-/- mice.

Animals↗
PubMed1980

[Studies on establishment and maintenance of persistent infection with measles virus in NC-37 cell. II. Effect of DNA-synthesis-suppressing factor (DSF) on the production of interferon in NC-37 cell infected with measles virus (author's transl)].

The attenuated strain of measles viruses, Schwarz, CAM-70, or subacute sclerosing panencephalitis (SSPE) virus of measles viruses, Halle, Mantooth was good interferon inducer, but the virulent strain, Edmonston, Toyoshima induced few amount of interferon or not. Furthermore, an inverse relationship seemed to exist between the ability to induce interferon and DNA synthesis suppressing factor (DSF). The attenuated strain or SSPE virus which had not a capacity to produce DSF could induce interferon and establish persistent infection in human lymphoid cell NC-37, while virulent strain did not induce interferon but DSF. Maximum yield of progeny virus was precede the detection of interferon in culture fluids. A persistently infected cells also produced continuously interferon and progeny virus. It is demonstrated that DSF suppressed interferon production by infection of measles virus and that DSF had not an activity like interferon.

Cells, Cultured↗
PubMed2002

The effects of gamma interferon on replication of foot-and-mouth disease virus in persistently infected bovine cells.

Foot-and-mouth disease virus (FMDV) causes a highly contagious viral disease of cloven-hoofed animals, which has a considerable socio-economic impact on the countries affected. In addition, persistent infection can occur following clinical or sub-clinical disease in either vaccinated or non-vaccinated cattle. The mechanism(s) by which FMDV persistence is established and maintained is not fully understood. To better understand the basic mechanisms controlling the virus infection in cattle, the effects of interferon gamma (IFN-gamma) on the replication of FMDV was evaluated in vitro in persistently infected-epithelial cells isolated from FMDV infected cattle. Initially primary bovine thyroid (BTY) cells were treated with varying doses of bovine recombinant IFN-gamma. The cytokine activity was measured by detection of viral antigen in cell supernatants and viral RNA expression compared with cells without INF-gamma treatment. Pretreatment with IFN-gamma profoundly affected FMDV growth in BTY cells. The replication of FMDV was affected in the presence of more than 2.5 u/ml of IFN-gamma and the effect was both dose-dependent and related to the time of exposure. Analysis of the mechanism of inhibition suggests that IFN-gamma did not inhibit the viral replication through induction of nitric oxide. More interesting is the finding that continuous treatment with IFN-gamma severely restricts FMDV replication or even cures persistently infected bovine epithelial cells, indicating that a cytokine-mediated pathway may be involved in the in vivo clearance of persistent FMDV.

Animals↗
PubMed1976

Accidental persistent infection of cell lines by Newcastle disease virus, showing three unusual features--defective neuraminidase, temperature sensitivity and intranuclear inclusions.

A persistent, defective infection by an unknown strain of Newcastle disease virus (NDV) appeared accidentally in established lines of pig, ox and sheep kidney cells. Virus particles released from the persistently infected cells were not infectious and were deficient in neuraminidase activity. Synthesis of some of the virus-specified proteins in the persistently infected cells was temperature-sensitive. Co-cultivation of mixed populations of carrier cells and healthy chick embryo cells induced cell fusion with the formation of multinucleate heterokaryons and intra-nuclear inclusions. The development of inclusions in the chicken nuclei was not accompanied by 'rescue' of infectious NDV.

Animals↗
PubMed1981

Isolation of a replication-efficient mutant of West Nile virus from a persistently infected genetically resistant mouse cell culture.

Flavivirus-resistant mouse embryofibroblasts (C3H/RV) that were infected with West Nile virus, strain E101 (WNV), yielded fewer infectious virions than did cultures of congenic susceptible cells (C3H/HE). Analysis of intracellular viral RNA synthesis indicated that the incorporation of [3H]uridine into 40S genome RNA was markedly reduced in resistant cells, and about 100-fold less labeled 40S RNA was found in pelleted extracellular virions from resistant cultures than in those from susceptible ones. A non-temperature-sensitive mutant of WNV isolated from culture fluid of a persistently infected culture of genetically resistant mouse cells was found to produce higher yields of infectious virus than the parental WNV used to initiate the persistent infection. Analysis of intracellular actinomycin D-resistant RNA indicated that the mutant virus (WNV-RV) was more efficient at incorporating [3H]uridine into 40S RNA in resistant cells than was the parental virus. WNV-RV also synthesized 40S RNA more efficiently than parental virus in congenic susceptible cells and in BHK cells. Analysis of the incorporation of [35S]methionine into viral proteins was likewise enhanced in WNV-RV-infected cells. The WNV-RV mutant provides a tool for studying the regulation of transcription of flavivirus RNA.

Animals↗
PubMed1990

Immunohistological detection of bovine viral diarrhoea virus antigen in the central nervous system of persistently infected cattle using monoclonal antibodies.

In a total of 25 cattle persistently infected with bovine viral diarrhoea virus (BVDV) the distribution of viral antigens in the central nervous system was studied. Using a panel of monoclonal antibodies (anti pestivirus C16; anti cytophathic BVDV C38; anti cytopathic and non-cytopathic BVDV C42; anti gp53 BVDV CA-1 and CA-3) and the indirect immunoperoxidase technique, BVDV antigen was located exclusively in neurons. Predilection sites for viral persistence were cerebral cortex and hippocampus. Morphological cellular alterations were not seen. Reactive perivascular lymphocytic infiltrations were occasional findings.

Animals↗
PubMed1981

Induction of transformed phenotypes in sheep fibroblasts by culture fluids from cells persistently infected with bovine leukemia virus.

FLK cells are fetal lamb kidney cells persistently infected with bovine leukemia virus (BLV). 3178 cells, originating from calf-form bovine lymphosarcoma, also showed persistent production of BLV and alteration of cell morphology, after treatment with 5'-iodo-2'-deoxyuridine. In the present paper, the first in vitro transformation of sheep fibroblasts by inoculation with BLV materials from these two cell lines is described. In a few passages after inoculation with these viral materials, morphological alteration occurred. The morphologically altered cells were grown as stable cultures and showed such transformed phenotypes as growth in soft agar medium, increased uptake of 2-deoxy-D-glucose and tumorigenicity in athymic nude mice. This result, together with our previous observation of simultaneous induction of BLV expression and morphological alteration of 3178 cells, suggests the presence of some transforming capacity in these BLV materials similar to that in, for example, murine or avian acute leukemia viruses. The possible acquisition of such capacity during the prolonged passage is discussed.

Animals↗
PubMed2005

Mig-14 is an inner membrane-associated protein that promotes Salmonella typhimurium resistance to CRAMP, survival within activated macrophages and persistent infection.

Salmonella enterica serovar Typhimurium (S. typhimurium) infects a wide variety of mammalian hosts and in rodents causes a typhoid-like systemic disease involving replication of bacteria inside macrophages within reticuloendothelial tissues. Previous studies demonstrated that the mig-14 and virK genes of Salmonella enterica are important in bacterial resistance to anti-microbial peptides and are necessary for continued replication of S. typhimurium in the liver and spleen of susceptible mice after orogastric inoculation. In this work we report that inflammatory signalling via interferon-gamma (IFN-gamma) is crucial to controlling replication of mig-14 mutant bacteria within the liver and spleen of mice after oral infection. Using a Salmonella persistence model recently developed in our laboratory, we further demonstrate that mig-14 contributes to long-term persistence of Salmonella in the spleen and mesenteric lymph nodes of chronically infected mice. Both mig-14 and virK contribute to the survival of Salmonella in macrophages treated with IFN-gamma and are necessary for resistance to cathelin-related anti-microbial peptide (CRAMP), an anti-microbial peptide expressed at high levels in activated mouse macrophages. We also show that both Mig-14 and VirK inhibit the binding of CRAMP to Salmonella, and demonstrate that Mig-14 is an inner membrane-associated protein. We further demonstrate by transmission electron microscopy that the primary locus of CRAMP activity appears to be intracytoplasmic, rather than at the outer membrane, suggesting that Mig-14 may prevent the penetration of the inner membrane by CRAMP. Together, these data indicate an important role for mig-14 in anti-microbial peptide resistance in vivo, and show that this resistance is important to the survival of Salmonella in systemic sites during both acute and persistent infection.

Animals↗
PubMed2006

Persistent infection with bovine viral diarrhea virus in an alpaca.

CASE DESCRIPTION: A 2.5-month-old female alpaca that had been born prematurely was examined because of moderate mucopurulent nasal discharge and high rectal temperature. CLINICAL FINDINGS: In addition to pyrexia and clinical signs of disease of the upper portion of the respiratory tract, the cria had inappetence and was in an unthrifty condition. Hematologic abnormalities included low WBC count, low hemoglobin concentration, and low PCV. Samples of blood were submitted for bovine viral diarrhea virus (BVDV) isolation and serologic evaluation. Other adults and newborn crias in the herd were similarly examined. Bovine viral diarrhea virus was detected in the cria, and a diagnosis of persistent infection with BVDV was made at 5.5 months of age. Persistent BVDV infection was suspected in another cria born into the herd but was not identified in any of the adult alpacas. TREATMENT AND OUTCOME: Despite several treatments with antimicrobials, no permanent improvement of the cria's condition was achieved. Because of the poor prognosis, the owners requested euthanasia of the cria; BVDV was isolated from specimens of multiple organs collected at necropsy. CLINICAL RELEVANCE: To date, BVDV infection in New World camelids has not been regarded as a major disease entity. Findings in the cria of this report illustrate that some strains of BVDV readily infect alpacas. Clinical description of the disease plus clinicopathologic findings suggest that persistent BVDV infection may be greatly overlooked as a cause of chronic anemia and failure to thrive in alpacas.

Animals↗
PubMedDate not supplied

On the potential usefulness of exchange plasmapheresis in the immunotherapy of cancer and of some chronic persistent infections.

In an individual sensitized to an antigen, Withdrawal of the corresponding antibody and of the accompanying antigen-antibody complexes stimulates antibody production: the end result is thus not unlike the effect of a booster dose of that antigen. Conversely, a sufficient concentration of antigen-antibody complexes will eventually shut off the antibody production to that antigen. The body is able to regulate through this mechanism the amplitude of the immune response, using the feed-back interaction of antigen-antibody complexes with the immune system. Without such a control system any antigenic stimulation would result in an uncontrolled out-pouring of antibodies, as is observed in myeloma. The regulation of cell mediated immunity is also indirectly affected by the concentration of circulating antigen-antibody complexes. Other mechanisms of immunoregulation are also at work, using the mediation of so-called suppressor cells, identified as sub-populations of T and B cells acting both specifically and non-specifically on immune effectors cells. It is likely that a major factor contributing to the pathogenesis of some persistent chronic infections such as syphilis, brucellosis, chronic viral hepatitis, leprosy, vaccinia, congenital cytomegalovirus infection persisting in childhood, and so on, and in conditions such as cancer, is an inadequate initial production of antibodies, further aggravated by the ensuing immunosuppression brought about by the formation of antigen-antibody complexes. Antigen-antibody complexes have indeed been identified as playing a prominent role in some of these diseases. It is also suggested that the magnitude of the initial antigenic dose may influence the ensuing immune response: while a large antigen dose could induce a "classic" and efficient immune response, a low antigen dose, such as an incipient neoplasm, could result in a minimal antibody response, further suppressed by the appearance of antigen-antibody complexes. Through this mechanism, a premature failure to eradicate the disease would follow. I suggest that a significant and sudden lowering of the concentration of relevant entibodies and antigen-antibody complexes through exchange plasmapheresis, would trigger a fully adequate and therapeutic immune response. This possibility is discussed.

Antibody Formation↗
PubMed1997

A congenital persistent infection of bovine virus diarrhoea virus in pigs: clinical, virological and immunological observations.

We report on a lifelong 'carrier' state of non-cytopathic bovine virus diarrhoea virus (BVDV) in an otherwise healthy pig. Three out of 13 pigs of a litter congenitally infected with BVDV survived for more than 3 months. One pig was BVDV seropositive at 1 month, the second seroconverted between 6 and 8 months, and the third remained viraemic and BVDV-immunotolerant until slaughter at 26 months. The latter pig, a boar, excreted virus in oropharyngeal fluid, urine and semen. Ejaculates, however, did not contain spermatozoa. The persistently infected pig had leucopenia from 3 months onwards, though differential white cell counts and thrombocyte counts remained normal. The antibody response of this pig after vaccination against foot-and-mouth disease and after infection with porcine parvovirus was not affected. The antibody response after vaccination against hog cholera, however, was delayed. In contrast, superinfection with antigenically related cytopathic BVDV strains did not alter the status of BVDV immunotolerance, nor did it induce clinical signs resembling mucosal disease as observed in cattle persistently infected with BVDV. Although the role of pigs in the epizootiology of bovine virus diarrhoea infections may be limited, the existence of healthy BVDV carrier pigs should be noted wherever control or eradication measures are applied.

Animals↗
PubMed1982

Heterologous response of antiserum-treated cell clones from a persistently infected DBT cell line to mouse hepatitis virus.

From DBT cells persistently infected with mouse hepatitis virus JHM strain (JHM-CC), a cell line producing neither infectious virus nor intracellular viral antigen was obtained after two passages in the presence of antiserum. In addition, 11 cell clones were manipulated from JHM-CC and found to be also free from the virus. These newly obtained cell line and 4 of 11 cell clones were shown to be resistant to JHM and the virus recovered from JHM-CC (JHM-CCV), while the other 7 cell clones were susceptible to both JHM and JHM-CCV as well as vesicular stomatitis virus. The susceptibility of all the cell clones and the newly obtained cell line to JHM and JHM-CCV became higher with passages. The observations were discussed in relation to the viral persistency in JHM-CC.

Animals↗
PubMed1977

An electron microscopic study of MDBK cells persistently infected with Newcastle disease virus.

Ultrastructural examination of a line of MDBK cells persistently infected with Newcastle disease virus (MDBKpi cells) revealed the presence of cytoplasmic aggregates of both smooth and granular nucleocapsids. Only granular nucleocapsids aligned under modified areas of plasma membrane and were incorporated into virus particles. On the grounds of morphogenesis, there was no apparent explanation for the persistent, not-cytocidal nature of the infection. Both nuclear and cytoplasmic aggregates of smooth nucleocapsids were present in MDBKpi cells which had been held without subculture for between 40 and 130 days (aged MDBKpi cells). Modified areas of plasma membrane with associated alignment of nucleocapsids were not present in aged MDBKpi cells, and neither budding nor released virus particles were observed, indicating a block in virus maturation. It is suggested that the granular material coating granular nucleocapsids allows them to interact with modified areas of plasma membrane, thereby inducing virus budding. A deficiency of this material, as apparently occurs in aged MDBKpi cells, would therefore cause a block in virus maturation. The nature of this granular material is discussed, and we suggest that it consists of M protein.

Animals↗
PubMed1992

Cell phenotypes in the efferent lymph of sheep persistently infected with Border disease virus.

The prefemoral efferent lymphatics of sheep persistently infected (PI) with Border disease virus (BDV) were cannulated in order to study the effects of the virus on cells of the immune system. Efferent lymphocytes recovered from PI sheep were phenotyped using a panel of monoclonal antibodies (MoAb) specific for ovine cell-surface markers and compared to lymphocytes recovered from normal, healthy controls. PI sheep had an increased percentage of cells expressing the T cell-associated molecules CD5, CD4, CD8 and T19, also an increase in cells expressing CD1 and a population of cells expressing low levels of the T19 molecule which was not present in control sheep. The lymphocytes were examined for the presence of BDV using virus-specific MoAb. On average 8.5% of the efferent lymphocytes from PI sheep carried virus antigen. BDV antigen was also found in the mononuclear cells and connective tissue of lymph nodes indicating widespread virus dissemination within the lymphoid system of PI sheep.

Animals↗
PubMed1993

Immune response to other agents of calves persistently infected with bovine virus diarrhoea virus (BVDV).

The ability of calves persistently infected (PI) with bovine virus diarrhoea virus BVDV to respond immunologically to defined antigens other than BVDV was studied. Five clinically healthy PI calves were studied together with 5 non-PI calves serving as controls. The humoral immune response was tested by measuring the serum antitoxin titre following immunization against tetanus. The cellular immune response was tested by the ability to develop a positive reaction in a cutaneous tuberculin test performed 1 month after immunization against Johne's disease (paratuberculosis). Finally, a skin-sensitizing agent, dinitrochlorobenzene (DNCB), was employed to study whether PI calves would react by hypersensitization following skin exposure to DNCB for 7 consecutive days followed by application of DNCB to a new skin area remote from the area that had first been exposed. The response of PI calves to the various types of antigenic stimuli applied was not significantly different from that of the control calves. Thus, PI calves developed a potent antitoxin response after tetanus immunization, they showed a positive reaction to tuberculin skin test after immunization against paratuberculosis, and were skin sensitized with DNCB.

Animals↗
PubMed2006

The properties of recombinant Sendai virus having the P gene of Sendai virus pi strain derived from BHK cells persistently infected with Sendai virus.

We prepared the chimeric recombinant Sendai virus [rSeV(Ppi)] by replacing the P gene of the Z strain with that of pi strain for analyzing the function of Ppi, Vpi and Cpi proteins. Intriguingly, HA production by rSeV(Ppi) is significantly lower at 38 degrees C than at 32 degrees C, showing that virus growth of rSeV(Ppi) is slightly suppressed at 38 degrees C. However, the main phenotypes of SeVpi, a marked temperature sensitivity as viral replication and an ability of establishing persistent infection, are not explained by the Ppi, Vpi and Cpi proteins. The V and C proteins form inclusion bodies in L929 cells infected with rSeV(Ppi) and incubated at 38 degrees C. L929 cells infected with rSeV(Ppi) and L929 cells stably expressing the Cpi protein show resistance to interferon-beta at 32 and 38 degrees C, indicating that the Cpi protein per se is not temperature-sensitive to inhibition of IFN signaling. The complete genome sequences of Sendai virus (SeV) pi and parent Nagoya strains were determined. Fifty nucleic acid substitutions are found in the genome sequence of SeV pi strain in comparison with Nagoya strain. There are three nucleic acid substitutions in the leader sequence, while the trailer, intergenic, gene-end and gene-start sequences of both strains are completely identical. Deletions and insertions of nucleotide are not found. There are 32 amino acid substitutions in Sendai virus pi strain. The specific amino acid substitutions unique to the SeVpi are 18. Information about the complete genome sequences of SeVpi strain is important to totally understand the persistent infection and lower pathogenicity of SeV.

Cell Line↗