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At least 289 records · Page 16Linked to original sources
PubMed2002

Persistent infection of influenza virus in irradiated mice and its prevention by intranasal vaccination.

Effects of intranasal administration of influenza vaccine on persistent viral infection in gamma-ray irradiated mice were examined. BALB/c mice were exposed to a sub-lethal dose of gamma-ray (7Gy) and infected intranasally with non-lethal A/PR/8/34 (PR8, H1N1) viruses. The mice irradiated on days 0 or +2 of infection showed a significant weight loss with a slight decrease in survival rate 3 weeks after infection. These mice kept infective viruses in the nasal and/or lung sites even 3 weeks after infection (persistent viral infection) without IgA or IgG antibodies (Abs), although non-irradiated infected mice cleared the virus completely within 2 weeks. On the other hand, the pretreatment with the nasal adjuvant-combined vaccine (3 days before irradiation) prevented the persistent viral infection with the Abs. These results demonstrate that the exacerbation of influenza is induced by the irradiation during early days of infection (0-2 days) and that the exacerbation is prevented by the intranasal vaccination at least 3 days before irradiation.

Administration, Intranasal↗
PubMed1986

Specific human cytotoxic T cells recognize B-cell lines persistently infected with respiratory syncytial virus.

The T-lymphocyte response to respiratory syncytial (RS) virus has been invoked to explain the bronchiolitis and pneumonia caused by RS virus in human infants. However, T cells also appear to play a role in protection against RS virus infection. Although RS virus-specific human lymphocytes have been demonstrated, neither the phenotype nor the function of the lymphocytes was characterized. We describe here the induction of anti-RS virus cytotoxic T lymphocytes, in both bulk culture and restimulated cell lines, from human peripheral blood. Infection of Epstein-Barr virus-transformed human B-cell lines with RS virus in vitro readily caused a persistent infection; these cells continued to synthesize RS viral proteins and secrete infectious RS virus 4 months after infection. The persistently infected cells were used both to restimulate cytotoxic-T-cell precursors and as targets for RS virus-specific cytotoxic T cells.

Antibodies, Monoclonal↗
PubMed1997

The cell receptor level is reduced during persistent infection with influenza C virus.

Persistent influenza C virus infection of MDCK cells perpetuates the viral genome in a cell-associated form. Typically, virus production remains at a low level over extended periods, in the absence of lytic effects of replication. In this study, we demonstrate that persistently infected cells are very restricted in permissiveness for superinfection. By reconstitution experiments, using bovine brain gangliosides as artificial receptors, the degree of super-infection was markedly increased. Analysis of cellular receptor expression revealed reduced concentrations of sialoglycoproteins in general and a limited presentation of the major receptor gp40. Cocultures of persistently infected and uninfected cells (the latter carrying normal receptor levels) initiated a transient rise in virus titers. This kind of induction of virus synthesis appeared to be mainly receptor-linked, since a receptor-deprived subline, MDCK II, did not give rise to a similar effect. Susceptibility of MDCK II cocultures could be partly restored by ganglioside treatment. In accordance to related virus systems, these findings on influenza C virus suggest a role of cell receptor concentrations in the regulation of long-term persistence.

Animals↗
PubMed1994

Long-term persistent infection of swine monocytes/macrophages with African swine fever virus.

Long-term persistent infection was established in 100% of pigs (n = 19) experimentally infected with African swine fever virus (ASFV). Viral DNA was detected in peripheral blood mononuclear leukocytes (PBML) at greater than 500 days postinfection by a PCR assay. Infectious virus was not, however, isolated from the same PBML samples. In cell fractionation studies of PBML, monocytes/macrophages were found to harbor viral DNA during the persistent phase of infection. This result indicates that monocytes/macrophages are persistently infected with ASFV and that ASFV-swine monocyte/macrophage interactions can result in either lytic or persistent infection.

African Swine Fever↗
PubMed1995

Parvovirus B19 infection--persistence and genetic variation.

53 patients with acute B19 infection were studied; symptoms at acute infection were rash and arthralgia (n = 26), rash (n = 7), arthralgia (n = 16), aplastic crisis (n = 3), and intrauterine fetal death (n = 1). These patients were followed for 26-85 months (mean 57 months) and re-assessed for persistent symptoms, anti-B19 antibodies, and B19 DNA. At follow-up, 7 individuals were positive for serum B19 DNA, compared with none of the controls (2-tailed p value = 0.016). All 7 of those persistently infected were women, 3 of whom had symptoms; 1 had a chronic haemolytic anaemia (initial presentation was aplastic crisis); 1 had persistent arthralgia in both knees (initial presentation was bilateral knee arthralgia); and 1 had arthralgia in one knee and chronic fatigue syndrome (initial presentation was bilateral arthralgia in knees and shoulders). For the 7 persistently infected patients, serum from the time of diagnosis of acute B19 infection was available for 4, all of which contained B19 DNA. With single-stranded conformational polymorphism (SSCP) assay of these 11 PCR products, identical SSCP types were demonstrated in 5 of 7 follow-up isolates. In 2 of the 4 cases for which both acute and follow-up PCR product was available, the SSCP type of the follow-up product was different from that of the acute product. Two B19 virus types were demonstrated in one patient (with persistent arthralgia and chronic fatigue syndrome) at follow-up assessment.

Adolescent↗
PubMed1980

Viruses isolated from cells persistently infected with vesicular stomatitis virus show altered interactions with defective interfering particles.

Virus mutants isolated from persistent infections of vesicular stomatitis virus in BHK-21 cells were much less susceptible to interference mediated by the defective interfering particle used to establish the persistent infection. This mutational change occurred as early as 34 days in the persistent infection and continued for over 5 years. The earliest variants showed no oligonucleotide map changes and no difference in the temperature-sensitive phenotype from the original virus, but the later variants exhibited extensive map changes. These results suggest a possible role for defective interfering particles in the selection of the mutants.

Animals↗
PubMed1996

Investigation of IFN type-I receptor and IFN regulatory factor expression relating to induction of 2', 5'-oligoadenylate synthetase in cells persistently infected with the mumps virus.

Poor induction of interferon-induced 2', 5'-oligoadenylate synthetase (2-5AS) activity has been demonstrated in cells persistently infected with the mumps virus or human T-lymphotropic virus type-I (HTLV-I). The suppression of 2-5AS induction is the result of the repression of 2-5AS gene expression at the transcription level. In a general way, after the binding of interferon-alpha (IFN-alpha) to cell surface-specific receptors, expression of 2-5AS gene is thought to be regulated by some transacting factors, IFN-regulatory factors (IRF-1 and IRF-2) and the IFN-stimulated gene factor (ISGF-3, a complex consisting of STAT-1 alpha, STAT-2 and p48). To clarify the cause of the suppression mechanism(s), fluctuation in the number of IFN receptors and the levels of mRNAs in both IRF-1 and IRF-2 were examined in cells persistently infected with the mumps virus (FLMT and KBMT). There were few differences in the number of IFN receptors and the level of IRF-2 mRNA between persistently infected cells and uninfected control cells. After the treatment of cells with IFN, a slight reduction of IRF-1 mRNA was found in persistently infected cells as compared with that of the uninfected control cells.

2',5'-Oligoadenylate Synthetase↗
PubMed1989

Relationship between virulence of Chlamydia psittaci strains and establishment of persistent infection of McCoy cells.

The pathogenicity of chlamydial strains for their natural hosts and their ability to induce persistent infections in McCoy cells were compared. Both virulent and avirulent strains persistently infected McCoy cells, but the appearance of the cell culture varied between strains. Avirulent strains induced completely inapparent persistent infection (infection Type 1), while with invasive strains the culture alternated between periods of cell multiplication and periods of extensive cytopathic change (infection Type 2). The virulence of virulent strains was not attenuated, even after 6 months of culture, but after 2 or 3 months some avirulent strains produced infection Type 2 and became invasive for mice and abortive for ewes. This variation of virulence was accompanied by a modification of protein patterns.

Abortion, Veterinary↗
PubMed1981

In vitro curing of persistent infection of HVJ (sendai virus) carrier tumor cells by spleen cells.

The viral antigens of hamster tumor cells persistently infected with HVJ (Sendai virus) disappeared upon transplantation, showing that HVJ persistent infection can be cured in vivo. In order to analyze these phenomena, an attempt to achieve a similar cure in vitro was made. When HVJ carrier tumor cells (GM2-HVJpi) were cultured in the presence of sera from GM2-HVJpi- tumor-bearing hamsters or rabbit antiserum against glycoproteins (GP) of HVJ, the cells showed only weak stainability with fluorescent antibody (FA). Lymphokines produced by spleen cells from GM2-HVJpi-tumor bearers could not cause GM2-HVJpi cells to lose their viral antigens. However, the viral antigens of GM2-HVJpi cells became undetectable upon cocultivation with spleen cells from either normal of GM2-HVJpi tumor-bearing hamsters. These cells from which HVJ antigens had been lost were reconfirmed to be cured in vitro through single colony isolation and subsequent establishment of a new HVJ infection after superinfection of the isolated cells with HVJ. The above results indicate that the curing of virus persistent infections in HVJ carrier tumor cells by transplantation was due to the in vivo action of spleen cells against transplanted HVJ carrier tumor cells.

Animals↗
PubMed1997

Reinfection-induced increase of rubella persistently infected cells in a macrophage-like cell line.

The establishment and relevant characteristics of a long-term rubella persistent infected immortalised murine macrophage culture with a high proportion of persistent infected cells over uninfected is described. The high proportion of persistent infected macrophages was obtained through reinfection with the original virus. Prior to reinfection, 35-50% of the cells expressed viral antigen, 0.05-1.5% produced infective virus and extra-cellular virus was continuously produced with infective titers cyclically fluctuating between 10(2) and 10(7) TCID50/ml. After reinfection, the macrophages which expressed viral antigen and produced infective virus had increased to 75-90% and 30-45% respectively and extracellular virus was continuously produced with stable titer between 10(2)-10(3) TCID50/ml. Furthermore, in the reinfected culture no significant variation was observed in the percentage of cells expressing antigen, producing virus and in the titer of extracellular virus for longer than a year of passages.

Animals↗
PubMed1986

Vaccinia virus DNA sequences in the nucleus of persistently infected Friend erythroleukemia cells.

FL vac cell lines are Friend erythroleukemia cells persistently infected with vaccinia virus. These cells produce attenuated leukemia virus, virulent poxvirus, resist superinfection with vaccinia, and show high levels of spontaneous erythrodifferentiation and decreased tumorigenicity in syngeneic hosts (Pogo, G.T. and Friend, C. (1982) Proc. Natl. Acad. Sci. USA 79, 4805-4809). To determine whether resistance to superinfection was associated with the presence of vaccinia DNA in the nucleus, DNA from cells at different passage levels was hybridized to a vaccinia DNA probe. Vaccinia DNA sequences were detected in the nucleus of cells of lines that were productively infected with vaccinia. No such sequences were detected in productively infected with vaccinia. No such sequences were detected in productively infected L cells nor in persistently infected cell lines that no longer produced infectious particles but were resistant to superinfection. Although no evidence of integration of vaccinia DNA was observed, differences in the restriction patterns were detected at some passage levels. The presence of vaccinia virus DNA sequences in the nucleus apparently did not affect the size of the provirus, the integration pattern or the expression of the leukemia virus.

Animals↗
PubMed1993

Superinfection-induced apoptosis and its correlation with the reduction of viral progeny in cells persistently infected with Hz-1 baculovirus.

Differential induction of necrosis or apoptosis was found upon challenge of cells of the insect Spodoptera frugiperda productively or persistently infected with Hz-1 baculovirus, respectively. Unlike parental SF9 cells, which were essentially all killed by virally induced necrosis, persistently infected cells underwent a process of massive cell death by apoptosis; cells which were not killed by apoptosis then reestablished a cell monolayer. Upon viral challenge, the yield of viral progeny was reduced greatly in persistently virus-infected cells but not in parental cells. Immunolabelling of individual cells revealed that upon viral challenge, production of viral progeny was detectable only in necrotic cells and not in apoptotic cells. These results indicated that induction of apoptosis greatly reduces the yield of viral progeny in cells persistently infected with Hz-1 baculovirus. This is the first report of apoptosis induction in persistently infected cells upon viral superinfection.

Animals↗
PubMed1975

The meaning of persistent infections in nature.

Viruses that cause persistent infections maintain themselves more effectively in nature than those causing acute and limited infections. There is a tendency for persistent viruses to evolve towards a state of minimal pathogenicity in the host. Vertical transmission, with integration of viral into host genome, represents the state of perfect parasitism.

Animals↗
PubMed1995

Human foamy virus DNA forms and expression in persistently infected Dami megakaryocytic cells.

We have characterized human foamy virus (HFV) proviral DNA and determined HFV expression in a persistent infection model, the Dami megakaryocytic cell line. Molecular studies were performed on parental persistently infected cells (Dami-P), as well as on derived clones (Dami-Cl). We report that in these nonlytic and non-HFV producer cells, viral DNA was found to be integrated into the cellular genome and that the few free proviral forms detected in Dami-P cells were deleted in their 5' LTR. Our molecular analysis indicates the presence of undeleted 5' LTR forms in the integrated provirus within a proviral population mainly composed of deleted forms. In addition, the deletion in the bel1 trans-activator gene, previously described by Saïb et al., was found to be highly predominant. However, in 5-iodo-2'-deoxyuridine treated Dami-Cl cultures, virus production occurred, providing evidence for the presence of complete viral genome. Analysis of HFV expression in Dami-Cl cells, by Northern blot and immunoprecipitation, shows that the most striking difference between cytolytic and persistent HFV infection was the lack of expression of structural viral proteins, in contrast with Bet protein expression, which is maintained. Our data suggest that the Bet protein could be involved in the maintenance of viral persistency and that the persistently infected Dami system provides a suitable model for clarifying its function.

Blotting, Southern↗
PubMed1977

Hamster brain tumor cells persistently infected with measles-subacute sclerosing panencephalitis virus.

A persistent infection was established in a cell line derived from a hamster brain tumor (HBT) with the HBS strain of measles-subacute sclerosing panencephalitis (SSPE) virus. The persistently infected cells (HBT-M) were studied with regard to their growth in vitro and their transplantability in vivo. Although the growth of the HBT-M cells paralleled that of the HBT cells in vitro their transplantability was decreased in weanling hamsters. Hydrocortisone treatment of the hamsters abrogated the lowered transplantability restoring the tumor-producing capacity to levels comparable to the HBT cells. The decreased cell growth of the HBT-M cells in vivo was attributed to the acquisition of measles virus (MV) antigens and the host immune response directed against these new antigens.

Animals↗
PubMed1998

Selection in persistently infected murine cells of an MHV-A59 variant with extended host range.

Murine coronavirus MHV-A59 normally infects only murine cells in vitro and causes transmissible infection only in mice. In the 17 C1 1 line of murine cells, the receptor for MHV-A59 is MHVR, a biliary glycoprotein in the carcinoembryonic antigen (CEA) family of glycoproteins. We found that virus released from the 600th passage of 17 C1 1 cells persistently infected with MHV-A59 (MHV/pi600) replicated in hamster (BHK-21) cells. The virus was passaged and plaque-purified in BHK-21 cells, yielding the MHV/BHK strain. Because murine cells persistently infected with MHV-A59 express a markedly reduced level of MHVR (Sawicki, et al., 1995), we tested whether virus with altered receptor interactions was selected in the persistently infected culture. Infection of 17 C1 1 cells by MHV-A59 can be blocked by treating the cells with anti-MHVR MAb-CC1, while infection by MHV/BHK was only partially blocked by MAb-CC1. MHV/BHK virus was also more resistant than wild-type MHV-A59 to neutralization by purified, recombinant, soluble MHVR glycoprotein (sMHVR). Cells in the persistently infected culture may also express reduced levels of and have altered interactions with some of the Bgp-related glycoproteins that can serve as alternative receptors for MHV-A59. Unlike the parental MHV-A59 which only infects murine cells, MHV/BHK virus was able to infect cell lines derived from mice, hamsters, rats, cats, cows, monkeys and humans. However, MHV/BHK was not able to infect all mammalian species, because a pig (ST) cell line and a dog cell line (MDCK I) were not susceptible to infection. MHV/pi600 and MHV/BHK replicated in murine cells more slowly than MHV-A59 and formed smaller plaques. Thus, in the persistently infected murine cells which expressed a markedly reduced level of MHVR, virus variants were selected that have altered interactions with MHVR and an extended host range. In vivo, in mice infected with coronavirus, virus variants with altered receptor recognition and extended host range might be selected in tissues that have low levels of receptors. Depending upon the tissue in which such a virus variant was selected, it might be shed from the infected animal or eaten by a predator, thus presenting a possible means for initiating the transition of a variant virus into a new host as a model for an emerging virus disease.

Animals↗
PubMed1995

Characterization of DBT cell clones derived from cells persistently infected with the JHM strain of mouse hepatitis virus.

Twelve clones derived from the cells persistently infected with the JHM strain (JHMV) of mouse hepatitis virus (MHV) were established from mouse astrocytoma-derived DBT cells and characterized. All the cell clones were resistant to superinfection with MHV. Only one of the persistently infected cell clone synthesized viral RNA and proteins and produced virus particles. Viral RNA was detectable in some other cell clones without production of viral protein nor the virus. No cell clones exhibited contact fusion activity. The results suggested that such variety of cell clones might have resulted from persistent infection with JHMV.

Animals↗
PubMed1984

Further studies of the RNA synthesis phenotype selected during persistent infection with vesicular stomatitis virus.

Vesicular stomatitis virus (VSV) isolated from two independently established lines of persistently infected mouse L cells expressed an altered phenotype of RNA synthesis at 37 degrees, the temperature at which the persistently infected cultures were maintained (T.K. Frey and J.S. Youngner, 1982, J. Virol. 44, 167-174). In comparison to the viruses used to initiate the two lines, wild-type (wt) VSV and ts-0-23 (ts-, RNA+ complementation group III), the VSV expressing this RNA phenotype synthesized much less mRNA but equal or greater amounts of 40 S genomic RNA (rt- phenotype). In the line initiated with wt-VSV, at 17 days after initiation, when 85% of the clones were ts-, 36% of the ts- clones were rt-. By 63 days the VSV-PI population was uniformly ts- and rt- and this phenotype prevailed for at least 2 years of persistence. In the line initiated with ts-0-23, the rt- phenotype was stable for at least 3 years of persistence. To study the relationship of the ts- and rt- phenotypes which were coselected during persistence, ts+ revertants of a ts- rt- VSV-PI clone were isolated. All of the ts+ revertants expressed a wt-VSV phenotype of RNA synthesis at 37 degrees (rt+), indicating that the two phenotypic markers may be pleiotropic manifestations of the same mutation. rt-VSV inhibited host cell RNA and protein synthesis more slowly than did wt-VSV. However, rt-VSV synthesized equivalent or greater amounts of all the virus proteins, compared to wt-VSV, despite the reduced amount of mRNA transcription. The attenuated shutoff of host cell macromolecular synthesis by rt- VSV and the concomitant efficient 40 S genome replication and virus protein synthesis may in part explain the selective advantage of the rt- mutation during persistence. The rt- phenotype was not unique to persistent infection; ts- rt- mutants also evolved during serial undiluted passages of wt-VSV in L cells and one ts- rt- mutant was identified in a group of spontaneous mutants isolated from a wt-VSV stock.

Animals↗