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PubMed1980

Peculiarities of the virus-host cell relationship in a calf kidney cell line persistently infected with measles virus.

Persistent infection with measles virus established in a calf kidney cell line differed in some features from other measles virus carrier systems. After a variable life span, ranging from 50 to 1100 days, six of the chronically infected cell lines showed an evolution towards lytic infection. Only one of these lines, the K-2 cell line, exhibited marked morphological, growth and chromosomal alterations suggesting in vitro cellular transformation. The transformed K-2 cells released infectious measles virus with several modified biological parameters. Persistent infection was not due to the accumulation of thermosensitive mutants or defective particles. The role of the host-cell factor and of the selection of the virus population during its passage in RV cells are discussed.

Animals↗

PubMed1983

Characterization of four cell lines persistently infected with measles virus.

Persistently infected cell lines were established by infecting Vero cells with four different strains of measles virus: Edmonston "wild type", Schwarz vaccine strain passaged at high multiplicity of infection, Hallé SSPE strain, and a temperature sensitive mutant of Edmonston strain, designated ts 841. The four cell lines have continued to produce virus at a constant low level over a period of more than two years, although cytopathology and hemagglutinating ability have varied with cell passage. Only virus from cells originally infected with ts 841 appears to be temperature sensitive. In each of the cell lines a sizable population of low density, interfering virus particles was generated, indicating that this is an important mechanism for these four cell lines in maintenance of the measles virus persistent infection.

Animals↗

PubMed1977

Temperature-sensitive mutants of measles virus produced from persistently infected HeLa cells.

A persistent infection with the Edmonston strain of measles virus was established in HeLa cells in the absence of measles virus antibody (HeLaPI cells). By hemadsorption or immunofluoresnce virtually 100 per cent of the cells possessed measles virus components. HeLaPI cells produced no interferon and were not resistant to superinfection with Newcastle disease virus. HeLaPI cells contained both smooth (15--18 nm) and rought (20--35 nm) nucleocapsids as detected by electron microscopy. The virus produced from the HeLaPI cells (MVPI) varied in titer between 1.5 X 10(2) and 5.5 X10(4) PFU/ml, had a smaller plque size and was more heat resistant than wild-type measles virus. MVPI was also found to be temperature-sensitive. The temperature-sensitivity of MVPI was determined by the efficiency of plaquing at 33 degrees and 39 degrees C in Vero cell monolayers. When HeLaPI cells were incubated at 33 degrees C, there was a 50-fold increase in virus production as well as a slight increase in the percentage of cells forming infectious centers compared to HeLaPI cells grown at 37 degrees C. MVPI readily established a persistent infection in HeLa cells which also rleased temperature-sensitive virus.

Antigens, Viral↗

PubMed1995

An immunohistochemical study of the distribution of border disease virus in persistently infected sheep.

Three seronegative sheep persistently infected with Border disease virus and six seropositive, non-viraemic sheep were examined for the cellular distribution of the agent. These animals originated from a closed flock which had been kept in an isolation facility for 5 years. They were killed and immediately necropsied. There were no gross abnormalities other than reduced body weight of the persistently infected sheep. Two samples of each major organ were collected. The first sample was fixed by immersion in formalin and processed for histological examination, which showed no lesions unequivocally attributable to the viral infection. The second sample was snap-frozen for immunohistochemical examination. This revealed viral antigen in all organs of the persistently infected, but in none of the seropositive animals. The infected cells included smooth muscle cells of hollow organs and blood vessels, epithelial cells of the alimentary tract and urogenital organs, lymphocytes in lymphoid organs, endocrine cells, neurons and glial cell.

Animals↗

PubMed1981

Persistent infection of Vero cells with Tacaribe virus.

Persistently infected cultures have been established from Vero cells surviving primary infection with Tacaribe virus (Vero-T). The growth rate and morphological characteristics of the persistently infected cells were indistinguishable from normal Vero cells. Virus release declined during the first 6 passages, a cyclical pattern was observed between passages 6 and 16, and subsequently no virus infectivity could be detected. Co-cultivation with normal RK-13 or Vero cells enhanced virus yield from virus-producing cultures of Vero-T cells (passage 15), but the addition of susceptible cells had no effect on non-producer Vero-T cultures (passage 19). Only a small proportion (less than 1%) of the persistently infected cells tested during the first 16 passages produced infectious virus. The virus released during the early stages of persistence was temperature-sensitive if grown at 40 degree C, more thermolabile at 50 degree C than parental virus, and unable to initiate a persistent infection in Vero cells. Vero-T cells consistently showed refractoriness to homotypic Tacaribe virus superinfection and a selective graded resistance to other arenavirus replication. The possible use of viral susceptibility of persistently infected cultures as marker of antigenic relationship among Tacaribe complex viruses if considered.

Animals↗

PubMed1987

Virus-lymphocyte interaction: T cells of the helper subset are infected with lymphocytic choriomeningitis virus during persistent infection in vivo.

The lifelong persistence of lymphocytic choriomeningitis virus (LCMV) in neonatally or congenitally infected mice is accompanied by a suppression of virus-specific T-cell responses. In this study, we identified the subset of T cells infected with LCMV during persistent infection in vivo. Using specific monoclonal antibodies to separate the different lymphocyte cell populations and employing both an infectious center assay and immunofluorescence to detect the virus, we found that infection is confined primarily to T cells of the helper subset (L3T4+ Lyt2-), with minimal involvement of cytotoxic T cells (Lyt2+ L3T4-) and mature B cells. About 0.54 to 1.1% of L3T4+ T cells were producing the virus, as determined by the infectious center assay. In contrast, 9.1 to 12.2% of these L3T4+ T cells contained viral antigen, as shown by immunofluorescence studies. This finding suggested that, at any given time, a substantial number of infected T cells were not producing infectious virus. This infection of T helper cells may be involved in the suppression of LCMV-specific T-cell responses observed in persistently infected mice.

Animals↗

PubMed1996

Morphologic changes and immunohistochemical detection of viral antigen in ovaries from cattle persistently infected with bovine viral diarrhea virus.

OBJECTIVE: To identify morphologic differences in ovaries from cows persistently infected with bovine viral diarrhea virus (BVDV) and determine ovarian cell types infected in these cows. DESIGN: A comparative study of ovaries in cattle persistently infected with BVDV and cattle not persistently infected with BVDV, using morphologic and immunohistochemical analysis. ANIMALS: 6 postpubertal cows persistently infected with BVDV and 6 postpubertal cows not persistently infected with BVDV. PROCEDURE: Ovaries were compared morphologically by counting the number of normal structures present on 3 histologic sections taken from each ovary. Immunohistochemistry was accomplished, using an indirect, monoclonal antibody-linked, avidin-biotin-peroxidase complex procedure. RESULTS: Significant (P < 0.01) decrease in the number of tertiary follicles, graafian follicles, atretic follicles, and corpus hemorrhagicum/luteum/albicans was observed in cows persistently infected with BVDV. No difference in numbers of primordial or secondary follicles was observed. Immunostaining of BVDV antigen in luteal cells and macrophage-like cells was evident in ovaries from cows persistently infected with BVDV. CONCLUSIONS: Cows persistently infected with BVDV appear to have significant morphologic changes in their ovaries that suggest reduction in normal ovarian activities. Furthermore, BVDV antigen can be identified in specific ovarian cell types in cattle persistently infected with BVDV. CLINICAL RELEVANCE: The changes observed may reduce reproductive performance in cows persistently infected with BVDV, and may be of importance when trying to salvage valuable genetic material from persistently infected cows through embryo transfer. It is yet to be determined whether similar findings are true in cows acutely infected with BVDV.

Animals↗

PubMed2006

E sequence analysis of persistently infected mutant Japanese encephalitis virus strains.

A persistent infection model was established after human hepatoma cells infected by Japanese encephalitis viruses were subcultured for several times. Viral titers of mutant viruses in persistently infected cells were examined by plaque methods using BHK cells. Nucleotides of the E coding region of two wild and two mutant viruses were amplified by RT-PCR. PCR products were sequenced by ABI-PRSM 310 sequencing system. Compared to JaGAr-01 wild strains, four amino acids were replaced (E61Tyr --> Asp, E219His --> Tyr, E384Val --> Glu, E418Pro --> Ala) in the E sequence of JaGAr-01 persistently-infected mutant strains. Eleven amino acid replacement (E51Arg --> Ser, E61Tyr --> Asp, E83Lys --> Glu, E123Ser --> Arg, E209Arg --> Lys, E227Pro --> Ser, E276Asp --> Ser, E290Arg --> Lys, E387Lys --> Arg, E418Leu --> Pro, E454Arg --> Gly) was also noted when we compared the E sequence between persistently infected Nakayama and its wild strains. A lot of similarities of amino acid sequence between mutant strains JaGAr-01 and Nakayama were also noted. It was concluded that geno-variation existed in E region of mutant viruses and the mutant protein encoded by E region, especially the mutation of E61 (Tyr --> Asp) may contribute to the maintenance of the persistent infection of Japanese encephalitis virus.

Animals↗

PubMed1983

Accumulation of radiolabelled fatty acids in the neutral lipid fraction of measles virus persistently infected BGM cells.

The effect of measles virus infection (acute and persistent) on fatty acid metabolism has been studied in BGM (African green monkey kidney) cells. In persistently infected cells, there was an increase in the incorporation of radiolabelled fatty acids into the neutral lipid fraction. Compared to uninfected cells, the increase was up to 2-fold for palmitic, stearic and oleic acids and 8-14 fold for arachidonic acid. The lipid metabolism in measles virus acutely infected cells was unmodified. The radiolabelled fatty acids incorporated into the neutral lipids in persistently infected cells were principally associated with the triglyceride fraction. The implications of a virus- induced modification of lipid metabolism are discussed.

Animals↗

PubMed1990

Extrachromosomal HIV-1 DNA in persistently infected U937 cells.

Persistent human immunodeficiency virus type 1 (HIV-1) infection of U937 monocytic cells resulted in the accumulation of novel forms of extrachromosomal viral DNA. These DNA species are larger than the genome size of HIV-1 and persist indefinitely. The extrachromosomal viral DNA species (E-DNA) were shown to be structurally stable by subcloning of infected cell lines and restriction fragment analysis. Similar E-DNA structures were observed in independent infections. Persistently infected monocytic cells had low levels of viral antigens, reflecting the low levels of viral RNA that were detected. These results support a role for E-DNA in persistent HIV-1 infection of monocytic cells.

Cell Line↗

PubMed2000

Expression of mutated poliovirus receptors in human neuroblastoma cells persistently infected with poliovirus.

Poliovirus (PV) is able to establish persistent infections in human neuroblastoma IMR-32 cells [Colbère-Garapin et al. (1989) Proc. Natl. Acad. Sci. USA 86, 7590]. During persistent infection, PV mutants are selected that display substitutions of residues in regions of the capsid known to interact with the PV receptor (PVR), a glycoprotein of the immunoglobulin superfamily. The mechanism of persistent infection in IMR-32 cells may therefore involve the selection of mutant PVRs. To test this hypothesis, the sequences of the PVR mRNAs in uninfected IMR-32 cells and in two independent IMR-32 cell cultures persistently infected with the Mahoney strain of PV type 1 (PV1/Mahoney) were determined. The PVR mRNA population of uninfected cells was homogeneous, and no mutation was repeatedly found, whereas that of persistently infected cells displayed missense mutations. Particular mutations were repeatedly detected, and all of them mapped to the N-terminal domain of PVR (domain 1), which interacts directly with PV. These mutations generated several types of PVR variants with the following substitutions: Ala67-->Thr alone, Ala67-->Thr associated with Gly39-->Ser, and Arg104-->Gln. Functional analysis of PVR in murine LM cells, stably expressing each of the PVR forms, showed that the PVR forms selected during persistent infection conferred on LM cells partial resistance to PV1/Mahoney-induced lysis. Although adsorption onto PVR seemed to be independent of the PVR form, an analysis of the conformational changes of the capsid during the early steps of the PV cycle provided evidence that the Ser39/Thr67 and Gln104 substitutions almost halved the conversion of 160S infectious particles into 135S A particles associated with the PV-PVR interaction. Altogether, these findings indicate that during persistent infection, specific mutations were selected in the domain 1 of PVR and that these mutations increased the resistance of cells to PV-induced lysis. These results are discussed in view of the position of the mutations on PVR.

Amino Acid Substitution↗

PubMed1991

Infection of lymphocytes by a virus that aborts cytotoxic T lymphocyte activity and establishes persistent infection.

For viruses to establish persistent infections in their hosts, they must possess some mechanism for evading clearance by the immune system. When inoculated into adult immunocompetent mice, wild-type lymphocytic choriomeningitis virus (LCMV ARM) induces a CD8(+)-mediated cytotoxic T lymphocyte (CTL) response that clears the infection within 7-14 d (CTL+ [P-]). By contrast, variant viruses isolated from lymphoid tissues of persistently infected mice fail to induce a CTL response and are thus able to establish a persistent infection in adult mice (CTL- [P+]). This report compares the interaction of CTL+ (P-) and CTL- (P+) viruses with cells of the immune system. Both types of virus initially bind to 2-4% of CD4+ and CD8+ T lymphocytes and replicate within cells of both subsets. The replication of CTL- (P+) and CTL+ (P-) viruses in lymphocytes in vivo is similar for the first 5 d after initiating infection. Thereafter, in mice infected with CTL- (P+) variants, lymphocytes retain viral genetic information, and infectious virus can be recovered throughout the animals' lives. In contrast, when adult mice are infected with wild-type CTL+ (P-) LCMV ARM, virus is not recovered from lymphocytes for greater than 7 d after infection. A CD8(+)-mediated anti-LCMV CTL response is induced in such mice. Clearance of infected lymphocytes is produced by these LCMV-specific CTLs, as shown by their ability to lyse lymphocytes expressing LCMV determinants in vitro and the fact that depletion of CD8+ lymphocytes before infection with CTL+ (P-) viruses results in levels of infected lymphocytes similar to those found in undepleted CTL- (P+)-infected mice. Hence, CTL-mediated lysis of T lymphocytes carrying infectious virus is a critical factor determining whether virus persists or the infection is terminated.

Animals↗

PubMed1997

Establishment and characterisation of a porcine rubulavirus (LPMV) persistent infection in porcine kidney cells.

Porcine rubulavirus (LPMV) can establish persistent infections in porcine kidney cells. Cell cultures characterised at passages 25 and 65 demonstrated haemadsorption, formation of syncytia, and a slower growth rate. The nucleoprotein (NP) and haemagglutinin-neuraminidase (HN) protein were present in all cells, although not to the same extent as in wild type infected cells. Incubation of the cell cultures with virus neutralising antibodies could not cure them from the infection. The cells were resistant to LPMV high multiplicity superinfection, but lysed rapidly upon infection with VSV. These cells thus fulfilled the criteria of a true persistent infection. Viral particles were released into the medium from the persistently infected cells as measured by HA and infection of PK-15 cells with medium from the persistently infected cells. The infectious titer of the virus released from the persistently infected cells was 3 logs lower compared to wild type virus, the HN titer still being comparable. Virus released from the persistently infected cells was unable to cause a lytic infection in PK-15 cells, and showed a reduced ability to spread when compared to a LPMV lytic infection.

Animals↗

PubMed1990

Alterations in lymphocyte subpopulations in peripheral blood of sheep persistently infected with border disease virus.

Fourteen sheep persistently infected with border disease virus were investigated to examine the effects of persistent viraemia on lymphocyte subpopulations in peripheral blood and their responses to the mitogen phytohaemagglutinin (PHA) in vitro. Persistently infected sheep had significantly more CD8+ (cytotoxic-suppressor) T-lymphocytes than uninfected sheep of the same age (P less than 0.001). The total number of CD4+ (helper) T-lymphocytes were not significantly different but there were more T-lymphocytes (CD5+) which were CD4- and CD8- in normal sheep than persistently infected sheep (P less than 0.001). Peripheral lymphocytes obtained from persistently infected sheep showed significantly reduced blastogenesis induced by PHA than those obtained from normal sheep (P less than 0.001).

Animals↗

PubMed1985

M protein instability and lack of H protein processing associated with nonproductive persistent infection of HeLa cells by measles virus.

Persistent infections such as subacute sclerosing panencephalitis (SSPE) which do not produce infectious virus particles (nonproductive persistence) are often accompanied by a reduced steady-state amount of the viral matrix (M) protein and/or reduced hemadsorption activity. The possible causes of these aberrations associated with nonproductive persistence were investigated by following changes in the viral proteins with time in pulse-chase experiments. Three HeLa cell lines persistently infected with measles virus; K11, K11A, and HG111; were compared to each other and to acutely infected HeLa cells. K11 produces infectious virions at a low level (productive persistence). K11A and HG111 are both nonproductive persistently infected cell lines derived from K11. K11A cells have a reduced steady-state amount of viral M protein and reduced hemadsorption activity. HG111 cells have reduced hemadsorption but a normal level of viral M protein. As such, these cell lines serve as good model systems for the study of nonproductive persistent infection associated with SSPE. The reduced amount of M protein in K11A was found to result from rapid degradation of the protein. Degradation of the protein resulted from changes in the protein itself rather than from cellular changes. The hemagglutination (H) protein was found to be present at a low level in K11A cells. In addition, in both K11A and HG111 cells, conversion of the sugar moiety of the H glycoprotein from the high mannose form to the complex sugar form did not take place. Such modification usually occurs concomitant with transport of glycoproteins onto the cell surface. As such, lack of processing could preclude the appearance of functional H proteins on the cell surface. This could account for the reduced hemadsorption activity in these cells. The roles that these changes may play in the generation of nonproductive persistence are discussed.

Cell Transformation, Viral↗

PubMed1992

Phagolysosomes of Coxiella burnetii-infected cell lines maintain an acidic pH during persistent infection.

Coxiella burnetii, the agent of Q fever, is an obligate intracellular bacterium that multiples within vacuoles of phagolysosomal origin. Persistently infected cell lines were maintained in continuous culture for months. We studied the pH of the phagolysosomes by using two murine cell lines during early propagation of the bacteria and after establishment of persistent infection. Three strains of C. burnetii were studied because of the purported propensity of each strain to cause acute or chronic disease and to be resistant or susceptible to antibiotics. The pHs were calculated from fluorescence experiments with fluoresceinated dextran as a lysosomal probe. Phagolysosomal vacuoles maintained an acidic pH during a 36-day infection. Minimal variation of the pH occurred over the duration of the experiment with strains that caused either acute or chronic disease. Phagolysosomal pH remained stable for as long as 153 days with the Nine Mile phase II isolate. Thus, neither the course of C. burnetti infection nor the diversity of antibiotic susceptibility of the strains is related to variations in the phagolysosomal pH.

Animals↗

PubMed2001

Establishment of persistent infection with non-cytopathic bovine viral diarrhoea virus in cattle is associated with a failure to induce type I interferon.

The establishment of persistent infections with non-cytopathic bovine virus diarrhoea virus (ncpBVDV) is crucial for the maintenance of BVDV in cattle populations. Also, super-infection of persistently infected individuals with antigenically homologous cytopathic BVDV (cpBVDV) results in fatal mucosal disease. Persistent infection with ncpBVDV is established by infection of the foetus during the first trimester of pregnancy. It has been shown previously that foetal infection with cpBVDV does not result in persistent infection. Infection of cells in vitro has demonstrated that cpBVDV induces type I interferon (IFN), whereas ncpBVDV fails to induce IFN. In this study we demonstrate that foetal challenge with cpBVDV results in IFN production, whereas ncpBVDV does not. These findings strongly suggest that the ability of ncpBVDV to inhibit the induction of type I IFN has evolved to enable the virus to establish persistent infection in the early foetus.

Amniotic Fluid↗

PubMed2000

Vaccination to treat persistent viral infection.

Persistent infections caused by such agents as the human immunodeficiency virus, hepatitis B virus, Epstein-Barr virus, etc., present formidable medical problems. A defining characteristic of these infections is that anti-viral cytotoxic T lymphocytes (CTL) may be lost or, if present, fail to clear the infection. Here we report a vaccination strategy which was successful in generating lytic CTL in persistently infected mice. Vaccination with an immunodominant CTL epitope derived from the nucleoprotein of lymphocytic choriomeningitis virus (LCMV) delivered in the form of a lipopeptide incorporating a universal CD4 helper epitope successfully induced lytic MHC-restricted CTL in mice persistently infected with LCMV since birth. However, induction of such CTL did not eliminate the virus, most likely because the CTL were generated at low frequencies and had 2 to 3 logs lower affinity than CTL generated in uninfected mice inoculated with the vaccine. Both CTL populations from either uninfected or persistently infected mice produced significant and similar amounts of interferon-gamma and IL-6. Vaccine-induced low-affinity CTL were still inadequate at complete removal of the virus when combined with LCMV-specific CD4 helper T lymphocytes. Thus, our results establish that CTL can be generated in persistently infected mice and that a crucial factor for clearing viral infection is the affinity of the CTL.

Adoptive Transfer↗