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PubMed1979

Changes in the virus-host cell relationship in a stable non-virogenic cell line persistently infected with measles virus (BGM/MV).

A non-virogenic African green monkey kidney cell line BGM/MV persistently infected with a neurotropic mouse brain-adapted strain of measles virus, was found to have undergone significant changes in the virus-host cell relationship between passages 35 and 119. Rather than the stable non-cytopathic relationship previously reported in which approximately 100% of the cells contained measles antigens and less than 1% of the cells expressed cell surface measles antigen, we observed cyclic manifestations of c.p.e. together with changes in the percentage of cells expressing intracellular and cell surface measles antigens. Treatment of BGM/MV cells with actinomycin D effected an increase in the percentage of cells expressing cell surface virus haemagglutinin (HA) at times when the percentage of cells with surface HA was less than the percentage of cells with intracellular measles antigens. Superinfection studies employing measles virus and vesicular stomatitis virus revealed a consonant cyclic refractivity and essentially no refractivity, respectively. Endogenous, infectious measles virus was not detected nor was interferon. It was concluded that a host cell factor other than interferon was modulating the cyclic expression of the measles virus infection.

Animals↗
PubMed1991

Advantages of a human immunodeficiency virus type 1 (HIV-1) persistently infected HeLa T4+ cell line for HIV-1 indirect immunofluorescence serology.

A HeLa T4+ cell line persistently infected with human immunodeficiency virus type 1 (HIV-1) was used in an indirect immunofluorescent antibody assay (IFA) system to explore its potential suitability as an alternative source of viral antigen for confirmatory IFA in HIV serology. In a study of 121 serum samples chosen because they were reactive on repeat examination by enzyme immunoassay but nonspecific by IFA by using HIV-1-infected H9 cells (H9 IFA) or gave discrepant results by enzyme immunoassay and H9 IFA, the specificity and sensitivity of the HeLa T4+ IFA were comparable to those of Western blot (immunoblot), and identification of the true positive samples among these discrepant or nonspecific samples by HeLa T4+ IFA was approximately twice that by H9 IFA. The primary advantages of using the HeLa cell line rather than lymphoid cell lines in IFA are that cells can be grown as a monolayer and that the individual cells are much larger. The cell membrane, cytoplasm, and nucleus are easily discernible; this allows specific and nonspecific staining to be distinguished. At least eight different nonspecific nuclear and cytoplasmic staining patterns were identified in this study by using T4+ cells.

Evaluation Studies as Topic↗
PubMed2001

Neospora caninum in persistently infected, pregnant cows: spontaneous transplacental infection is associated with an acute increase in maternal antibody.

Nine cows which were naturally and persistently infected with Neospora caninum were housed and observed intensively throughout pregnancy. No recrudescence of a latent infection was detected by PCR tests on maternal blood but fetal infection, implying a recrudescence of maternal parasitosis, was associated with a marked increase in maternal antibody. The increase occurred in the second half of pregnancy in five cows which infected their calves, and before mid-pregnancy in one cow which aborted. There was no change in the avidity of the antibody, which remained high and characteristic of long-term infection. In three infected cows that gave birth to uninfected calves there was no marked increase in maternal antibody. Antigen-specific interferon gamma responses of peripheral blood mononuclear cells were observed in all the infected cattle but they did not vary significantly either during pregnancy, or whether the cows did or did not infect their calves, although the responses were consistently higher in the latter. There was no change in the plasma concentrations of cortisol or acute phase proteins associated with the recrudescence of the parasite. Three uninfected cows housed with the infected cows remained uninfected throughout the experiment. No immunosuppressive event was detected which might have provoked parasite recrudescence but the acute antibody rise associated with transplacental infection provides a valuable, non-invasive marker for further studies to investigate the cause and consequences of parasite recrudescence in N caninum infection in cattle.

Animals↗
PubMed1990

Sequence variability of simian immunodeficiency virus in a persistently infected rhesus monkey.

A juvenile rhesus monkey that was inoculated intravenously with molecularly cloned SIVmac239 became persistently infected. A modified polymerase chain reaction (PCR) procedure was used to specifically amplify full-length envelope (env) gene sequences from DNA extracted from peripheral blood mononuclear cells (PBMC), lymph node tissue, and cells infected with recovered virus at 69 and 93 weeks post-infection. Extensive sequence variability accumulated in vivo in spite of infection with molecularly cloned virus. In the central portion of env. sequence variability was largely confined to three discrete regions.

Amino Acid Sequence↗
PubMedDate not supplied

[Amplification of the activity of HIV-1 isolates purified from seropositive children after cryopreservation of persistently-infected cells].

HIV-1 strains MC-1974 and MC-1978 were isolated from children infected in hospital. Both children presented with symptoms of HIV infection by the moment the blood samples for virus isolation were collected. In vitro the isolated strains showed weak infective activity and caused no cytopathic effect in sensitive cells. It may be explained by azidothymidine antiviral therapy or by initial immunodeficient status of both children not caused by HIV infection. Virus activity was enhanced in both cultures after reactivation of Jurkat-tat cells persistently infected with MC-1974 and MC-1978 strains after cryopreservation. Viruses isolated from culture fluid effectively infected Jurkat-tat cells. The infection was associated with formation of syncytia, accumulation of viral particles detected by electron microscopy and of intracellular antigens detected by fluorescent antibody technique and by immunoblotting. The results suggest the presence in the body of infected children and in Jurkat-tat-1974 and Jurkat-tat-1978 persistent lines of a viral genome containing all virusspecific genes necessary for productive expression of HIV-1.

Cell Line↗
PubMed2002

Pathomorphological changes in hyaline cartilage during focal persistent infection.

We studied morphological changes in hyaline cartilages of different localization in adult male rabbits with focal persistent infection produced by Staphylococcus aureus strain 209. Local chronic inflammation produced systemic atrophic and degenerative changes in the cartilage tissue. The severity of pathological changes depended on genetically determined repair and metabolic activity of the cartilage tissue.

Animals↗
PubMed1977

Effect of input multiplicity on the establishment of simian virus 40 persistent infections in rhesus monkey kidney cells.

Monolayer cultures of LLC-MK2 rhesus monkey kidney cells become persistently infected with simian virus 40 after infection at input multiplicities of 100, 10, or 1 plaque-forming unit per cell. After 3 weeks, all cells of the cultures infected at a multiplicity of 1 plaque-forming unit per cell produced the simian virus 40 T antigen. In contrast, 8 to 11 weeks elapsed before all the cells in the cultures infected at a multiplicity of 100 plaque-forming units per cell produced T antigen. Defective interfering particles and interferon production were not evident during this time.

Antigens, Viral↗
PubMed1973

Temperature-sensitive defect of mutants isolated from L cells persistently infected with Newcastle disease virus.

The temperature-sensitive defects of virus mutants isolated from L cells persistently infected with Newcastle disease virus (NDV) were analyzed. Genetic grouping of the mutants by complementation tests was attempted by using several different methods, including yield analysis, RNA synthesis, and heterozygote formation at 42 to 43 C, the nonpermissive temperature. In each case, specific interference prevented detection of complementation. This interference was shown to occur prior to or at the level of virus RNA synthesis. Temperature-shift experiments with five different NDV(pi) clones showed that virus replication begun at 37 C could not be completed at the nonpermissive temperature. The activity of the NDV-specific RNA-dependent RNA polymerase in the cytoplasm of infected chicken embryo cells was not stable and could not be demonstrated directly. However, indirect measurement of RNA polymerase activity at the nonpermissive temperature was accomplished by studying the kinetics of virus-specific RNA synthesis in infected cells after temperature shift. Two types of response were obtained: with three NDV(pi) clones, virus-specific RNA synthesis ceased immediately upon transfer of infected cells to 42 to 43 C, whereas in cells infected with two other NDV(pi) clones, RNA synthesis continued for several hours at this temperature. These results suggested that there may be two types of ts defects in NDV(pi), both associated with virus-specific RNA polymerase activity.

Animals↗
PubMed1975

Temperature-sensitive virus derived from BHK cells persistently infected with HVJ (Sendai virus).

BHK-HVJ cells, a cell line of baby hamster kidney cells persistantly infected with HVJ (Sendai virus), started to produce infectious virus by shifting down the incubation temperature from 38 to 32 C. The virus derived from BHK-HVJ cells, designated as HJV-pB, was effectively neutralized with antibody against wild-type virus (HVJ-W) which was used for the establishment of BHK-HVJ cells. HVJ-pB replicated in eggs at 32 C, but not at 38 C, while HVJ-W grew equally well at both temperatures. When BHK cells infected with HVJ-PB were incubated at 38 C, production of infectious virus, hemagglutinin, and neuraminidase was markedly restrained, whereas a considerable amount of viral nucleocapisid and envelope antigens was detected in the cells by complement fixation tests. These viral activities became detectable immediately after temperature shift-down from 38 to 32 C even at the later stage of infection. HVJ-pB was indistinguishable from HJV-W with respect to particle size, density, and morphological characteristics, but appeared to possess a higher neuraminidase activity and was inactivated more rapidly at 50 C than HVJ-W. HVJ-pB was less cytocidal and could easily cause latent infection in BHK and mouse L cells.

Animals↗
PubMedDate not supplied

[Persistent infection of pig embryo kidney cell cultures caused by a variant of tick-borne encephalitis virus].

The results of modelling and study of persistent infection of pig embryo kidney cell cultures (PEK) with MF variant of tick-borne encephalitis (TBE) virus are presented. In the life of chronically infected cultures periods of formation and stabilization were observed which were characterized by different types of relationships between the persisting virus and the cells. By the characters under study the persisting virus did not differ significantly from the initial MF variant. Inoculation of PEK and BHK-21 cell monolayers with samples of DNA from chronically infected cultures permitted to isolate transfected agents. Their identification by the neutralization tests and the indirect immunofluorescence procedure confirmed that they belonged to TBE virus. It is suggested that the mechanism of TBE virus persistence in PEK-MF system is based on the integration of TBE virus genome with DNA of chronically infected PEK cells.

Animals↗
PubMed2000

Infectivity, persistence, and antibody response to domestic and sylvatic Trichinella spp. in experimentally infected pigs.

Groups of pigs were inoculated with genotypes of Trichinella belonging to: Trichinella spiralis, Trichinella nativa, Trichinella britovi, Trichinella pseudospiralis (from Caucasus), T. pseudospiralis (from USA), Trichinella murrelli, Trichinella sp. (from North America), and Trichinella nelsoni. The pigs were sacrificed between 5 and 40weeks p.i., and the number of muscle larvae per gram (l.p.g.) of tissue was determined as an average of 18 muscles. All Trichinella genotypes were infective for pigs, but both their infectivity and persistence varied: 5weeks p.i., T. spiralis muscle larvae were present in high numbers (mean=427l.p.g.), while T. britovi, T. nelsoni, and T. pseudospiralis larvae were present in moderate numbers (means=24-52l.p.g.); larvae of the remaining genotypes were recovered only in low numbers (means=0.05-5. 00l.p.g.). The total larval burden (live weight of pigxl.p.g.) was constant over time for T. spiralis, T. britovi, and T. nelsoni, but declined significantly (P<0.05) for the other genotypes. Antibody responses could be detected 3-4weeks p.i. by seven different Trichinella ES antigens, but the antibody levels and dynamics differed significantly among the experimental groups. In pigs inoculated with T. spiralis, T. britovi, or T. nelsoni, the antibody level increased rapidly between weeks 3 and 5 p.i. and was stable or increased slightly throughout the experimental period. In pigs inoculated with T. nativa, T. murrelli, or Trichinella (T6) (from North America), a rapid increase was detected between weeks 3 and 5 p.i., but for these genotypes a reduction in the antibody levels was seen thereafter. In the pigs inoculated with T. pseudospiralis, the antibody level increased more gradually over a period from week 3 p. i. to weeks 15-20 p.i., and decreased thereafter. In general, all species of Trichinella were detected by any of the seven ES antigens, which points to the potential use of one common antigen for surveillance and epidemiological studies on both domestic and sylvatic Trichinella in pigs. Homologous ES antigens were slightly more sensitive in detecting antibodies to the corresponding Trichinella species.

Animals↗
PubMed2001

Antigen-presenting cells from calves persistently infected with bovine viral diarrhoea virus, a member of the Flaviviridae, are not compromised in their ability to present viral antigen.

The aim of this study was to assess whether the infection of antigen-presenting cells (APC) in vivo, evident in calves persistently infected (PI) with bovine viral diarrhoea virus (BVDV), compromised their ability to stimulate virus-specific T cell responses. Major histocompatibility complex (MHC) molecule-identical cattle were identified from the inbred family at the Institute for Animal Health. One was PI and immunotolerant to BVDV. Virus was not isolated from the remaining calves, which were classified as BVDV-immune or BVDV-naïve depending on the presence or absence of BVDV-specific antibodies in sera. Two-colour flow-cytometric analysis of PBMC from the PI calf showed that 40% of CD14(+) monocytes were infected in vivo. Monocytes from the PI calf (PI monocytes) were used as naturally infected ex vivo APC with CD4(+) or CD8(+) T cells isolated from the BVDV-naïve or BVDV-immune animals. PI monocytes stimulated proliferative responses with CD4(+) and CD8(+) T cells from BVDV-immune animals, but not from BVDV-naïve calves. This provided evidence for the presence of virus-specific CD4(+) and CD8(+) memory T cells after acute infection and indicated that ex vivo monocytes from PI, immunotolerant calves stimulated both MHC class I- and MHC class II-restricted T cell responses to BVDV. Additionally, naturally infected ex vivo monocytes cultured in vitro for 3 days stimulated effective T cell responses to the virus with which they were infected.

Animals↗
PubMed2006

Persistent infection of RAW264.7 macrophages with the DA strain of Theiler's murine encephalomyelitis virus: An in vitro model to study viral persistence.

Theiler's murine encephalomyelitis virus (TMEV) is a member of the Picornaviridae family and causes a virus strain dependent pathology in the central nervous system of mice. The GDVII strain induces an acute and mostly fatal encephalomyelitis. In the few mice that survive, the virus is cleared by the immune system. In contrast, infection with the DA strain leads to a persistent infection, marked by inflammation and demyelination that resembles multiple sclerosis. In the DA-induced disease, macrophages play a crucial role because they contribute to demyelination by the secretion of toxic mediators. Moreover, they represent the main viral reservoir, hereby also underlining their essential role in TMEV persistence. The mechanism of this persistence is not yet understood and tools to investigate it directly, without the complexity imposed by experimental animals, are largely missing. By studying TMEV infection of RAW264.7 macrophages, we found that the DA strain establishes a persistent infection in these cells, in contrast to the neurovirulent GDVII strain. Whereas the GDVII strain was cleared within 4 to 5 days post infection, DA virions were still present after 1 year of cell cultivation. This persistently DA-infected macrophage cell line, which we have called DRAW, provides a model to investigate the interactions between the cellular and viral factors influencing persistence and to screen for anti-TMEV agents.

Animals↗
PubMedDate not supplied

[A comparison of 2 T-lymphoid cell lines persistently infected with the human immunodeficiency virus (HIV-1) with different productive capacities].

T-lymphoid cell lines (H9/CBL-4 and CEM/CBL-4) persistently infected with HIV-1 were observed simultaneously for 6.5 months. The virus activity was characterized by such parameters as the number of infected cells determined by fluorescent antibody technique, the total level of virus--specific protein synthesis determined by immune blotting method, and the capacity to infect H9 and CEM cells. A comparative analysis of the two cell lines helped define the evaluation criteria for high and low productivity cultures. It was shown that a short-term virus persistence could exist in high-productivity cultures and long-term persistence in low-productivity cultures. The cytopathic activity of virus in cultures could be judged by accumulation of virus protein p24 in cell-free supernatants, this being one of the factors defining the efficacy of infection of H9 and CEM T-lymphoid cells.

Cell Line↗
PubMed1983

Analysis of genetic variation in Theiler's virus during persistent infection in the mouse central nervous system.

The genetic changes occurring in the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV) during persistent infection in the mouse central nervous system (CNS) were studied. RNase T1-oligonucleotide fingerprinting of the RNAs of 28 BeAn viruses isolated at various times postinfection (p.i.) demonstrated that mutation occurred throughout the infection. Although plaque-purified BeAn virus was used to inoculate mice intracerebrally, genetically different viruses were recovered from the CNS. One to three oligonucleotide changes were found up to Day 152 p.i., but all three viruses isolated at Day 180 had four to nine oligonucleotide changes. No pattern of oligonucleotide changes occurring in different virus isolates was found, yet three viruses isolated from different animals at Day 180 had the same four new oligonucleotides. Overall, the number of oligonucleotide changes represented a 0.1 to 1.2% change in the virus genome. In addition, the analytical two-dimensional gel technique of P.Z. O'Farrell, H.M. Goodman, and P.H. O'Farrell (Cell 12, 1133-1142, 1977) suggested that mutation occurred in all virus isolates. In nine isolates, one to three proteins were found to have charge changes, and in general, as many nonstructural proteins had charge changes as structural proteins. P20, a nonstructural protein probably equivalent to the protease described for encephalomyocarditis virus, was found to have shifted cathodally in six different viruses. Several virus isolates had doublet patterns, suggesting the possibility that within the CNS, subpopulations existed which had proteins of slightly different charge or that virus-specified proteins had been modified after translation. Finally, antigenic variation of neutralizing site(s) on BeAn virus isolates as a way for virus to evade immune surveillance and thereby maintain the persistent state was studied. The ability of mouse serum to neutralize persisting virus isolates was not significantly different from the ability to neutralize the infecting virus. Therefore, antigenic variation does not appear to be a factor in TMEV persistence.

Animals↗
PubMed1993

T cell memory specific for self and non-self antigens in rats persistently infected with Borna disease virus.

We have studied CD4+ Th1 T cell responses in Borna disease (BD), a virus-mediated immune disease of the central nervous system (CNS), and demonstrate the priming of virus-specific as well as autoreactive T cells specific for myelin antigens in the course of viral infection. The fate of these in vivo generated T cells was subsequently assessed by in vitro proliferation assays with lymphocytes from different lymphoid organs of diseased animals over a long period of time. Virus-specific T cell responses continuously decreased during the establishment of persistent infection and could no longer be detected after 5-6 months post infectionem, when inflammatory reactions in the brain had ceased. By contrast, autoantigen-specific T cells kept their ability to mount characteristic secondary responses--although at an overall rather low level--over long periods of time; these autoreactive T cells homed to a specific lymphoid organ, the perithymic lymph node. Our study thus describes for the first time a complete decline of virus-specific T cell memory in a persistent viral infection, and raises the question how long-lasting T cell autoreactivity is controlled.

Amino Acid Sequence↗
PubMed2004

T-cell senescence: a culprit of immune abnormalities in chronic inflammation and persistent infection.

Long-lived clonal T cells deficient in CD28 expression are commonly found in patients with inflammatory syndromes and persistent infections. Considering that CD28 loss is the most consistent immunological marker of aging, we propose that, in pathological states, CD28(null) T cells represent prematurely senescent cells resulting from persistent immune activation. These unusual lymphocytes have aberrant functions that contribute to disease-related immune abnormalities, and the degree of accumulation of CD28(null) T cells predicts the severity of clinical manifestations. We suggest that understanding of the biological properties of T cells that have reached replicative senescence will influence the future management of certain diseases. Indeed, studies on the molecular basis for the loss of CD28 are already providing information on methods to functionally rescue senescent T cells.

CD28 Antigens↗