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At least 685 records · Page 38Linked to original sources
PubMed1978

Properties of the viruses selected during persistent infection of L cells with VSV.

Two virus clones, VSV-mp and VSV-sp, were isolated from L cells persistently infected with VSV (New Jersey serotype). Both clones were more temperature sensitive than the parent virus, VSV-o, and grew more slowly, gave smaller plaques, less c.p.e. and lower virus yields in L cells. Unlike the parent virus, both persistent viruses induced interferon production in L cells. Stable carrier cultures could be obtained from L cells infected with VSV-sp at low multiplicities without pretreatment with interferon. This may be related to the fact that VSV-sp is more sensitive to interferon than either VSV-mp or VSV-o.

Cell Fusion↗
PubMed1992

Persistent infection of human adenovirus type 5 in human monocyte cell lines.

Adenovirus infection of human monocyte hybridoma cell lines and the fusion partner U937 was investigated. Adenovirus adsorbed poorly to these cells as well as primary human alveolar macrophages. The virus-binding experiments showed a 100-fold reduction in apparent viral binding to these cells compared to the permissive HeLa cells. Adsorption of adenovirus to these cells could be enhanced by preincubation of adenovirus with its antiserum. Following entry into the cells amplification of adenovirus DNA was detected starting at 2 days postinfection but few mature virus particles were produced. The infected cultures survived the infection and continued to grow for more than a year. In these chronically infected cultures, linear adenovirus DNA persisted up to 200 copies per cell and a small amount of mature virus was produced. Infectious center assay and cell cloning experiments showed that the majority of the cells in the chronically infected cultures harbor adenovirus genome. These results indicate that restriction of replication of human adenovirus type 5 at the late phase results in persistent infection of U937 and the human monocyte hybridoma cell lines.

Adenoviruses, Human↗
PubMed1985

Site of suppression of Banzi viral replication by an antiviral factor released from Aedes albopictus cells persistently infected with Banzi virus.

The ability of the antiviral factor present in culture medium of Aedes albopictus cells persistently infected with the flavivirus, Banzi virus, to inhibit the replication of Banzi virus was examined. The anti-Banzi viral factor did not inhibit the uncoating of the virion. Levels of viral RNA were markedly reduced in mosquito cells treated with the antiviral factor. Syntheses of negative-strand and of positive-strand viral RNA species were inhibited to approximately the same extent. This inhibition was virus-specific in that the anti-Banzi viral factor had no effect on the synthesis of viral RNA in mosquito cells infected with either Japanese encephalitis or Eastern equine encephalitis viruses. The anti-Banzi viral factor inhibited the in vitro Banzi viral RNA synthesis but not that of Eastern equine encephalitis virus or of Japanese encephalitis virus.

Aedes↗
PubMed1996

Comparative study on four enzyme-linked immunosorbent assays and a cocultivation assay for the detection of antigens associated with the bovine viral diarrhoea virus in persistently infected cattle.

Four commercially available ELISAs for detection of antigens associated with the bovine viral diarrhoea virus in persistently infected cattle have been compared. The tests are equally specific (100%) and the sensitivity of three ELISAs is comparable with that of a conventional cocultivation assay. Performing ELISA on samples from young animals that received colostrum may yield false negative results because of interference of maternal antibodies in the tests. It is concluded that ELISA can be a valuable tool in eradications programs when large numbers of cattle are to be monitored.

Animals↗
PubMed1982

Establishment of cell cultures persistently infected with spotted fever group rickettsiae.

A cell line was established from the tunica vaginalis of meadow voles, Microtus pennsylvanicus, which could be persistently infected with the spotted fever group rickettsiae, Rickettsia rickettsii, R. rhipicephali, and R. slovaca. As determined by light and electron microscopy, all cells in the cultures became infected and remained so even after 20 serial passages over a period of months. The rickettsiae-infected vole cell line is an excellent experimental model to study the noncytolytic host-cell interactions required for persistence of spotted fever group rickettsiae in nature.

Animals↗
PubMed1986

Effect of interferon on Vero cells persistently infected with SSPE virus and lytically infected with measles virus.

The effect of lymphoblastoid interferon (IFN) on viral polypeptides synthesized in a Vero cell culture persistently infected with subacute sclerosing panencephalitis virus (SSPE-Vero) was compared to that of Vero cells infected with exogenous measles virus. After IFN treatment there was no significant decrease in the synthesis of SSPE viral proteins, but inhibition of synthesis of measles polypeptides was readily seen. In Vero and SSPE-Vero cells IFN was able to inhibit replication of Sindbis virus although the effect in Vero cells was significantly more sensitive. In both cell lines IFN was able to stimulate 2'--5' oligoadenylate synthetase (E enzyme) but not the protein kinase system. The SSPE-Vero cells showed a lower basal level of E enzyme activity than the Vero cells.

2',5'-Oligoadenylate Synthetase↗
PubMed1984

Characterization of genetic changes occurring in attenuated poliovirus 2 during persistent infection in mouse central nervous systems.

Genomic changes occurring in the attenuated W-2 strain of poliovirus 2 during persistent infection of the central nervous system of immunosuppressed mice were analyzed. The RNase T1 oligonucleotide fingerprints of 34 different viruses, isolated from the brains and spinal cords of paralyzed and nonparalyzed mice during a 105-day period, were used to quantitate and compare the mutations occurring in each isolate. Although mice were inoculated with plaque-purified virus, genetically distinct viruses were recovered from the central nervous system. The number of oligonucleotide changes occurring in isolates from paralyzed mice generally was greater than that observed in isolates from nonparalyzed mice. However, differences in the extent of mutation in isolates from the two groups of mice did not appear to be related to the level of virus replication. In paralyzed mice, the number of oligonucleotide changes on average was greater in viruses isolated during the first 60 days of the infection than in the last 45 days. The number of oligonucleotide changes was essentially constant throughout the infection, however, in viruses isolated from the brains of nonparalyzed mice. In addition, several specific oligonucleotide changes were found only in viruses isolated from paralyzed animals.

Animals↗
PubMed2006

Identification of herds with cattle persistently infected with bovine viral diarrhea virus by virological evaluation of three calves.

For the identification of herds with cattle persistently infected (PI) with bovine viral diarrhea virus, 1,272 animals from 20 herds were subjected to serum neutralizing (SN) test using the Nose strain and virus isolation. Eighteen PI cattle were detected from 5 herds. On the phylogenetic tree based on the nucleotide sequences of the 5' untranslated region, the isolates from the PI cattle were classified into genotypes-1a or -1b. Of 3 unvaccinated calves aged 6 to 12 months selected from each herd, the probabilities of obtaining 2 or more non-PI cattle with SN antibody titers of 64 or more (P(SN)), one or more PI cattle (P(VI)), and either of the conditions (P(Total)) were calculated using the hypergeometric probability model. P(Total) for the 5 herds with PI cattle was 1.000. P(SN) for 3 herds with many PI cattle within the selected age group was as low as 0.500 or less, and P(VI) was as high as 0.886 or more. P(SN) in the 2 other herds with few PI cattle was 1.000, and P(VI) was as low as 0.375 or less. P(Total) in 13 of 15 herds without PI cattle was 0.000, and was 0.714 or 0.774 for the 2 other herds. These results suggest that herds with PI cattle can be predicted with high accuracy when both SN test and virus isolation are performed on only 3 unvaccinated calves aged 6 to 12 months selected from a herd.

5' Untranslated Regions↗
PubMed2004

Action and reaction: Chlamydophila pneumoniae proteome alteration in a persistent infection induced by iron deficiency.

Chlamydophila pneumoniae is an obligate intracellular pathogen implicated in a variety of acute and chronic diseases. Long-term infections are associated with a persistent life stage, in which bacteria can stay for years. They are less accessible to antibiotic treatment but still prone to sustain an inflammatory response. Different in vitro models have been established to mimic and characterize chlamydial persistency. For C. pneumoniae and Chlamydia trachomatis, altered metabolic activities and changed antigenic profiles compared to acute infections have been reported. Most studies including transcriptome and proteome analyses describe persistency induced by IFNgamma treatment. Here, we use iron depletion of the infected cell culture that also leads into persistent infection. We describe differently regulated proteins found by subtractive proteome analysis comparing two early stages of infection with and without addition of the iron chelator deferoxamine-mesylate. While only one bacterial protein was up-regulated during iron deficiency up to 24 h post infection (p.i.), 11 were found to be up-regulated and eight to be down-regulated from 24-48 h p.i. Two down-regulated proteins could be identified by peptide mass fingerprinting as thioredoxin reductase and chromosome partitioning protein (ParB). The latter is involved in chromosome segregation. Thus, using a comparative approach we identified on a proteome level down-regulation of ParB in persistent chlamydial forms, which is in agreement with previous results describing changes in cell division and atypical altered morphology of persistent Chlamydiae.

Amino Acid Sequence↗
PubMed1999

Establishment of persistent infection with HIV-1 abrogates the caspase-3-dependent apoptotic signaling pathway in U937 cells.

Treatment of 26L cells, a subclone obtained from U937 cells, with TNF-alpha or DNA-damaging agents such as teniposide (VM26) and camptothecin (CPT) induced morphologically and biochemically typical apoptotic changes, including the activation of procaspase-3. The cells persistently infected with HIV-1 (26L/HIV), however, showed a marked resistance to VM26 and CPT, whereas they hardly lost the sensitivity to TNF-alpha. TNF-alpha-induced apoptosis of 26L/HIV cells proceeded without the increase in caspase-3 activity, indicating that signaling for apoptosis in the infected cells proceeded through an alternative caspase-3-independent pathway which could respond to TNF-alpha but not to VM26 and CPT. The evidence that p-toluenesulfonyl-l-lysine chloromethyl ketone (a trypsin-like serine protease inhibitor) blocked VM26- and CPT-induced apoptotic changes but not TNF-alpha-induced apoptosis also supported the existence of the alternative TNF-alpha-inducible pathway. The results also suggest that a TLCK-sensitive protease is involved upstream of the procaspase-3 activation process and that the protease is essential for the progress of VM26- and CPT-induced apoptosis. The similar effect of HIV-1-productive infection on the apoptosis induced by the DNA-damaging agents was also confirmed by utilizing U1 cells, which are latently HIV-1-infected U937 cells. The cells became resistant to these agents after induction of the viral production by pretreatment with PMA. These results suggest that persistent HIV-1 infection blocks an apoptotic pathway triggered by DNA damaging agents through the inhibition of the procaspase-3 activation process.

Apoptosis↗
PubMed1989

Extensive cell heterogeneity during persistent infection with foot-and-mouth disease virus.

Coevolution of viruses and the host cells occurred in BHK-21 cell cultures persistently infected with foot-and-mouth disease virus (FMDV) (J. C. de la Torre, E. Martínez-Salas, J. Diez, A. Villaverde, F. Gebauer, E. Rocha, M. Dávila, and E. Domingo, J. Virol. 62:2050-2058, 1988). In the present report we provide evidence of an extreme phenotypic heterogeneity of the cells, which was generated in the course of persistence. A total of 248 stable cell clones isolated from FMDV carrier cultures at early or late passages were analyzed. At least six distinct cell phenotypes were distinguished with regard to cell morphology, resistance to FMDV strain C-S8c1, and cell growth characteristics. No infectious FMDV or viral RNA was detected in variant cell clones, suggesting that the altered phenotypes were caused by inheritable cell modifications, selected in the course of persistence. Thus, the FMDV-BHK-21 carrier cell system must be described as a dynamic interaction between an evolving heterogeneous population of virus and multiple cell variants. We suggest that cell heterogeneity confers a selective advantage for long-term virus and cell survival by providing the cell population with a range of responses toward FMDV.

Animals↗
PubMed1981

Cellular source of interferon induced in human peripheral blood mononuclear leukocytes by mumps virus or by tumour cells persistently infected with mumps virus.

Human leukocyte interferon (IFN-a) was induced in cultures of human peripheral blood mononuclear leukocytes (PBML) from seropositive healthy donor infected by mumps virus, or by a human lung carcinoma cell line (Pc-10) persistently infected with mumps virus (Pc-10/M-V). Adherent cells (M0), non-T, non-B cells and B cells all produced IFN in response to mumps virus or Pc-10/MpV cells. The non-T, non-B cells co-cultured with Pc-10/MpV cells produced high-titred IFN. However, T cells did not produced any antiviral factors even in the presence of M0. Furthermore, T cells activated with phytohaemagglutinin (PHA-P), concanavalin A or treated with u.v.-irradiated mumps virus, or Pc-10/MpV cells pretreated with mitomycin C did not produce any antiviral factors in response to either mumps virus or Pc-10/MpV cells.

Carcinoma↗
PubMed1988

Influence of interferons alpha I1 and gamma and of tumour necrosis factor on persistent infection with bovine viral diarrhoea virus in vitro.

Non-cytopathic strains of bovine viral diarrhoea virus (BVDV) readily establish persistent infections in cells of bovine origin. The involvement of endogenous interferon (IFN) on the maintenance of the infection level, as well as the effect of exogenous IFN and tumour necrosis factor alpha (TNF-alpha), was studied. Although exogenous IFN suppressed the spread and replication of virus, it did not cure the infection, even when continuously present over many cell passages. TNF-alpha alone had no antiviral effect in this system. However, both TNF-alpha and IFN enhanced the cytopathic effect of cytopathic BVDV, and induced a BVDV-like cytopathic effect in cells infected with non-cytopathic BVDV. These data are discussed with regard to possible mechanisms of pathogenesis during fatal BVDV disease in cattle.

Animals↗
PubMed1974

Persistent infection of BSC-1 cells by defective measles virus derived from subacute sclerosing panencephalitis.

A line of cells (IP-3), persistently infected with defective measles virus, was developed from co-cultures of subacute sclerosing panencephalitis-derived brain cells with monkey kidney cells (BSC-1). The line, carried for more than 45 serial passages, produced neither infectious virus nor hemagglutinin. Cultures consistently displayed a cycling focal cytopathic pattern of infection characterized by formation of syncytia, necrosis, and plaques followed by healing. Fluorescent measles antigen was present in damaged areas only, especially in syncytia. The development of syncytia was suppressed by measles antibody. Syncytia were lysed by antibody plus rabbit complement. A variant noncytopathic subline (IP-3-Ca) was derived from the 16th passage. Infectious virus was not detected. Cells were minimally positive for hemadsorption. Fluorescent measles antigen was present in all cells. Co-cultures of IP-3-Ca cells with normal BSC-1 cells developed massive syncytia and extensive destruction. The IP-3-Ca cells multiplied in the presence of measles antibodies and were destroyed by antibodies plus complement. The possible relevance of these findings to the pathogenesis of subacute sclerosing panencephalitis is discussed.

Adolescent↗
PubMed1961

Variation of herpes simplex virus in persistently infected tissue cultures.

Hinze, Harry C. (University of Wisconsin, Madison), and Duard L. Walker. Variation of herpes simplex virus in persistently infected tissue cultures. J. Bacteriol. 82:498-504. 1961.-Cultures of human conjunctiva, HeLa, and KB cells infected with herpes simplex virus (HF strain) were cultured for prolonged periods in medium containing low levels of antibody. After continuous culture of the infected cell lines for 6 months, two major changes were noted in the character of the virus present in the cultures. These changes consisted of an alteration in the type of cytopathic effect produced by the virus and marked loss of virulence for mice. Further study of the virus from the cultures revealed that it was still antigenically similar to the original strain of herpes virus. It was found that the variant produced an altered, proliferative type of cytopathic effect only in the presence of herpes antibody. The variant multiplied more slowly in human conjunctiva cells in culture than did the parent virus, and the variant had lost practically all capacity for multiplication in the brain of mice.

Animals↗
PubMed1984

Formation of a host range mutant of the lymphotropic strain of minute virus of mice during persistent infection in mouse L cells.

Minute virus of mice (i), the lymphotropic strain of minute virus of mice, established a persistent infection in normally restrictive L cells. The carrier state, which lasted 150 days, exhibited three clearly distinguishable stages. During the early stage (days 1 to 10 postinfection), small amounts of virus were formed. A "crisis" then developed that lasted 50 to 60 days and was characterized by massive cell lysis and high titers of virus. This was followed by a 70- to 80-day period in which small but stable quantities of virus were produced. Virus shed by the carrier culture during the latter phase had acquired an altered host range, namely, it had lost its ability to replicate in T-lymphocyte cell lines and had adapted to growth in L cells. Virus isolated at this time from a single plaque in L cells, designated hr301, was shown to possess similar host range properties. No differences, however, could be found between the DNAs of minute virus of mice (i) and of hr301 by restriction enzyme analysis, suggesting that the mutation that affected the viral host range did not involve an extensive region of the viral genome.

Animals↗