SEARCH · PubMed Health

Results for “Persistent Infection”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

PubMed1976

Persistent infection of BHK cells with herpes simplex virus types 1 and 2 in the absence of specific anti-herpetic antibody.

Persistent infection of BHK-21 cells with 5 strains of herpes simplex virus (HSV) type 1 and a 1 strain of HSV type 2 is described. Acute infection only was obtained with two strains of type 1 and one strain of type 2. Persistent infection could not be established in HeLa and rabbit lung cells. Persistent infection of BHK cells proceeded in the absence of specific antibody. Persistently infected cells were more resistant to superinfection with homologous or heterologous HSV as compared to infection of normal BHK cells. No interferon activity was demonstrated in persistently infected cell cultures. The results of virus titration were in accordance with the demonstration of fluorescent antigen of HSV.

Animals↗

PubMed1978

Persistent infection of L cells with vesicular stomatitis virus: evolution of virus populations.

A previous report (Youngner et al., J. Virol. 19:90-101, 1976) documented that noncytocidal persistent infection can be established with wild-type vesicular stomatitis virus (VSV) in mouse L cells at 37 degrees C and that a rapid selection of RNA(-), group I temperature-sensitive (ts) mutants consistently occurs in this system. To assess the selective advantage of the RNA(-)ts phenotype, evolution of the virus population was studied in persistent infections initiated in L cells by use of VSV ts 0 23 and ts 0 45, RNA(+) mutants belonging to complementation groups III and V. In L cells persistently infected with ts 0 23, the ts RNA(+) virus population was replaced gradually by viruses which had a ts RNA(-) phenotype. VSV ts 0 45 (V) has another marker in addition to reduced virus yield at 39.5 degrees C: a defective protein (G) which renders virion infectivity heat labile at 50 degrees C. Persistent infections initiated with this virus (ts, heat labile, RNA(+)) evolved into a virus population which was ts, heat resistant, and RNA(-). These findings suggest that the ts phenotype itself is not sufficient to stabilize the VSV population in persistently infected L cells and also indicate that the ts RNA(-) phenotype may have a unique selective advantage in this system. In addition to the selection of ts RNA(-) mutants, other mechanisms which also might operate in the maintenance of persistent VSV infections of L cells were explored. Whereas defective-interfering particles did not seem to mediate the carrier state, evidence was obtained that interferon may play a role in the regulation of persistent infections of L cells with VSV.

L Cells↗

PubMed1991

Persistent infection of Vero cells by the flavivirus Murray Valley encephalitis virus.

Murray Valley encephalitis (MVE) virus strain OR2 was serially passaged on Vero cells to establish a persistent infection which was maintained for over 300 days. Supernatants from infected cells protected Vero cells from c.p.e. and caused up to a 95% reduction of wild-type virus yield. These protective and interfering effects suggest that defective interfering (DI) particles are responsible for the establishment and maintenance of the MVE virus persistent infection. The persistently infected cell supernatant preparations shared several features with DI particle preparations from other viral systems, such as their amplification to detectable levels after two to four passages of virus. However, results from this study suggest that DI particles of MVE virus differ from other studied systems in that they are able to affect only moderately the yield of infectious wild-type virus. The genetic drift of the parental virus during the course of a long term persistent infection in vitro appears to be minimal.

Animals↗

PubMedDate not supplied

A monoclonal ELISA for bovine viral diarrhoea pestivirus antigen detection in persistently infected cattle.

Detection of cattle persistently infected with bovine viral diarrhoea virus (BVDV) is crucial to controlling mucosal disease. A sandwich enzyme-linked immunosorbent assay (ELISA) using monoclonal antibodies raised against the 48-kDa glycoprotein and the 120/80-kDa protein was developed for detecting antigens in leucocytes of 3 persistently BVDV-infected calves. The test is simple, sensitive and rapid. Moreover the same ELISA was able to recognise Belgian field isolates of BVDV. These results show that the test can be applied in the field.

Animals↗

PubMed1979

Measles virus-specified polypeptide synthesis in two persistently infected HeLa cell lines.

Measles virus-directed protein synthesis was examined in two HeLa cell lines (K11 and K11A) that are persistently infected with wild-type measles virus. Four viral proteins (H, hemagglutination protein; P, nucleocapsid-associated protein; NP, the major nucleocapsid protein; and M, the matrix protein) were readily detected in both cell lines by immune precipitation of [(35)S]methionine-labeled cell extracts followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. When analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, three (H, NP, and M) of the four viral proteins in both K11 and K11A cells differed from the corresponding viral proteins synthesized in HeLa cells acutely infected with the parental wild-type virus. In addition, the M protein from K11A cells migrated significantly more slowly on sodium dodecyl sulfate-polyacrylamide gel electrophoresis than the M protein from K11 cells, and there appeared to be slight differences in the H and NP proteins between these two persistently infected cell lines. The altered viral proteins detected in K11 and K11A cells appeared to be the result of viral mutations rather than changes in the host cell, since virus recovered from these cells directed the synthesis of similar aberrant viral proteins in HeLa cells. Virus recovered from K11 cells and virus recovered from K11A cells were both temperature sensitive and grew more slowly than wild-type virus. HeLa cells infected with virus recovered from K11 cells readily became persistently infected, resembling the original persistently infected K11 cells. Thus, viral mutations are associated with persistent measles virus infections in cell cultures.

Capsid↗

PubMed1991

Antigenic and genetic variation in cytopathic hepatitis A virus variants arising during persistent infection: evidence for genetic recombination.

Variants of hepatitis A virus (pHM175 virus) recovered from persistently infected green monkey kidney (BS-C-1) cells induced a cytopathic effect during serial passage in BS-C-1 or fetal rhesus kidney (FRhK-4) cells. Epitope-specific radioimmunofocus assays showed that this virus comprised two virion populations, one with altered antigenicity including neutralization resistance to monoclonal antibody K24F2, and the other with normal antigenic characteristics. Replication of the antigenic variant was favored over that of virus with the normal antigenic phenotype during persistent infection, while virus with the normal antigenic phenotype was selected during serial passage. Viruses of each type were clonally isolated; both were cytopathic in cell cultures and displayed a rapid replication phenotype when compared with the noncytopathic passage 16 (p16) HM175 virus which was used to establish the original persistent infection. The two cytopathic virus clones contained 31 and 34 nucleotide changes from the sequence of p16 HM175. Both shared a common 5' sequence (bases 30 to 1677), as well as sequence identity in the P2-P3 region (bases 3249 to 5303 and 6462 to 6781) and 3' terminus (bases 7272 to 7478). VP3, VP1, and 3Cpro contained different mutations in the two virus clones, with amino acid substitutions at residues 70 of VP3 and 197 and 276 of VP1 of the antigenic variant. These capsid mutations did not affect virion thermal stability. A comparison of the nearly complete genomic sequences of three clonally isolated cytopathic variants was suggestive of genetic recombination between these viruses during persistent infection and indicated that mutations in both 5' and 3' nontranslated regions and in the nonstructural proteins 2A, 2B, 2C, 3A, and 3Dpol may be related to the cytopathic phenotype.

Animals↗

PubMed1992

Measles virus from a long-term persistently infected human T lymphoblastoid cell line, in contrast to the cytocidal parental virus, establishes an immediate persistence in the original cell line.

To investigate the mechanisms of measles virus (MV) establishment and maintenance of persistence in lymphoid cells, we have established a long-term persistent infection with MV, Edmonston strain, in the human T lymphoblastoid cell line MOLT4, which has been in continuous culture for over 8 years. In this culture, designated MOMP1, more than 98% of cells display viral antigens. The MOMP1 culture is immune to superinfection with MV and is not cured by anti-MV antibodies. No evidence of defective interfering particles was obtained. The persistently infected culture releases an infectious virus showing a miniplaque and thermoresistant modified phenotype that, unlike the parental virus Edmonston strain which produces a lytic infection with extensive cell fusion, establishes an immediate persistence in MOLT4 cells with neither significant loss of cell viability nor cell fusion. This suggests that the modification in the virus suffices to maintain the state of persistence without requiring a coevolution of the host cell during the infection, as has been reported in other persistent virus infections.

Antibodies, Viral↗

PubMed1979

Establishment of persistent infection in BHK-21 cells by temperature-sensitive mutants of Sindbis virus.

Twelve temperature-sensitive (ts) mutants of Sindbis were examined for their ability to establish persistent infection in BHK-21 cells at 39 degrees C. Five of these mutants were able to initiate colony formation in infected cultures, which followed an extensive c.p.e. Two of the mutants were able to establish persistent infections which survived beyond the fifth cell passage p.i. The ability to initiate colony formation was correlated with low reversion of the ts mutation, or with ability to interfer with the multiplication of the wild-type virus. Virus released from persistently infected cultures was not temperature-sensitive. The restriction of virus multiplication in persistently infected cells operated prior to virus-specified RNA synthesis. It is concluded that in this system establishment of persistent infection depends on an inhibition of virus multiplication early in infection and occurs in only a small proportion of infected cells.

Animals↗

PubMed1976

Characterization of measles viruses in establishment of persistent infections in human lymphoid cell line.

Human lymphoid cells (NC-37) were infected with attenuated measles vaccine virus (Schwarz, AIK-C, and CAM-70 strains), subacute sclerosing panencephalitis virus (Mantooth and Halle strains), neurovirulent TYCSA strain, and wild type virus (Edmonston and Toyoshima strains) at an input multiplicity of 0-01. These strains were divided into two groups by their capacity to establish carrier states. CAM-70, Toyoshima, and Edmonston strains did not set up persistent infections in NC-37 cells, whereas AIK-C strain induced chronic cyclic infection and the Schwarz, TYCSA, Mantooth and Halle strains could set up persistent infections and furthermore two types of persistent infections were recognizable. Cells persistently infected with Schwarz strain contained nucleocapsid structures in both nucleus and cytoplasm, and produced infectious virus of 10(4) to 10(5) p.f.u./ml over 100 days after the inoculation of the virus but the cap-formation of measles antigens on the cell membrane was seldom observed. However, in cells persistently infected with TYCSA strain, nucleocapsid structures were rarely observed in the nucleus, but the cap-formation of measles antigens on the cell membrane was often observed. The titre of carried virus was always higher than the number of cells in the range of 10(6) to 10(7) p.f.u./ml. Mantooth strain was similar to Schwarz strain and Halle strain was similar to TYCSA strain in the properties of their carrier states. These carrier states were stable and the cells grew normally for over one year.

Antigens, Viral↗

PubMed1992

Defective RNAs in mosquito cells persistently infected with Bunyamwera virus.

Viral protein and RNA synthesis were compared in BHK and Aedes albopictus C6/36 (mosquito) cells infected with Bunyamwera virus. In BHK cells host protein synthesis was inhibited and viral proteins were detected until the cells died; in C6/36 cells there was little inhibition of host proteins and viral proteins could not be detected after 36 h post-infection. Relatively more S segment RNA than L or M segment RNA was produced in infected C6/36 cells compared to BHK cells. A persistent infection of C6/36 cells was established and the cells were passaged at weekly intervals for over a year. The titre of virus released from the cells and the level of viral RNA in the cells at different passages fluctuated markedly, but there was no simple relationship between virus titre and the amount of viral RNA. Northern blot analysis of viral RNA extracted from persistently infected cells revealed the presence of subgenomic RNAs derived from the L RNA segment. These defective RNAs were not packaged into nucleocapsids. The presence of the defective RNAs did not correlate with resistance of cells cloned from the persistently infected population to superinfection with homologous virus. Hence the role of these defective RNAs in the maintenance of the persistent state remains to be elucidated.

Animals↗

PubMed1979

Interferon susceptibility of various cell lines persistently infected with haemagglutinating virus of Japan (HVJ).

Various cell lines persistently infected with para-influenza 1 virus, HVJ strain, were less susceptible to the antiviral action of interferon than the same cell lines when not infected with HVJ. When Vero cells persistently infected with a temperature-sensitive strain of HVJ were incubated at 38 degrees C, a non-permissive temperature, they became fully susceptible to interferon, whereas neither the haemadsorbing nor the cell-associated haemagglutinating activity of the virus was expressed. These findings suggest that the lowered interferon susceptibility of virus-carrier cells may be related to the maturation of virus in them. It was found that the low susceptibility of virus-carrier cells to interferon is not due to blocked adsorption of interferon or to inability of the cells to respond tointerferon. Studies with actinomycin D suggest that some step (or steps) before the synthesis of the messenger RNA for the antiviral protein is blocked.

Animals↗

PubMed1977

Persistent infections in L cells with temperature-sensitive mutants of reovirus.

Serial passage of reovirus temperature-sensitive (ts) mutant C(447) produced by passage 9 (P9) a heavily defective population of virus from which the double-stranded RNA genomic segments L(1), L(3), and M(1) were largely missing. Viral cores obtained from this P9 population were heterogeneous with respect to buoyant density in CsCl gradients, suggesting that particles were present with different combinations of deleted segments. Similar observations were made with the E(320) ts mutant of reovirus. By serial passage P15, 90% of the E(320) viral population was defective and the major missing genomic segments were L(1) and L(3). Persistent infections were readily established in monolayer cultures of L cells with P9 of C(447) virus and P15 of E(320) virus and in Vero cells with P9 of C(447) virus. Under similar conditions persistent infections could not be initiated with defective-free populations of C(447) or E(320) viruses. The greater the capacity of defective virus in the population to interfere with viral growth, the more readily persistent infection was initiated. During their maintenance persistently infected cells were subcultured approximately twice a week. More than 80% of the cells continuously produced virus. By subculture 6 the original ts infectious viral component had been replaced by a small-plaque mutant with a ts(+) phenotype. Defective virus was always present in the carrier cells. In addition to the more commonly observed defectives whose cores banded at approximately rho = 1.40 to 1.415 g/ml in CsCl gradients, a new class of defective core was seen banding in the region of 1.34 to 1.36 g/ml. This latter particle, which has not been thoroughly characterized as yet, is termed "light defective." Persistently infected cells underwent periodic crises during their maintenance, during which the cultures partially lysed and then rapidly grew to confluence. Crises corresponded to a burst of infectious virus from the cells and a relatively low concentration of light defectives. During quiescent periods the concentration of light defectives amounted to as much as 98% of the total viral population. The function of light defectives is not yet clear, but it seems essential to assign major importance to defective virus in maintaining persistent infections in this system.

Defective Viruses↗

PubMed1991

Defective function of leukocytes from cattle persistently infected with bovine viral diarrhea virus, and the influence of recombinant cytokines.

Cattle persistently infected with bovine viral diarrhea (BVD) virus have decreased neutrophil and lymphocyte functions. We reevaluated these functions and further characterized the inhibition of persistent BVD virus infection in neutrophils, using sensitive kinetic assays. In addition, the influence of in vitro incubation of neutrophils with recombinant bovine interferon gamma (rBoIFN gamma) and in vitro incubation of lymphocytes with recombinant bovine interleukin-2 was evaluated. Significant (P less than 0.05) decrease in random migration under agarose, Staphylococcus aureus ingestion, cytochrome-C reduction, iodination, antibody-independent cell-mediated cytotoxicity, oxidant production, and cytoplasmic calcium flux were observed in neutrophils from cattle persistently infected with BVD virus, compared with noninfected control cattle. Incubation of neutrophils from noninfected controls with rBoIFN gamma significantly (P less than 0.05) decreased random migration under agarose, cytochrome-C reduction, and cytoplasmic calcium flux. Neutrophils from cattle persistently infected with BVD virus also had decreased random migration under agarose after incubation with rBoIFN gamma; in addition, antibody-independent cell-mediated cytotoxicity, elastase release, and cytoplasmic calcium flux were significantly enhanced. The rBoIFN gamma induced significantly (P less than 0.05) different effects on chemotaxis, cytochrome-C reduction, iodination, and cytoplasmic calcium flux of neutrophils from infected and control cattle. The rBoIFN gamma was more effective at improving the function of neutrophils from cattle persistently infected with BVD virus, compared with neutrophils from controls. Lymphocytes from infected cattle had decreased blastogenesis in response to phytohemagglutinin, concanavalin A, and pokeweed mitogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

Establishment and characterization of a subacute sclerosing panencephalitis (measles) virus persistent infection in BGM cells.

Infection of BGM cells with the Halle isolate of subacute sclerosing panencephalitis (SSPE) gave rise to a persistent infection (BGM/Halle), whereas infection of another African green monkey kidney cell line (Vero) under identical conditions led to a lytic infection. The BGM/Halle cells multiplied more slowly than the non-infected cells (even when the medium was changed daily). Under such conditions 10(7) to 10(8) p.f.u./ml/24 h of measles virus was released into the medium. It was established that the persistent infection was not due to the accumulation of thermosensitive mutants and that the virus was not modified as measured by several biological parameters. The virus released from BGM/Halle cells had, however, acquired an ability to give rise to a persistent infection in Vero cells. The quantity of virus released from persistently infected Vero cells was very low (10(2) to 10(3) p.f.u./ml). It was concluded that a host-cell factor plays a role in the restriction of virus replication.

Cell Division↗

PubMed1990

[Patterns of acute and persistent infections in enteroviral heart diseases].

Enteroviruses are considered as the major etiologic agents of myocarditis in humans. Recent in situ hybridization studies on endomyocardial biopsies indicate that not only in acute myocarditis (pattern of acute infection), but also in chronic dilated cardiomyopathy enterovirus RNA can be detected (pattern of persistent infection). Our experimental studies on murine coxsackievirus B3 myocarditis provided evidence that persistent infection occurs also in mice. Quantitative in-situ hybridization and immunohistochemistry as well as electron microscopic in situ hybridization experiments were performed on ACA/SnJ mice three to thirty days after infection. The pattern of acute infection (days 3-9 p.i.) is characterized by rapid progression of myocardial lesions, an increasing number of inflammatory cells and a high number of infected myocytes. Hallmarks of the persistent pattern (day 15-30 p.i.) are reduced inflammation, reduced numbers of persistently infected cells and a slow progression of myocardial lesions. Infection is primarily restricted to degenerated, atrophic myocytes and to fibroblasts.

Acute Disease↗

PubMed1977

Interferon production and response to exogenous interferon in two cell lines of mouse brain origin persistently infected with Sendai virus.

Two persistently infected cell lines established from C3H mouse brain cells infected in vivo with Sendai virus were shown to differ with respect to interferon (IF) production and response to exogenous IF. MB/Sen carrier cells contained 1-5 per cent antigen positive cells when examined by immunofluorescence, and virus was occasionally recovered from the culture medium. MB/SenAS carrier cells were maintained with 0.16 per cent Sendai antiserum in the supernatant medium. All MB/SenAS cells contained viral antigen and infectious virus was present in the culture medium. MB/Sen released IF spontaneously into the culture medium. Further IF production could be stimulated in MB/Sen by superinfection with Newcastle disease virus (NDV) or vesicular stomatitis virus (VSV). Exogenous IF provided good protection against VSV challenge. In contrast, MB/SenAS produced no IF spontaneously but could be stimulated by NDV and VSV to produce IF. Exogenous IF failed to reduce the amount of VSV released into the supernatant fluid. Replication of VSV was restricted in MB/SenAS as shown by a 2.3 log10 lower virus yield compared to MB/Sen.

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↗

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↗