Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Persistent Infection”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 109 records · Page 6Linked to original sources
PubMed1993

Persistent infection with Ehrlichia chaffeensis.

Although persistent infection of animals by members of the genus Ehrlichia is well known and may be associated with subsequent severe or fatal illness, persistent infection of humans with Ehrlichia chaffeensis has not been reported. Herein we report a typical case of serologically documented acute ehrlichiosis; despite therapy with tetracycline and chloramphenicol, the patient's condition progressively worsened and he suffered multiple secondary infections and gastrointestinal hemorrhage. He died 68 days after his initial hospitalization. Retrospective immunohistologic examination of both acute-phase bone marrow specimens (obtained day 12 of illness) and postmortem liver tissue specimens (obtained day 68 after onset of disease) revealed E. chaffeensis morulae in mononuclear cells, presumably macrophages and monocytes. Findings of this case provide the first definitive evidence that E. chaffeensis is capable of establishing persistent human infection and suggest a role for this obligate intracellular bacterium in the induction of immune compromise associated with a fatal outcome.

Acute Disease↗
PubMed1977

The role of defective interfering particles in persistent infection of Vero cells by measles virus.

Persistent infections by measles virus were rapidly established in the majority of Vero cells when monolayers were infected with virus stocks that had been passed three to five times from an undiluted inoculum. These virus stocks had low infectivity titres but normal haemagglutinin titres and were able to cause interference. The ability of such virus stocks to establish persistent infections seems to be due to the presence of defective interfering particles rather than of virus mutants. Measles virus released from a persistently infected Vero cell line at the 93rd passage had properties similar to the undiluted passage virus that generated persistent infections.

Animals↗
PubMed1984

Feline calicivirus infection in kittens borne by cats persistently infected with the virus.

On the basis of repeated isolation of feline calicivirus (FCV) from oropharyngeal swabs four to eight months after exposure to FCV strain 255, four carrier queen cats were identified. These cats gave birth to 16 kittens. Litters were individually housed with their mothers until nine weeks of age and were monitored virologically and serologically from birth until 15 weeks old. All kittens became infected between three and nine weeks old and shed FCV consistently for periods of three to 11 weeks. Clinical signs of FCV were observed in 11 kittens but none developed severe respiratory disease. At the time of initial infection maternal antibody titres in the kittens ranged from 1:4 to 1:24. Within one to three weeks of infection titres began to rise. The results indicated that kittens of queen cats persistently infected with FCV frequently experience mild or subclinical immunising infections.

Age Factors↗
PubMed2001

Molecular approaches to elucidating innate and acquired immune responses to Babesia bovis, a protozoan parasite that causes persistent infection.

For many vector-transmitted protozoal parasites, immunological control of acute infection leads to a state of persistent infection during which parasitemias may cycle unnoticed in infected but otherwise clinically healthy animals. Achieving persistent infection is a strategy that favors parasitism, since both host and, therefore, parasite survive, and endemically infected animal populations provide a reservoir of parasites continually available for subsequent transmission. Examples of the major economically important protozoan pathogens that cause persistent infection in mammals include the related Theileria and Babesia parasites as well as Trypanosoma species. Control of acute infection and maintenance of clinical immunity against subsequent infection are determined by the interplay of innate and acquired immune responses. This review will focus on approaches taken to gain an understanding of the molecular basis for innate and acquired immunity against the hemoprotozoan parasite of cattle, Babesia bovis. Knowledge of mechanisms used by the parasite to survive within infected cattle from acute to persistent infection combined with definition of the correlates of protective immunity in cattle should be applicable to designing effective vaccines.

Animals↗
PubMed1983

Inhibition of onset of overt multiplication of Chlamydia psittaci in persistently infected mouse fibroblasts (L cells).

When monolayers of mouse fibroblasts (L cells) persistently infected with Chlamydia psittaci (strain 6BC) were dispersed in medium 199 and plated out in new flasks, the monolayers that grew out consisted almost exclusively of inclusion-free host cells that retained full resistance to superinfection with C. psittaci (covert infection). After a delay that was inversely proportional to the initial density of the newly transferred L cell population, the percentage of host cells containing visible chlamydial inclusions increased rapidly (overt infection), and most of the L cells were destroyed by extensive chlamydial multiplication (wipeout), leaving only a few survivors to start new persistently infected monolayers. When persistently infected L cell populations grown in medium 199 were transferred to Eagle minimal essential medium, the onset of overt multiplication was strongly suppressed although covert multiplication of C. psittaci continued unabated, as shown by host cell retention of resistance to superinfection and the prompt resumption of overt multiplication after transfer back into medium 199. The difference(s) between the two media responsible for the different expression of the persistently infected state was not determined. A single dose of 100 U of penicillin G per ml of medium 199 given at the time persistently infected monolayers were divided almost completely suppressed the appearance of visible signs of chlamydial infection for several weeks, although resistance to superinfection was retained at all times. The same amount of penicillin given 7 days after replating did not prevent the occurrence of the first expected wipeout, but there was a long period of inclusion-free L cell growth between the first wipeout and the second. It was concluded that covert multiplication of C. psittaci in persistently infected L cells may continue indefinitely without the appearance of visible signs of infection. The transition between covert and overt chlamydial multiplication appears to be a penicillin-sensitive, multistep process that is regulated, at least in part, by the host cell density and the composition of the growth medium.

Animals↗
PubMed1993

Precise missense and silent point mutations are fixed in the genomes of poliovirus mutants from persistently infected cells.

Poliovirus mutants selected in persistently infected human neuroblastoma cells have a modified cell tropism and can establish a secondary persistent infection in nonneural cells, such as HEp-2c cells. Nucleotide sequence analysis revealed that the genome of a persistent mutant, S11, differed from that of the parental lytic Sabin 1 poliovirus strain by 31 point mutations. Three mutations occurred in the noncoding regions. The other mutations resulted in 12 amino acid substitutions; 1 substitution occurred in a nonstructural protein (3A), while the other 11 substitutions were clustered in the capsid proteins VP2 and VP1. The same missense mutations, as well as many of the silent mutations that we observed in mutant S11, also accumulated in the genome of two other persistent viruses isolated from independent infections. This finding indicates that both missense and silent mutations are selected during the persistent infection of neuroblastoma cells and suggests that the secondary structure of RNA in the coding region may play a role in viral infection.

Capsid↗
PubMed1996

Cytotoxic-T-lymphocyte-mediated cytolysis of L cells persistently infected with Chlamydia spp.

Persistent chlamydial infections have been proposed as a means whereby chlamydiae evade immune resolution of infection. Such a mechanism would require evasion not only of the humoral immune responses but also of cell-mediated immune responses. We hypothesized that if such a mechanism is important, persistently infected cells should not be recognized by cytotoxic T cells. Persistent infections were simulated in vitro by treatment of Chlamydia trachomatis- or Chlamydia psittaci-infected cells with gamma interferon (IFN-gamma), penicillin, or tryptophan depletion. Cultures were examined for induction of a chlamydial stress response (measured by transcription of groesl RNA) and for the effects on viability, infectivity, morphology, and immune recognition. Although both IFN-gamma and penicillin induced aberrant chlamydial morphology and growth, we did not find evidence that these treatments elicited a classical stress response. In addition, T-cell-mediated lysis of Chlamydia-infected target cells treated with IFN-gamma or penicillin or grown in tryptophan-deficient media was examined. The immune cell-mediated lysis of these treated infected cells demonstrated that despite the effects of these compounds on chlamydial growth and development, the infected cells continued to be efficiently recognized and killed by cytotoxic T cells. Thus, it seems unlikely that these in vitro models of persistence represent functional mechanisms to evade immune clearance.

Base Sequence↗
PubMed2005

Establishment of Vero E6 cell clones persistently infected with severe acute respiratory syndrome coronavirus.

Little information is available on persistent infection of severe acute respiratory syndrome (SARS) coronavirus (CoV). In this study, we established persistent infection of SARS-CoV in the Vero E6 cell line. Acute infection of Vero E6 with SARS-CoV produced a lytic infection with characteristic rounding cytopathic effects (CPE) and the production of a large number of infectious particles in the culture fluid within 3 days post-infection. Upon subsequent culturing of the remaining adherent cells, the cells gradually proliferated and recovered normal morphology similar to that of the parental cells, and continued to produce large numbers of infectious viral particles during the observation period of 5 months. Among a total of 87 cell clones obtained from the persistently infected Vero E6, only four cell clones (named #13, #18, #21, and #34) were positive for viral RNA. Clones #13, #18, and #34 shifted to viral RNA-negative during subsequent cultures, while #21 continuously produced infectious particles at a high rate. The SARS-CoV receptor, angiotensin-converting enzyme 2, was almost completely down regulated from the cell surface of persistently infected cells. Western blot analysis as well as electron microscopy indicated that the ratios of spike to nucleocapsid protein in clone #21 as well as its parental persistently infected cells were lower than that in the cells in the acute phase of infection. These Vero E6 cells persistently infected with SARS-CoV may be useful for clarifying the mechanism of the persistent infection and also for elucidating the possible pathophysiologic significance of such long-term maintenance of this virus.

Angiotensin-Converting Enzyme 2↗
PubMed1984

Persistent infection of mouse fibroblasts with Coxsackievirus.

Infection of fibroblast cell lines initiated from BALB/c or NFR mice with coxsackievirus B3 (CBV-3) or B4 (CBV-4) resulted in infections which persisted for a limited number of subpassages of the infected cells in most cases, but for over a year in one case. In all instances primary acute infections were characterized by cytopathology and release of infectious virus progeny. Viral antigen could be detected during the acute phase of infection, but not in subcultured infected cells. Infectious center assays showed that every cell was infected during the acute phase of infection, but that from the first subcultivation on, the numbers of cells which were able to initiate infection were greatly reduced. The long term persistent CBV-3 infection was characterized by wide fluctuations in titers of virus released into the supernatant fluids. Interferon did not appear to play a role in maintenance of the persistent infection. Information derived from studies on mechanisms of CBV persistence in the in vitro model may help to elucidate the role of CBV in chronic human diseases such as myocarditis.

Animals↗
PubMed1996

Persistent infection of mammalian cells by Rift Valley fever virus.

Infection of mammalian cells with Rift Valley fever virus (RVFV) leads generally to the production of virus and cell death. In this paper we examined the fate of Vero cells infected with three strains of RVFV and observed that, while a large proportion of cells exhibited a clear cytopathic effect (CPE), a small but significant fraction did not undergo a lytic infection but was able to proliferate and establish a persistent infection. Several independent RVFV persistently infected cell lines have been established and passaged for more than 1 year after infection with a virulent strain (ZH548) and two attenuated strains (C13 and MP12). Although the viruses used for the primary infection were plaque-purified, we do not know whether defective-interfering particles were responsible for the establishment of the persistent infection. The persistently infected cells became resistant to superinfection with RVFV but not with other viruses and shed low amounts of infectious, lytic and non-lytic virus during a limited number of passages. In all the passages tested, the three genomic segments or related products were synthesized as well as the structural nucleoprotein N and glycoproteins G1 and G2. Abnormal defective RNAs were detected, migrating faster or slower than their respective counterparts. The faster-migrating RNAs were internally deleted, some of them possessing only the very terminal part of the 5' genomic end.

Animals↗
PubMed2005

Reinfections, persistent infections, and new infections after general population screening for Chlamydia trachomatis infection in the Netherlands.

OBJECTIVES: The objectives of this study were to determine the rate of new infections and reinfections or persistent infections with Chlamydia trachomatis to define appropriate screening intervals and to identify risk factors for reinfection. DESIGN: This was a cross-sectional study among a subsample of participants in a population-based screening. SETTING: This study was conducted in urban and rural areas in The Netherlands. PARTICIPANTS: A total of 21,000 15- to 29-year-old women and men were invited for home-based urine testing. One year after the study, a subsample of 299 participants were offered retesting. MAIN OUTCOME MEASURES: The authors studied the rate of infection with C. trachomatis. Serovar determination was used to potentially discriminate between new infections and reinfections or persistent infections. RESULTS: Nine C. trachomatis infections were found among 187 responders (4.8% confidence interval, 1.7-7.9). The prevalence was 10.4% (5 of 48) in previous positives and 2.9% (4 of 139) in negatives. Three of 5 repeatedly positive participants were infected with a different C. trachomatis serovar. CONCLUSIONS: Our study indicates that infected persons found in a systematic, population-based screening should be re-screened within 1 year. Optimal screening intervals still need to be determined.

Adolescent↗
PubMed1981

Establishment of a persistently infected cell line with Rinderpest virus.

Persistent infection of rinderpest virus in Vero cells was established and designated as VRP34. Virus specific antigens were present in nearly 100 per cent of the cells. Cytopathic effect (CPE) consisting of syncytium formation and vacuolation is a unique feature of VRP34. Spontaneously released virus mainly consisted of non-temperature-sensitive virus populations and was able to initiate persistent infection in both normal Vero and RK13 cells. The results indicate that mutation of virus is responsible for the establishment of persistent infection.

Animals↗
PubMed1990

Effect of antiviral antibody on maintenance of long-term rubella virus persistent infection in Vero cells.

A Vero cell line with a long-term rubella virus persistent infection was maintained for 45 weeks in the presence of anti-rubella virus antibody of sufficient titer to completely neutralize the virus in the culture fluid to determine the effect of the presence of antibody on the maintenance of the persistent infection. Prior to antibody treatment, virus was continuously detected as plaque-forming units in the persistently infected culture fluid. Virus clones that were plaque purified from the persistently infected culture fluid were temperature sensitive and exhibited a reduced efficiency of replication and ability to induce cytopathic effects in Vero cells at the persistently infected culture temperature compared with the standard virus used to initiate the persistently infected culture. Defective interfering RNAs were the major intracellular virus-specific RNA species present in the persistently infected cells. Treatment with antibody failed to cure the persistently infected culture of virus, and the cells retained the ability to release virus after antibody treatment was discontinued. Interestingly, the presence of antibody led to the selection of a population of virus which was markedly less cytopathic for Vero cells than the virus population which was selected during persistent infection in the absence of antibody.

Animals↗
PubMed2002

Characteristics of a respiratory syncytial virus persistently infected macrophage-like culture.

A persistently infected culture obtained from immortalized murine macrophage-like cells, which survived respiratory syncytial virus (RSV) infection at multiplicity of one, was established and characterized. The presence of RSV through the passages was confirmed and monitored by (a) detection of infectious virus by TCID(50)/ml, (b) defective particles by viral infectivity interference and buoyant density determinations, (c) cell surface antigen by indirect immunofluorescence and FACS, and (d) expression of a viral gene by RT-PCR. Moreover, cell morphology changes by comparison of macrophage area and perimeter were determined. A second culture was obtained by cell cloning out of this culture, and a third culture was established by superinfection with the original virus, in which 92-95% of the macrophages expressed viral antigen without cell destruction and released defective particles but low levels of infectious virus. Although the three cultures maintained the characteristics of persistently infected cells, concentrations of released infectious virus, defective particles, and percentages of cells bearing viral antigen varied. RSV persistently infected murine macrophage cultures provide an in vitro model to study viral-macrophage interaction and to allow the experimental use of a cell important in disseminating the infection. In addition, due to the wide array of cellular and humoral reagents in the mouse, studies on immunologic aspects of viral immunity are facilitated.

Animals↗
PubMed1977

Persistent infection of cultured mammalian cells by Japanese encephalitis virus.

Persistent infections were established by serial undiluted passage of flavivirus Japanese encephalitis virus in a line of rabbit kidney cells (MA-111). The persistently infected cells resembled uninfected cells in most respects. Low levels of infectious virions were released from a small percentage of cells, and a larger and more variable percentage was shown to possess viral antigen by fluorescent-antibody staining. Released viruses were shown to interfere with replication of wild-type Japanese encephalitis virus. Persistently infected MA-111 cells could not be superinfected with homologous wild-type Japanese encephalitis virus but could be superinfected with two heterologous viruses. Transfer of cell culture medium from persistently infected MA-111 cells to a line of African green monkey kidney cells (Vero) resulted in similar persistent infections in the latter cells. Temperature sensitivity and host-cell interferon production were not involved in establishment or maintenance of persistence. Determination of ratios of physical particles to infectious particles revealed that many defective, noninfectious viruses were present, suggesting that defective interfering particles may be responsible for persistency.

Cell Division↗
PubMed1990

Detection of anti-rabies virus cytotoxic T lymphocytes in mice of four distinct H-2 haplotypes using target cells persistently infected with ERA rabies virus.

Cells persistently infected with Evelyn-Rokitnicki-Abelseth (ERA) rabies virus were established. The cells were used as stimulator and target cells to compare H-2 restricted cytotoxic T lymphocyte (CTL) responses specific for rabies virus in A/WySnJ (H-2a), C57BL/6J (H-2b), BALB/cByJ (H-2d), A.SW/SnJ (H-2s) and SJL/J (H-2s) mice. Using a 51chromium release assay, it was determined that an effector/target (E/T) ratio of 5:1 was necessary to demonstrate specific lysis of ERA virus persistently infected mouse neuroblastoma (MNB) (H-2a), EL-4 (H-2b) and P815 (H-2d) cells. Effectors at an E:T ratio of only 0.05:1 specifically lysed an SV-40 transformed SJL/J mouse fibroblast (SSSV) (H-2s) target monolayer. The CTL destruction of the SSSV monolayer was observed visually following Giemsa staining. This is the first instance in which a detailed method for detection of murine anti-rabies virus CTLs has been reported. Furthermore, it is the first time target cells persistently infected with rabies virus were used as stimulator cells to amplify CTLs in vitro and as target cells in the CTL assay. It also is the initial report in which rabies specific CTLs were characterized in H-2d and H-2s rabies virus infected mice.

Animals↗
PubMed1999

Suppression of interferon response gene expression in cells persistently infected with mumps virus, and restoration from its suppression by treatment with ribavirin.

Persistent infections with mumps virus were established in human B-lymphoid cell line Akata and in the human chronic myelogenous leukaemia cell line K562. Even after IFN treatment a drastic decrease in STAT-1alpha (signal transducers and activators of transcription-1alpha), STAT-2 and p48 (ISGF-3gamma: IFN-stimulated gene factor-3gamma), which are closely correlated with the IFN-signaling pathway, was found in these persistently infected cells (Akata-MP1 and K-MTP). Therefore, the IFN-signaling pathway is thought to be defective in these persistently infected cells. In other words, most of the IFN-inducible genes in these cells persistently infected with mumps virus may not be able to respond to IFN treatment. Indeed, poor induction of 2',5'-oligoadenylate synthetase (2-5AS), dsRNA activated protein kinase (PKR), and MxA protein mRNAs were demonstrated in these cell lines after IFN treatment. Expression of MHC class-I antigen was also significantly reduced in the persistently infected cell lines as compared with that of uninfected control cells. HLA antigen was augmented by IFN-alpha in Akata and K562 cells, but not in persistently infected cells. Furthermore, suppression of IFN-induced 2-5AS induction and MHC class-I expression was restored by treatment of persistently infected cells with ribavirin through inhibition of virus replication. The result of restoration was also confirmed by IFN-induced STAT-1 induction in persistently infected cells treated with ribavirin.

Antiviral Agents↗
PubMed1982

Novel phenotype of RNA synthesis expressed by vesicular stomatitis virus isolated from persistent infection.

Vesicular stomatitis virus (VSV) stocks isolated from two persistently infected mouse L-cell lines (designated VSV-PI stocks) express an altered phenotype of RNA synthesis. This phenotype is different from the RNA synthesis phenotype expressed by the viruses used to initiate the persistently infected lines, wild-type VSV and VSV ts-0-23 (a group III, ts-, RNA+ mutant). At 34 and 37 degrees C in L cells productively infected with VSV-PI stocks derived from the two cell lines, transcription of virus mRNA was significantly reduced, whereas replication of the 40S genomic RNA species was enhanced compared with wild-type VSV or ts-0-23. At 34 and 37 degrees C, both VSV-PI stocks replicated with equal or greater efficiency than wild-type VSV; 37 degrees C was the temperature at which the persistently infected cultures were maintained. At 40 degrees C, both VSV-PI stocks were temperature sensitive, and clonal VSV-PI isolates from both cell lines belong to complementation group I (RNA-). Standard ts- mutants (derived by mutagenesis of wild-type VSV) belonging to RNA- complementation groups I, II, and IV do not express the VSV-PI RNA synthesis phenotype at the permissive temperature, making this phenotype distinctive to persistent infection. Since the two VSV-PI populations from persistently infected cell lines initiated with different viruses both evolved this unique phenotype of RNA synthesis, the expression of this phenotype may play an important role in the maintenance of persistence.

Animals↗