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Results for “Persistent infection”

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PubMed1976

RNA synthesis in BHK 21 cells persistently infected with vesicular stomatitis virus and rabies virus.

Virus-induced RNA synthesis was studied in BHK 21 cells persistently infected with vesicular stomatitis virus (VSV) and rabies virus by labelling RNA synthesized in the presence of antinomycin D. During persistent infection the species of messenger RNA synthesized were similar in size and relative proportions to those seen during acute infection, but there were some minor differences. Full-sized B virion RNA was generally not detected during persistent infection, and new species (probably DI virion RNA) appeared.

Animals↗

PubMed1977

Antigenic shift of visna virus in persistently infected sheep.

Visna viruses isolated from persistently infected sheep were antigenically distinct from the plaque-purified virus used for inoculation. The selection of antigenic variants under antibody pressure, thought to occur in vivo, was reproduced in sheep cell cultures inoculated with plaque-purified visna virus and maintained in antibody. Antigenic shift may be a mechanism for persistence of virus in slow or recurrent viral infections.

Animals↗

PubMed1979

A comparative study of tick-borne encephalitis virus RNA synthesis in acutely and persistently infected cells.

Rate zonal and buoyant density gradient centrifugation did not reveal any difference between tick-borne encephalitis virus virions released from acutely or persistently infected cells. All three RNA species characteristic for flavivirus replication were found both in acutely or persistently infected cells, but increased levels of intracellular 42S RNA polyadenylation was observed in persistently infected cells.

Animals↗

PubMed1979

Pneumoviruses: the cell surface of lytically and persistently infected cells.

Human embryonic lung (MRC-5), feline embryo (FEA), mink lung (Mv1Lu) and monkey kidney (BSC-1) cells infected by respiratory syncytial virus showed characteristic morphological changes when viewed by scanning electron microscopy. The surfaces of respiratory syncytial virus-infected cells developed a profusion of slender filaments after 48 h incubation at 31 degrees C. Similar changes in surface morphology were observed in BSC-1 cells infected by murine pneumonia virus. Filament production therefore appears to be a common property of pneumo-viruses. Filaments were not observed in cells infected with either syncytial and non-syncytial herpes simplex virus, the cytocidal vesicular stomatitis and Batai (Bunyaviridae) viruses, or the focus-inducing rabbit fibroma virus. Filament production was not observed in cells infected with ts mutants of respiratory syncytial (RS) virus during incubation at the restrictive temperature, or in a persistently infected culture of BSC-1 cells at 37 degrees C. The persistently infected cells (the RS ts 1/BSC-1 line) had some of the characteristics of cells transformed by oncogenic viruses, namely ability to overlap adjacent cells and agglutination by a low concentration of concanavalin A. The pseudo-transformed phenotype was temperature-dependent, however, and suppressed by raising the temperature of incubation to 39 degrees C. The presence of virus antigen at the cell surface was similarly temperature-dependent in these cells, diminished at high temperature (39 degrees C) and enhanced at low temperature (31 degrees C), suggesting that the changes in the host cell were the result of insertion of virus protein into the cell membrane. Evidently, persistent infection by a cytoplasmic virus can produce alterations in the host cell usually associated with transformation by nuclear viruses.

Animals↗

PubMed2025

SARS-CoV-2 genomic diversity and within-host evolution in individuals with persistent infection in the UK: an observational, longitudinal, population-based surveillance study.

BACKGROUND: Persistent SARS-CoV-2 infections in hospitalised immunocompromised individuals are known to facilitate accelerated within-host viral evolution, potentially contributing to the emergence of highly divergent variants. However, little is known about the evolutionary dynamics and transmission risks of persistent infections in the general population. We aimed to characterise the within-host evolution of SARS-CoV-2 during persistent infections identified through a large community surveillance study. METHODS: We used data from the Office for National Statistics COVID-19 Infection Survey (ONS-CIS), a large-scale, longitudinal, population-based surveillance study conducted in the UK from April, 2020, to March, 2023. For this analysis, we focused on infections with high viral load (cycle threshold ≤30) and available genome sequences, from seven major SARS-CoV-2 lineages (alpha, delta, BA.1, BA.2, BA.4, BA.5, and XBB). ONS-CIS participants were randomly selected from the general population and tested regularly by RT-PCR, regardless of symptoms. We defined persistent infections as those with sustained or rebounding high viral RNA titres for 26 days or longer. We examined associated host characteristics and used raw sequence data to identify de novo mutations and estimate within-host synonymous and non-synonymous evolutionary rates across the SARS-CoV-2 genome. FINDINGS: Between Nov 2, 2020, and March 21, 2023, we identified 576 persistent infections with at least two sequences, including 11 alpha, 106 delta, 102 BA.1, 204 BA.2, 16 BA.4, 133 BA.5, and 4 XBB. Persistent infections were more common in males than females (p<0·0001) and individuals older than 60 years (p=0·0027). The median within-host genome-wide evolutionary rate was 7·9 × 10-4 substitutions per site per year (IQR 7·0-9·0 × 10-4), with high inter-individual variability driven largely by non-synonymous mutations, particularly in the N-terminal and receptor-binding domains of the spike protein. Longer infection duration was associated with higher evolutionary rates, while no associations were found with age, sex, vaccination status, previous infection, or virus lineage. We found no clear evidence of transmission beyond the first month of infection in any of the 84 persistent infections lasting 56 days or longer. In total, we identified 379 recurrent mutations, including many with known or predicted negative fitness effects and low prevalence at the population level, as well as de novo reversions to the Wuhan-Hu-1 reference sequence, which were likely under positive selection within those individuals. INTERPRETATION: This study highlights the heterogeneous nature of within-host SARS-CoV-2 evolution in individuals with persistent infection in the community. Notably, a small subset of persistent infections with high viral loads underwent accelerated viral evolution or recurrently acquired hallmark mutations found in novel variants. In addition, onward transmission from a persistent infection during the later stages of infection is likely to be rare. These insights have important implications for prioritising genomic surveillance and managing patients with persistent infections. FUNDING: Department of Health and Social Care.

Humans↗

PubMed1979

Chronically persistent infection with human cytomegalovirus in human lymphoblasts.

Cells from a line of human lymphocytes originating from a leukemic patient were persistently infected with human cytomegalovirus. Assays of infectious centers and fluorescent antigen staining indicated that 1%--10% of the cells were infected. It appears that persistent infection is due to an equilibrium between the release of virus by infected host cells and the growth of uninfected cells rather than to defective virus or temperature-sensitive mutants.

Antigens, Viral↗

PubMed1979

Effects of ribavirin on BHK-21 cells acutely or persistently infected with mumps virus.

The effects of ribavirin on BHK-21 cells acutely infected with mumps virus were compared to the effects of the drug on the same cell line persistently infected with mumps virus. Visible cytotoxicity was minimal for both cell types; however, there was an inhibition of cell replication with increasing drug concentrations. Ribavirin had marked antiviral activity against both the acute and persistent infections as determined by an inhibition of hemadsorption plaque formation, decreased immunofluorescence, and a reduction in the release of infectious virus. Even after the drug had been on the persistently infected cells for 72 h, there was still antigen production detectable by immunofluorescence, although the cells no longer hemadsorbed chicken erythrocytes. Ribavirin removal from both types of infection resulted in the renewed synthesis of virus.

Animals↗

PubMed1979

Characterization of measles virus-specific proteins synthesized in vivo and in vitro from acutely and persistently infected cells.

Measles virus protein synthesis has been analyzed in acutely and persistently infected cells. To assess the role of measles in subacute sclerosing panencephalitis (SSPE), measles viral proteins synthesized in vivo or in vitro were tested for reactivity with serum from a guinea pig(s) immunized with measles virus and sera from patients with SSPE. Guinea pig antimeasles virus serum immunoprecipitates the viral polypeptides of 78,000 molecular weight (glycosylated [G]), 70,000 molecular weight (phosphorylated [P]), 60,000 molecular weight (nucleocapsid [N]), and 35,000 molecular weight (matrix [M]) from cells acutely infected with measles virus as well as from chronically infected cells, but in the latter case, immunoprecipitated M protein has a reduced electrophoretic migration. Sera of SSPE patients immunoprecipitated all but the G protein in acutely infected cells and only the P and N proteins from chronically infected cells. In immunoprecipitates of viral polypeptides synthesized in a reticulocyte cell-free translation system, in response to mRNA from acutely or persistently infected cells, the 78,000-molecular-weight form of the G protein was not detected among the cell-free products of either mRNA. Guinea pig antimeasles virus serum immunoprecipitated P, N, and M polypeptides from the products of either form of mRNA, whereas SSPE serum immunoprecipitated the P and N polypeptides but not the M polypeptide. The differences in immunoreactivity of the antimeasles virus antiserum and the SSPE serum are discussed in terms of possible modifications of measles virus proteins in SSPE.

Cell Line↗

PubMed1978

Recovery of a Sendai virus variant with temperature-sensitive hemolytic activity from persistently infected cells from mouse brain.

A persistently infected cell line designated MB/Senas was established by cultivation of mouse brain cells from four-day-old C3H mice infected intracerebrally at birth with 10(6) PFU of Sendai virus, strain 52. After 5 passages, 0.16 per cent of Sendai52 antiserum (containing two 50 per cent plaque reducing doses/ml of serum) was introduced into the culture medium. The addition of antiserum was accompanied by a rise in cell-associated viral antigen from a level of 5 per cent antigen positive cells to 100 per cent demonstrable by both intracellular and membrane immunofluorescence. A variant of Sendai52 virus, designated Sendaias, was recovered from MB/Senas by inoculation of supernatant medium into chick embryos. Infection of chick embryos at 37 degrees C was abortive. Fifty per cent or less of chick embryos infected at dilutions 10(-1) to 10(-9) yielded detectable virus. Hemagglutination (HA) was weak but could be improved by trypsinization of allantoic fluids. Neuraminidase (NA) activity was barely detectable. Hemolysis (HE) was absent. Propagation of Sendaias virus at 33 degrees C showed no change from weak HA and NA activities but HE activity was now apparent which was temperature sensitive. Mortality of infected chick embryos increased to 100 per cent. HE activity and lethality for chick embryos was thermolabile at 45 degrees C.

Cell Line↗

PubMedDate not supplied

Infectious lymphocytes in mice persistently infected with lymphocytic choriomeningitis virus.

During persistent infection of mice with the lymphocytic choriomeningitis (LCM) virus approximately 3% of leukocytes were found to contain viral antigen and to produce infectious virus. Morphologically, infected cells were shown not to be lymphoblasts and their numbers were not reduced by removal of mononuclear phagocytes. We conclude that in LCM virus carrier mice true lymphocytes participate in the infectious process.

Animals↗

PubMed1979

Clonal analysis of mammalian cell cultures persistently infected with Japanese encephalitis virus.

More than 200 cells were cloned from populations of mammalian cells persistently infected with Japanese encephalitis virus. Only four cloned cultures contained cells that had viral antigen measurable by immunofluorescence and that released infectious virus, yet all clones harbored virus-specific RNA. Superinfection of cloned cells with wild-type Japanese encephalitis virus did not produce cytopathic effects, but resulted in production of viral antigen and infectious virus in formerly nonproducing clones. Cocultivation of nonproducer clone cells with normally permissive cells did not induce virus production, nor did treatment of nonproducer clones with various inhibitors of DNA, RNA, or protein synthesis. It is suggested that the cloning procedure may have selected for a particular subpopulation of cells and that defective virus is also involved in establishment and maintenance of persistent infection.

Animals↗

PubMed1979

Border disease: persistant infection with the virus.

Two genetically related sheep that produced border disease-affected lambs from successive pregnancies were identified. These sheep, and some of their progeny, were found to be persistently infected with a virus antigenically related to bovine virus diarrhoea/mucosal disease virus. Only one of the sheep developed detectable serum antibody to the virus, and this animal only produced it 12 months after being detected as infected. The epidemiological significance of sheep persistently infected with border disease virus is discussed.

Animals↗

PubMed2025

Shedding dynamics of a DNA virus population during acute and long-term persistent infection.

Although much is known of the molecular mechanisms of virus infection within cells, substantially less is understood about within-host infection. Such knowledge is key to understanding how viruses take up residence and transmit infectious virus, in some cases throughout the life of the host. Here, using murine polyomavirus (muPyV) as a tractable model, we monitor parallel infections of thousands of differentially barcoded viruses within a single host. In individual mice, we show that numerous viruses (>2600) establish infection and are maintained for long periods post-infection. Strikingly, a low level of many different barcodes is shed in urine at all times post-infection, with a minimum of at least 80 different barcodes present in every sample throughout months of infection. During the early acute phase, bulk shed virus genomes derive from numerous different barcodes. This is followed by long term persistent infection detectable in diverse organs. Consistent with limited productive exchange of virus genomes between organs, each displays a unique pattern of relative barcode abundance. During the persistent phase, constant low-level shedding of typically hundreds of barcodes is maintained but is overlapped with rare, punctuated shedding of high amounts of one or a few individual barcodes. In contrast to the early acute phase, these few infrequent highly shed barcodes comprise the majority of bulk shed genomes observed during late times of persistent infection, contributing to a stark decrease in bulk barcode diversity that is shed over time. These temporally shifting patterns, which are conserved across hosts, suggest that polyomaviruses balance continuous transmission potential with reservoir-driven high-level reactivation. This offers a mechanistic basis for polyomavirus ubiquity and long-term persistence, which are typical of many DNA viruses.

Animals↗

PubMed1979

Cyclic expression of antigen and infectious virus in a BHK cell line (0-853) persistently infected with an SSPE strain of measles virus.

Establishment and characteristics of a baby hamster kidney cell line (BHK 0-853) persistently infected with a subacute sclerosing panencephalitis (SSPE) strain of measles virus (Lec strain) is described. The persistent infection was easily and repeatedly established and no special conditions were required. There was a predictable fluctuation in expression of virus intracellular and membrane antigens which varied from greater than 90% to less than 1% of the cells demonstrating these antigens during the first 6 or 7 passages. Thereafter, fluctuation of antigen and infectious virus expression continued in an unpredictable fashion.

Animals↗

PubMed1978

An insect cell line persistently infected with a baculovirus-like particle.

A persistent infection by a baculovirus-like particle was found in the established lepidopteran (Heliothis zea) cell line, IMC-HZ-1. The virus caused CPE in less than 1% of the IMC-HZ-1 cells, as measured by phase-contrast and electron microscopy. Transmission tests showed that four lepidopteran cell lines were susceptible to the persistent virus (designated as IMC-HZ-I-NOV). In inoculated TN-368 cell cultures, 90--100% infection was achieved. The ultrastructure and development of IMC-HZ-I-NOV in cell cultures were similar to known baculoviruses, and it is probable that this persistent virus is a member of the family Baculoviridae. Two lepidopterous species (Estigmene acrea and H. zea) inoculated with IMC-HZ-1-NOV by intrahemocoelic injection and/or per os feeding of larvae were not susceptible.

Cell Line↗

PubMed1975

Immune enhancement of the tumorigenicity of hamster brain tumor cells persistently infected with measles virus.

Studies were conducted on the tumorigenicity of a hamster brain tumor (HBT) cell line persistently infected with measles virus (MV). This cell population, termed HBT-M, exhibited decreased tumorigenicity in weanling hamsters when implanted intracutaneously. The lowered tumorigenicity of the HBT-M cells could be counteracted by concurrent hydrocortisone treatment restoring the tumor-producing capacity to levels comparable to those of the highly tumorigenic HBT cells. It was also determined that prior immunization of hamsters with MV resulted in enhancement of tumor formation from usually subtumorigenic doses of HBT-M cells. This increase in tumorigenicity appeared to correlate with high titers of MV antibody. Treatment of hamsters with cyclophosphamide resulted in a reduction of MV antibody titers and effected a decrease of HBT-M cell tumorigenicity to control levels. Preliminary studies with passive immunizations indicated that the enhancing factor could be transferred in the sera from hamsters hyperimmunized with MV. These data suggested that MV antibody may potentiate the development of neoplasia of cells persistently infected with MV in a manner similar to the enhancement of tumor growth by blocking antibody.

Animals↗

PubMed1976

Relationship between establishment of persistent infection of haemagglutinating virus of Japan and the properties of the virus.

The infectious virus (HVJ-pi) obtained from BHK cells persistently infected with haemagglutinating virus of Japan was found to be temperature-sensitive as well as causing little or no cytopathic effect (c.p.e.) and leading to establishment of carrier cultures in several cell lines at both permissive (32 degrees C) and non-permissive (38 degrees C) temperature. In order to obtain information about the role of HVJ-pi in the establishment of persistent infection, comparative studies were made of some phenotypic properties of HVJ-pi and HVJ-38 which was obtained by passing wild-type HVJ in eggs at 38 degrees C and was proved to be highly cytopathic. HVJ-pi differed from HVJ-38 in (1) temperature sensitivity in its ability to produce virus progeny, (2) infectivity for embryonated eggs, (3) neuraminidase activity, (4) the thermal stability of HA and neuraminidase activity, and (5) the polypeptide composition of BHK-grown viruses. B cells infected with HVJ-pi release haemagglutinin more efficiently, and less HA was accumulated on the cell membrane. In considering these results, it was concluded that the difference of envelope proteins might be involved in the striking difference in c.p.e. between HJV-pi and HVJ-38.

Cell Line↗

PubMed1976

Mononuclear cell fraction carrying Herpesvirus saimiri in persistently infected squirrel monkeys.

Circulating lymphocytes from squirrel monkeys persistently infected with Herpesvirus saimiri (HVS) were separated into B- and T-lymphocyte fractions by a rosette-enrichment technique. HVS was isolated only from lymphocyte fractions forming rosettes or from unseparated lymphocytes; this indicated that T-lymphocytes were the target cells for HVS in the natural host, squirrel monkeys.

Animals↗