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At least 1,225 records · Page 68Linked to original sources
PubMed1992

Inhibition of intrahepatic hepatitis B virus replication by antiviral drugs in a novel transgenic mouse model.

Transgenic mice which carry the integrated human hepatitis B virus (HBV) genome and produce HBV particles in the liver were treated with antiviral compounds, and the amount of viral DNA in the liver and serum was monitored by Southern analyses. Mouse alpha interferon (200,000 U per injection, twice daily for 3 days) and a novel nucleoside, oxetanocin G (15 mg/kg of body weight per injection, twice daily for 7 days), inhibited viral DNA synthesis in the liver almost completely. This animal model should prove useful in evaluating anti-HBV agents.

Animals↗
PubMed1974

Vaccinia virus replication in enucleate BSC-1 cells: particle production and synthesis of viral DNA and proteins.

The growth of vaccinia virus in monolayers of BSC-1 cells enucleated by centrifugation in the presence of cytochalasin B has been studied. No evidence for the production of infectious virus in these cells was obtained, and the production of virus particles was reduced to 8.3% compared with the yield from cytochalasin-treated, uncentrifuged cells. Virus DNA and early and late polypeptides were synthesized with normal timing in enucleate cells, but in reduced amounts; cleavage of structural polypeptide precursors P4a and Px also occurred in enucleate cells. Factories containing immature virus particles were demonstrated in enucleate cells by electron microscopy; these factories were reduced in number and size compared with those found in cytochalasin-treated, uncentrifuged cells.

Amino Acids↗
PubMed2000

Hepatitis A virus replication: an intermediate in the uncoating process.

Dense, RNase-sensitive, VP2-containing, non-infectious hepatitis A virus (HAV) particles were found to be formed at early times after the infection of cultured cells. These particles formed with kinetics mirroring those reported for HAV uncoating. The kinetics of the formation of dense HAV particles corresponded to a decrease in detectable, mature input virions, as detected by RNA dot blot hybridization of CsCl density gradient fractions. The dense HAV particles did not appear to have altered sedimentation coefficients, and as the fate of small capsid protein VP4 is not yet known, these particles cannot yet be termed 'A particles' or 'infectosomes', as have the uncoating intermediates in some picornavirus-cell systems.

Animals↗
PubMed1992

Measles virus replication in lungs of hispid cotton rats after intranasal inoculation.

Hispid cotton rats were inoculated intranasally with either measles virus (MV) Edmonston, a multipassaged, tissue culture-adapted strain of MV, or with one of three clinical MV isolates that had limited passages (three to five times) in tissue culture cells. MV Edmonston was recovered from the lungs of every (n = 37) hispid cotton rat inoculated with this virus for at least 7 days after virus inoculation. Peak pulmonary titers occurred on Day +4 (3.3-4.4 log10/g lung). Scattered areas of inflammation were observed interstitially in lung sections from infected animals stained with hematoxylin and eosin, and a similar pattern of diffuse fluorescence was seen in cryostat sections stained with an indirect fluorescent antibody procedure specific for virus antigens. Fluorescent antibody and virus isolation studies on lung lavage cells both suggested that lung leukocytes were a primary target of the virus. In contrast to these findings, virus was isolated only sporadically from hispid cotton rats inoculated with any of the clinical measles virus isolates. Despite the restricted growth of MV in these animals, cotton rats may be useful for studying certain aspects of measles virus pathogenesis and for screening potential antiviral compounds in vivo.

Administration, Intranasal↗
PubMedDate not supplied

The effect of cell density on influenza virus replication in CV-1 cells.

The number of hemadsorbing cells in CV-1 cell monolayers infected with influenza A virus was higher in semi-confluent cultures than in dense contact-inhibited monolayers. The level of virus-specific protein synthesis as well as the accumulation of virus progeny were also inversely correlated with cell density. At a high multiplicity of infection the majority of these cells in dense monolayers did not express HA on the cell surface, did not synthesize virus-specific proteins and survived at least 96 hours after infection. However, these cells developed a partial shut-off of cell protein synthesis and could not be efficiently superinfected. Analysis of the data of virus protein synthesis, progeny virus accumulation, and the assessment of hemadsorption suggest that CV-1 cells in dense monolayers can be infected at a sufficiently high multiplicity of infection, but only a fraction of the infected cells is capable of amplification of virus protein synthesis and progeny virus accumulation. No cell-density effects of comparable extent could be observed in MDCK cells.

Animals↗
PubMedDate not supplied

Ultrastructural study of mouse thymus virus replication.

With the exception of thymocytes, no other cell types have been reported to be involved in mouse thymus virus (MTV) infection. The ultrastructure of thymuses of mice infected with MTV were examined. The earliest sign of infection was detected 5 days p.i.; lymphocytes, epithelial and phagocytic (macrophages) reticular cells were shown to be affected. Viral particles and filamentous structures were present in both the nucleus and the cytoplasm of these cells. At more severe stages of cellular necrosis, 6 and 7 days p.i., cytoplasmic granulation as well as loss in definition of cytoplasmic organelles became apparent. This was followed by nuclear degradation and aggregation of cells. After 9 days p.i. necrotic lesions were still observed but viral particles were no longer detectable. This study provides evidence of the susceptibility of macrophages to MTV.

Animals↗
PubMed1979

Macrophage restriction of Marek's disease virus replication and lymphoma cell proliferation.

Macrophages are shown to restrict the replication of Marek's disease virus (MDV) and isotope uptake by spleen cells from chickens bearing Marek's disease (MD) tumors. The titer of virus from duck embryo fibroblasts (DEF) co-cultivation with MDV-spleen cells pretreated to deplete marcophages was 4- to 18-fold higher than with untreated cells. Treated MDV-spleen cells increased isotope uptake by 2-fold. These restrictive activities are attributable to macrophage regulation of cell proliferation.

Animals↗
PubMed2005

Inhibition of hepatitis B virus replication by recombinant small interfering RNAs.

RNA interference (RNAi) is a biological phenomenon in which introduction of a small, double-stranded interfering RNAs (siRNAs) into a cell causes a specific degradation of homologous single-stranded RNA. siRNA can be delivered into the cell by different approaches including synthetic RNA, in vitro transcribed RNA and RNA transcribed from polymerase III-based recombinant vectors. As hepatitis B (HB) represents a worldwide health problem, we attempted to develop a fast and easy approach to generation and screening of specific siRNA-targeted HB virus (HBV) genes. Using PCR amplification, specific siRNA expression cassettes (SECs) were developed and used to generate effective siRNAs against HB virus (HBV) replication and gene expression in mammalian cells. After screening, we identified two SECs that expressed siRNAs which efficiently decreased the level of HBV pre-c/c gene expression in transfected Bel-7402 cells by 81.9% and 87.3%, respectively. In addition, the level of HBV DNA was decreased by 83.5% and 85.2% in HepG2 2.2.15 cells, respectively. This study provides (i) a new effective application of RNA interference to study viral gene function and viral replication and (ii) a new tool for the prevention and treatment of human HBV infection.

DNA, Viral↗
PubMedDate not supplied

The trans-activator gene of HTLV-III is essential for virus replication.

Studies of the genomic structure of human T-lymphotropic virus type III (HTLV-III) and related viruses, implicated as the causal agent of acquired immune deficiency syndrome (AIDS), have identified a sixth open reading frame in addition to the five previously known within the genome (gag, pol, sor, env and 3'orf). This gene, called tat-III, lies between the sor and env genes and is able to mediate activation, in a trans configuration, of the genes linked to HTLV-III long terminal repeat (LTR) sequences. We now present evidence that the product of tat-III is an absolute requirement for virus expression. We show that derivatives of a biologically competent molecular clone of HTLV-III, in which the tat-III gene is deleted or the normal splicing abrogated, failed to produce or expressed unusually low levels of virus, respectively, when transfected into T-cell cultures. The capacity of these tat-III-defective genomes was transiently restored by co-transfection of a plasmid clone containing a functional tat-III gene or by introducing the TAT-III protein itself. As HTLV-III and related viruses are the presumed causal agents of AIDS and associated conditions, the observation that tat-III is critical for HTLV-III replication has important clinical implications, and suggests that specific inhibition of the activity of tat-III could be a novel and effective therapeutic approach to the treatment of AIDS.

Deltaretrovirus↗
PubMed2006

Relationships between hepatitis C virus replication and CXCL-8 production in vitro.

The chemokine CXCL-8 (interleukin-8) is induced by many viruses, including hepatitis C virus (HCV). In the current study, we examined CXCL-8 levels in the context of acute and chronic HCV replication in vitro. Two different small interfering RNAs were used to silence CXCL-8 mRNA and protein expression in Huh7 and BB7 replicon cells. HCV RNA synthesis in BB7 cells was inhibited by CXCL-8 knockdown. Furthermore, antibody neutralization of endogenous CXCL-8 activity inhibited HCV replication, while addition of recombinant human CXCL-8 stimulated NS5A protein expression. Moreover, CXCL-8 protein levels correlated positively with HCV RNA levels in four independent subgenomic and genomic replicon lines (R = 0.41, P = 0.0013). However, CXCL-8 mRNA levels correlated inversely with CXCL-8 protein and HCV RNA levels in all replicon lines and in Huh7 cells. Transient replication assays with strongly permissive and weakly permissive Huh7 cells and three independent subgenomic replicons with various replicative capacities revealed that CXCL-8 protein levels were higher in weakly than in strongly permissive cells. The JFH-1 subgenomic replicon, which replicated to high levels in both strongly and weakly permissive Huh7 cells, induced CXCL-8 protein to high levels in both cell types. The data indicate that in the replicon system, CXCL-8 protein levels are positively associated with chronic HCV replication and that CXCL-8 removal inhibits HCV replication. During acute HCV replication, CXCL-8 production may be inhibitory to viruses with low replicative capacity. The data underscore the complex regulation of CXCL-8 mRNA and protein expression and further suggest that in addition to contributing to HCV pathology via proinflammatory actions, CXCL-8 may have opposing antiviral and proviral effects depending on the level of HCV replication, the cellular context, and whether the infection is acute or chronic.

Cell Line, Tumor↗
PubMed1999

In vivo regulation of hepatitis B virus replication by peroxisome proliferators.

The role of the peroxisome proliferator-activated receptor alpha (PPARalpha) in regulating hepatitis B virus (HBV) transcription and replication in vivo was investigated in an HBV transgenic mouse model. Treatment of HBV transgenic mice with the peroxisome proliferators Wy-14,643 and clofibric acid resulted in a less than twofold increase in HBV transcription rates and steady-state levels of HBV RNAs in the livers of these mice. In male mice, this increase in transcription was associated with a 2- to 3-fold increase in replication intermediates, whereas in female mice it was associated with a 7- to 14-fold increase in replication intermediates. The observed increases in transcription and replication were dependent on PPARalpha. HBV transgenic mice lacking this nuclear hormone receptor showed similar levels of HBV transcripts and replication intermediates as untreated HBV transgenic mice expressing PPARalpha but failed to demonstrate alterations in either RNA or DNA synthesis in response to peroxisome proliferators. Therefore, it appears that very modest alterations in transcription can, under certain circumstances, result in relatively large increases in HBV replication in HBV transgenic mice.

Animals↗
PubMed2005

A cell-based system for hepatitis B virus replication: significance of clinically enhanced viral replication in relation to deletions in viral core promoter.

The core promoter of hepatitis B virus (HBV) is crucial in viral replication. Our previous investigation in clinical serum samples indicated that deletions in the viral core promoter (from nucleotide 1758 to 1777 and 1749 to 1768 respectively) may lead to increase in viral replication. We propose to characterize these deletion mutants in a cell-based system that supports HBV replication. Replicative HBV genome developed in our laboratory was used as template to generate deletions in viral core promoter corresponding to those found in clinical samples. These deletion constructs were used to transfect HepG2 cells, which then support the subsequent infection of cells from these deleted but replicative genomes. The effect of deletion on the viral replication was measured by comparing the amount of hepatitis B virus surface antigen (HBsAg) secreted in the culture medium with that from cells transfected with the wild type HBV genome. The amount of secreted HBsAg in cells transfected with deletion mutants was significantly lower than those transfected with the wild type genome. Our results provide a new system for molecular characterization of mechanism of HBV replication. Contrary to the increased replication observed in clinical samples, the reduced viral replication in genomes carrying deletions in the core promoter suggests a complex regulatory mechanism of viral replication which may involve other elements in the viral core promoter.

Gene Deletion↗
PubMed2006

Amantadine inhibits the function of an ion channel encoded by GB virus B, but fails to inhibit virus replication.

A chemically synthesized peptide representing the C-terminal subunit (p13-C) of the p13 protein of GB virus B (GBV-B), the most closely related virus to hepatitis C virus (HCV) showed ion channel activity in artificial lipid bilayers. The channels had a variable conductance and were more permeable to potassium ions than to chloride ions. Amantadine but not hexamethylene amiloride (HMA) inhibited the ion channel function of p13-C in the lipid membranes. However, neither agent was able to inhibit the replication and secretion of GBV-B from virus-infected cultured marmoset hepatocytes, which were harvested from a marmoset that was infected in vivo or inhibit replication after in vitro infection of naive hepatocytes. These data suggest that the GBV-B ion channel, contrary to the data derived from the lipid membranes, is either resistant to amantadine or that virus replication and secretion are independent of ion channel function. As the p7 protein of HCV also has ion channel activity that is apparently resistant to amantadine in vivo, the former possibility is most likely. Ion channels are likely to have an important role in the life cycle of many viruses and compounds that block these channels may prove to be useful antiviral agents.

Amantadine↗
PubMed1982

Influenza virus replication in human alveolar macrophages.

Studies with animal models suggest that alveolar macrophages may be important cells in some respiratory virus infections, but little is known about the role of these cells in virus infections in man. In this study human alveolar macrophages were obtained by fibreoptic bronchoscopy and infected in vitro with a variety of influenza viruses. After infection with the NWS strain of influenza virus the haemagglutinin and nucleoprotein viral antigens were demonstrated in greater than 90% of cells at 24 h by immunofluorescence with specific antisera. There was no cytopathic effect at this time, and no virus release was detected by plaque assay of culture fluids on MDCK cells. Alveolar macrophages were also infected with a human vaccine strain (H1N1) of influenza virus and with two recent isolates (H1N1 and H3N2). In each case viral nucleoprotein antigen was produced in 10-20% of the cells by 24 h postincubation, but there was no release of infectious virus. There was no cytopathic effect and the phagocytosis of IgG-coated latex beads was unimpaired 24 h after in vitro infection.

Cells, Cultured↗
PubMed1987

Protection of C58 mice from lactate dehydrogenase-elevating virus-induced motor neuron disease by non-neutralizing antiviral antibodies without interference with virus replication.

The paralytic poliomyelitis induced in old, immunosuppressed C58 mice by a primary infection with the lactate dehydrogenase-elevating virus (LDV) is prevented by the presence of anti-LDV antibodies in the virus inoculum or by passive transfer of LDV-free plasma from chronically LDV-infected mice one day before infection. Non-neutralizing antibodies were protective and specifically directed to the lowest molecular weight form of the envelope glycoprotein of LDV (VP-3), which seems to exist in virions in at least ten molecular forms ranging from 24 to 44 kDa. The antibodies did not prevent the productive infection of the subpopulation of macrophages that represents the primary permissive cell type in the mouse as evidenced by normal plasma LDV levels nor the spread of LDV to the central nervous system. Many non-neuronal cells containing LDV RNA were detected by in situ hybridization in the spinal cords of mice that had been infected with LDV in the presence of protective antibodies. However, no LDV RNA-positive neurons were detected, which are normally found coincidental with the development of paralytic symptoms in LDV-infected C58 mice. We propose that an early event after infection is critical for the infection of neurons and is inhibited by the presence of non-neutralizing antibodies to the LDV glycoprotein.

Animals↗
PubMed1990

Analysis of bovine parainfluenza-3 virus replication in bovine embryonic lung cells by indirect fluorescent antibody and hemadsorption assays.

The temporal manifestation of bovine parainfluenza-3 virus (BPI3V) proteins in the cytoplasm and on the surface of bovine embryonic lung (BEL) cells was characterized by indirect fluorescent antibody (IFA) and hemadsorption (HAd) assays. Intracellular proteins appeared earliest at 0.5 h post inoculation (p.i.) and the infection spread to virtually all cells by 48 h p.i. Viral proteins on the surface of cells were seen first at 16 h p.i., and by 48 h p.i. the entire cell monolayer was IFA positive. Hundred-fold less virus in the inoculum delayed appearance of the intracellular as well as cell-surface viral proteins by 24 h and allowed the infection of only about 1/3 of the cells by 48 h p.i. Kinetics of the development in the proportion of HAd-positive cells correlated with those of the surface fluorescence-positive cells. Morphology of the manifestation of BPI3V proteins is characterized by microphotography.

Animals↗