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At least 433 records · Page 24Linked to original sources
PubMed1983

Virus replication in infected epithelial cells is coupled to cell shape-responsive metabolic controls.

The cell shape of monkey epithelial cells was varied from flat to spheroidal by gradually reducing the substrate adhesiveness with poly (HEMA) films of increasing thickness. The decrease in cell spreading is accompanied by a dramatic response in cellular macromolecular metabolism in the nucleus. Within 14 to 16 hr, DNA and RNA syntheses are inhibited by more than 95%, while the level of protein synthesis is reduced by only twofold after 24 hr in spheroidal-suspension culture. When epithelial cells, spread to various degrees, are infected with SV40 or herpes virus a parallel inhibition of virus replication and cellular macromolecular metabolism occurs. However, VSV can proliferate in the metabolically active cytoplasm of epithelial cells in which nuclear activity is inhibited owing to alterations in cell shape. The results suggest that the metabolic restrictions imposed on epithelial cells, owing to changes in cell spreading, are a dominant phenomenon that cannot be overcome by virus infection. Rather, virus replication, which is dependent on the cellular metabolic machinery, is inhibited in parallel with the inhibition of cellular macromolecular metabolism.

Animals↗
PubMedDate not supplied

Delta infection in asymptomatic carriers of hepatitis B surface antigen: low prevalence of delta activity and effective suppression of hepatitis B virus replication.

We examined the prevalence of serum anti-delta antibody among 769 intravenous drug abusers in Taiwan. delta infection was found extremely common in the HBsAg-positive carriers with drug abuse, because 128 (85%) of 151 carriers were positive for anti-delta. However, most of antibody titers were low (less than 1:5,000). By molecular hybridization, delta RNA genomes were detectable in only five (4%) of 128 asymptomatic carriers positive for anti-delta. The results suggested that most of them had previous, instead of ongoing, delta infection. We also studied the serum markers reflecting hepatitis B virus replication in these carriers and a control group. Hepatitis B e antigen was positive in only 12 (10%) of 115 anti-delta positive carriers in contrast to 22 (23%) of 95 age- and sex-matched HBsAg-positive, anti-delta negative volunteers donating blood (p less than 0.025). Furthermore, in contrast to the close association between HBeAg and hepatitis B virus DNA generally present in HBsAg carriers (concordance in this series: 79%), among the 12 HBeAg-positive subjects of the delta infected group, only two, or 17%, had serum hepatitis B virus DNA (p less than 0.003). Such suppressing effects did not require a simultaneous presence of the delta agent, as shown by the lack of delta RNA genomes in the serum by sensitive assay. We conclude that although delta superinfection is common in the asymptomatic HBsAg carriers with intravenous drug abuse in the nonendemic area of Taiwan, continuous delta activities are uncommon in them. In addition, the previous delta infection probably exerts effective suppression on the hepatitis B virus replication in these HBsAg carriers.

Adult↗
PubMed2006

In vitro inhibition of human influenza A virus replication by chloroquine.

Chloroquine is a 9-aminoquinolone with well-known anti-malarial effects. It has biochemical properties that could be applied to inhibit viral replication. We report here that chloroquine is able to inhibit influenza A virus replication, in vitro, and the IC50s of chloroquine against influenza A viruses H1N1 and H3N2 are lower than the plasma concentrations reached during treatment of acute malaria. The potential of chloroquine to be added to the limited range of anti-influenza drugs should be explored further, particularly since antiviral drugs play a vital role in influenza pandemic preparedness.

Chloroquine↗
PubMed1964

INFECTIOUS BOVINE RHINOTRACHEITIS VIRUS REPLICATION, CYTOPATHOLOGY, AND PLAQUE FORMATION IN THE PRESENCE AND ABSENCE OF NUCLEIC ACID ANALOGUES.

Stevens, Jack G. (University of Washington, Seattle), and Neal B. Groman. Infectious bovine rhinotracheitis virus replication, cytopathology, and plaque formation in the presence and absence of nucleic acid analogues. J. Bacteriol. 87:446-453. 1964.-Cytopathology induced by infectious bovine rhinotracheitis (IBR) virus was correlated with the one-step growth cycle. Nuclear alterations, including the development of inclusion bodies, preceded the appearance of virus. It was found that similar effects occurred in the presence of 5-bromodeoxyuridine (BUDR) and 5-fluorodeoxyuridine (FUDR), compounds which depress the yield of "standard" virus from a range of 116 to 500 to less than 0.5 plaque-forming units per cell. As with known members of the herpesvirus group, IBR virus plaques developed and enlarged indefinitely in the presence of specific antibody. An analysis of the mechanism operative in this process was undertaken. The evidence suggested that neither viral nor subviral particles capable of replicating "standard" virus passed between cells during the first 8 hr of infection. This is the time preceding the release of extracellular virus from initially infected cells. With BUDR and FUDR, it was shown that plaques also developed in this system in the virtual absence of production of "standard" infectious virus. However, a class of analogue-dependent virus was found which may have been at least partly responsible for plaque formation in the analogue-treated system. The relative contributions of subviral particles or of a self-sustaining molecular disorganization to the process have not been completely assessed as yet.

Animals↗
PubMed1991

Stimulation of measles virus replication by cyclic guanosine monophosphate.

Measles virus (MV) replication in acutely infected human cells was markedly stimulated following exposure to guanosine 3',5'-monophosphate (cyclic GMP). Addition of cyclic GMP to tissue culture fluids immediately following infection with the virus resulted in acceleration of virus-mediated cell fusion, increased synthesis of virus-specified proteins and a 50-fold increase in infectious particle production. No evidence of altered viral protein phosphorylation was found. The results suggest that cyclic GMP stimulates multiple stages of the MV replication cycle.

Cell Line↗
PubMed1973

Effects of adrenal glucocorticoids on polyoma virus replication.

Treatment of polyoma virus-infected fibroblasts from mouse embryos and virus-infected 3T3 cells with physiological concentrations of the glucocorticoids enhances plaque formation at least 10-fold. The data suggest that this effect results from an increased rate of virus production. Steroid specificity studies indicate that the cytoplasmic receptors that mediate the physiological actions of these hormones are also involved in the present effect.

Animals↗
PubMed2004

2'-fluoro-2'-deoxycytidine inhibits Borna disease virus replication and spread.

Borna disease virus (BDV) causes neurological diseases in a variety of warm-blooded animal species, possibly including humans. To date, there is no effective treatment against BDV infection. Recently, we reported on the antiviral activity of 1-beta-D-arabinofuranosylcytosine (Ara-C). However, Ara-C's cytotoxic side effects are a major obstacle for its therapeutic use. Herein, we demonstrate that the nucleoside analog 2'-fluoro-2'-deoxycytidine (2'-FdC) exhibits potent antiviral activity against BDV. Importantly, 2'-FdC-associated cytotoxicity is negligible, indicating 2'-FdC as an excellent candidate for the development of antiviral therapy against BDV.

Animals↗
PubMed1987

Thioglycollate elicited macrophages demonstrate enhanced virus replication and depressed bacterial killing.

Thioglycollate elicited peritoneal macrophages of Balb/c mice exhibited minimal antibacterial activity against Listeria monocytogenes but were fully permissive for the replication of ectromelia virus. By comparison, resident and LPS elicited macrophages did not exhibited depressed antibacterial activity nor did they support viral replication. The thioglycollate effects were demonstrated in macrophages cultured in vitro and also in intact Balb/c mice. Mice given thioglycollate intraperitoneally and challenged by the same route suffered overwhelming virus and bacterial infections as a result of early local proliferation within peritoneal macrophages with subsequent spread to the liver. Balb/c mice challenged intravenously with similar doses of the virus of bacterial pathogen after administration of thioglycollate by the i.p. route did not succumb to either infection. Thus the ability of thioglycollate to compromise cellular host defenses against the infectious agents appears to be site specific; i.e. restricted to the peritoneal cavity where exudate macrophages and challenge inocula first come into contact.

Animals↗
PubMed2002

Viral RNA mutations are region specific and increased by ribavirin in a full-length hepatitis C virus replication system.

High rates of genetic variation ensure the survival of RNA viruses. Although this variation is thought to result from error-prone replication, RNA viruses must also maintain highly conserved genomic segments. A balance between conserved and variable viral elements is especially important in order for viruses to avoid "error catastrophe." Ribavirin has been shown to induce error catastrophe in other RNA viruses. We therefore used a novel hepatitis C virus (HCV) replication system to determine relative mutation frequencies in variable and conserved regions of the HCV genome, and we further evaluated these frequencies in response to ribavirin. We sequenced the 5' untranslated region (5' UTR) and the core, E2 HVR-1, NS5A, and NS5B regions of replicating HCV RNA isolated from cells transfected with a T7 polymerase-driven full-length HCV cDNA plasmid containing a cis-acting hepatitis delta virus ribozyme to control 3' cleavage. We found quasispecies in the E2 HVR-1 and NS5B regions of untreated replicating viral RNAs but not in conserved 5' UTR, core, or NS5A regions, demonstrating that important cis elements regulate mutation rates within specific viral segments. Neither T7-driven replication nor sequencing artifacts produced these nucleotide substitutions in control experiments. Ribavirin broadly increased error generation, especially in otherwise invariant regions, indicating that it acts as an HCV RNA mutagen in vivo. Similar results were obtained in hepatocyte-derived cell lines. These results demonstrate the potential utility of our system for the study of intrinsic factors regulating genetic variation in HCV. Our results further suggest that ribavirin acts clinically by promoting nonviable HCV RNA mutation rates. Finally, the latter result suggests that our replication model may be useful for identifying agents capable of driving replicating virus into error catastrophe.

Amino Acid Sequence↗
PubMed1999

Delay effect in a model for virus replication.

As biology becomes more quantitative, it appears that the increasing use of mathematics in this area is inevitable. In 1996, Nowak & Bangham (1996, Science 272, 74-79) proposed three mathematical models to explore the relation between antiviral immune responses, virus load, and virus diversity. In this paper we investigate the delay effect in a model which considers the interaction between a replicating virus and host cells. We assume that there is a finite time lag between infection of a cell and the emission of viral particles. Even with the introduction of this delay, the steady states of the model--as suggested by Nowak & Bangham--remain stable. The result also gives a condition for how the parameter values should be chosen when analysing clinical data so that the model remains tenable.

Humans↗
PubMed1993

Inhibition of type 1 human immunodeficiency virus replication by a tat antagonist to which the virus remains sensitive after prolonged exposure in vitro.

The transactivator of transcription, Tat, of human immunodeficiency virus type 1 (HIV-1) is required for viral replication. Inhibition of Tat function could have the potential to keep integrated provirus in dormancy. In the presence of Tat, Ro 24-7429, an analog of Ro 5-3335, inhibited expression of indicator genes controlled by the HIV-1 long terminal repeat promoter in transient transfection assays and in a constitutive cell line at noncytotoxic concentrations. Reduction of steady-state mRNA of the indicator gene by the compound correlated with reduction of the gene product in the constitutive cell line. Ro 24-7429 has broad activity against several strains of HIV-1 in different cell lines, peripheral blood lymphocytes, and macrophages (IC90 = 1-3 microM). Importantly, Ro 24-7429 inhibited viral replication in both acute and chronic infection in vitro, a characteristic expected of a Tat antagonist and not shared by viral reverse transcriptase inhibitors. Consistent with this, the compound reduced cell-associated viral RNA and proteins and partially restored cell-surface CD4 in chronically infected cells. After 2 years of continued weekly passage of the virus in fresh CEM cells grown in the presence of the compound at 1 or 10 microM, the virus did not develop resistance to the drug. These results indicate that the compound's action might involve a cellular factor.

Alkaline Phosphatase↗
PubMed2005

Antiviral mode of action of a synthetic brassinosteroid against Junin virus replication.

The antiviral mode of action of the synthetic brassinosteroid (22S,23S)-3beta-bromo-5alpha,22,23-trihydroxystigmastan-6-one (6b) against Junin virus replication in Vero cells was investigated. Time-related experiments showed that 6b mainly affects an early event of virus growth cycle. Neither adsorption nor internalization of viral particles was the target of the inhibitory action. The analysis of the effect of 6b on viral RNA synthesis demonstrated that the presence of the compound adversely affects virus RNA replication by preventing the synthesis of full length antigenomic RNA. Although 6b was most effective the earlier it was added to the cells after infection with JV, a high level of inhibition of JV yield and fusion activity of newly synthesized viral glycoproteins was still detected when the compound was present during the last hours of infection. Therefore, we cannot rule out an inhibitory action of 6b on later events of JV replicative cycle.

Animals↗
PubMed1987

Expression of pre-S gene-encoded proteins in liver and serum during chronic hepatitis B virus infection in comparison to other markers of active virus replication.

Pre-S gene-encoded proteins of the hepatitis B virus (HBV) were studied in the liver by immunofluorescence and in serum by radioimmunoassay in 30 patients with chronic HBV infection. The results were compared with molecular hybridization analysis of HBV-DNA in liver and serum, with serum hepatitis B e antigen/antibody (HBeAg/anti-HBe) status and with underlying liver histology. Pre-S peptides were detected in the serum of 11 patients, 10 of whom were positive for serum HBV-DNA and/or liver hepatitis B core antigen. Only 4 of these patients were HBeAg positive. The prevalence of serum pre-S among HBV replicating carriers was 59% (10/17) compared to only 8% (1/13) among those with non-replicating virus (P less than 0.01). All patients with circulating pre-S peptides had active liver disease. Anti-pre-S was detected in the serum of only 4 patients, 3 with integrated HBV-DNA. In contrast to serum findings, pre-S peptides were detected in the liver of all patients with histochemically demonstrable hepatitis B surface antigen (HBsAg), regardless of HBV replicative status. HBsAg carriers with integrated HBV-DNA had abundant cytoplasmic pre-S1 and pre-S2 localized in numerous ground-glass hepatocytes. It is concluded that pre-S peptides are usually displayed in the liver simultaneously with histochemically detectable HBsAg; they are secreted in the serum in association with high HBV replication and release of HBV particles, but in the absence of episomal HBV replication, pre-S peptides seem to be largely retained within hepatocytic membranes.

Adult↗
PubMed1999

A functional measles virus replication and transcription machinery encoded by the vaccinia virus genome.

Measles virus encodes three proteins required for the encapsidation, transcription and replication of viral genomes. The genes for these proteins have been inserted into the vaccinia virus genome together with the gene for the bacteriophage T7 RNA polymerase. Cells infected with this recombinant virus were able to encapsidate, transcribe and replicate a CAT gene positioned in the negative polarity behind a T7 promoter and flanked by measles virus genomic termini. Inhibition of the accumulation of the nucleocapsid proteins by actinomycin D led to an increase in CAT expression. Thus the measles virus polymerase activity, encoded by the vaccinia genome, was regulated by the level of measles proteins just as the authentic polymerase. The recombinant vaccinia described in this study could be useful for the production of measles virus-like particles encoding foreign genes and employed in vaccination or gene therapy strategies.

Bacteriophage T7↗
PubMed1990

Friend virus replication in normal and immunosuppressed C57BL/6 mice.

Young adult C57BL/6 mice are resistant to the replication of Friend virus. We show here that this resistance is not absolute. In 7-week old C57BL/6 mice injected with NB-tropic Friend virus iv, high titers of SFFV could be recovered from the spleen at 8 days after infection but by 21 days, no virus was detectable. A single dose of anti-Thy 1.2 monoclonal antibody iv before FV infection permitted continued replication of SFFV in these animals. This finding strongly supports the hypothesis that SFFV replication in C57BL/6 mice is restricted by a T cell-mediated immune response.

Aging↗
PubMed2003

Dynamics of hepatitis C virus replication in human liver.

Hepatitis C virus (HCV) replication at the cellular level is not fully understood. This study describes an optimized system for quantifying replication of HCV in hepatocytes and in liver tissues. A digital image analysis method was developed to quantify signal intensities of HCV genomic and replicative-intermediate RNAs in infected human liver tissues and to examine their spatial distribution. The average number of viral genomes per productively infected hepatocyte ranged from 7 to 64 RNA molecules. The maximal concentrations of genomic and replicative-intermediate RNAs at the single cell level were 74 and 34 molecules per hepatocyte, respectively. A gradient dispersion of genomes was observed around virus-producing cells, suggesting infection of neighboring hepatocytes as one mechanism of viral spread in the liver. There was no significant difference in total hepatic load of HCV genomes between the post- and nontransplant patients, whereas serum titers in the former group were much higher that that in the latter group. HCV replication varied among infected hepatocytes, occurred in a subset of cells, and proceeded at a low level, confirming one mechanism by which individual hepatocytes are cumulatively able to generate steady state concentrations of millions of HCV genomes per milliliter of blood. Lower viral clearance rates in circulating blood may explain the phenomenon of increased serum titers of viral RNA in posttransplant immunosuppressed patients.

Genome, Viral↗
PubMed1998

The presence of active hepatitis C virus replication in lymphoid tissue in patients coinfected with human immunodeficiency virus type 1.

The existence of extrahepatic replication sites of hepatitis C virus (HCV) remains controversial. Highly strand-specific Tth-based reverse transcriptase-polymerase chain reaction was used to search for the presence of viral RNA negative strand in lymph nodes from 16 patients with AIDS and in peripheral blood mononuclear cells (PBMC) from 14 other human immunodeficiency virus (HIV)-positive patients. Negative-strand HCV RNA was detected in lymph node samples from 10 patients (63%) and in PBMC from 5 (36%). This suggests that, at least under circumstances of impaired immunity associated with HIV infection, HCV is lymphotropic in vivo. However, the clinical implications of these findings need to be further investigated.

Acquired Immunodeficiency Syndrome↗