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At least 325 records · Page 18Linked to original sources
PubMed2000

Inhibition of influenza virus replication by cocaine.

Cocaine has been shown to have a number of diverse effects on the immune system. The current investigators have previously demonstrated an inhibitory effect of cocaine on murine hepatitis virus replication in peritoneal macrophages in vitro. The present study was undertaken to examine the effects of cocaine on influenza virus replication and to further characterize that effect in an animal model. Cocaine was capable of inducing a dose-dependent reduction in influenza PR-8 replication using MDCK cells in vitro. Concentrations of 100 microg/ml caused a 50% reduction of virus. To further characterize the effect in vivo, C57Bl/6 mice infected with influenza PR-8 by intranasal instillation were given daily ip injections of 10 mg/kg cocaine just prior to and for 4 days after exposure to influenza. Lungs from mice exposed to cocaine had viral titers that were reduced approximately 50% compared to controls as demonstrated by hemagglutination titers. Additional studies suggest that this reduction appears to be caused by an increase of cocaine-induced interferon.

Animals↗
PubMed1988

Loss of CD4 membrane expression and CD4 mRNA during acute human immunodeficiency virus replication.

Using mAbs and genomic probe to the CD4 molecule, the HIV receptor, we demonstrated that HIV replication induces the disappearance of its functional receptor from the cell surface by two distinct mechanisms. First, after being expressed onto the cell surface, HIV envelope gp110 will complex CD4, efficiently masking the CD4 epitope used by the virus to bind its receptor. This phenomenon occurs on the surface of each infected cell and is not due to the release of soluble gp110; infection with recombinant HIV/vaccinia viruses expressing a mutated HIV env gene designed to prevent gp110 release from the cell surface induces a similar gp/CD4 complexes formation. Second, virus replication induces a dramatic and rapid loss of CD4 mRNA transcripts, preventing new CD4 molecules from being synthesized. These two mechanisms of receptor modulation could have been developed to avoid reinfection of cells replicating the virus as well as to produce more infectious particles. These results suggest that the classical virus interference documented for other retroviruses might not only be due to receptor/envelope interaction, but might also depend on receptor gene expression.

Cell Membrane↗
PubMed2002

Conditional virus replication as an approach to a safe live attenuated human immunodeficiency virus vaccine.

Despite intensive efforts, no safe and effective vaccine has been developed for the prophylaxis of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). Studies with the simian immunodeficiency virus (SIV)/macaque model demonstrated that live attenuated viruses are the most effective vaccines tested thus far. However, due to ongoing low-level replication of the attenuated virus and the error-prone replication machinery, the attenuated virus may regain replication capacity and become pathogenic. We therefore designed a novel vaccine strategy with an HIV-1 virus that replicates exclusively in the presence of the nontoxic effector doxycycline (dox). This was achieved by replacement of the viral TAR-Tat system for transcriptional activation by the Escherichia coli-derived Tet system for inducible gene expression. This designer HIV-rtTA virus replicates in a strictly dox-dependent manner and may represent an improved vaccine strain because its replication can be turned on and off at will. Spontaneous virus evolution resulted in optimization of the components of the Tet system for their new function to support virus replication in human cells. The optimised Tet system may be of particular use in other applications such as inducible expression of gene therapy vectors in the brain.

AIDS Vaccines↗
PubMed1993

Induction of IFN-alpha by HIV-1 in monocyte-enriched PBMC requires gp120-CD4 interaction but not virus replication.

IFN-alpha is in plasma of HIV-1 infected patients during early and late-stage disease and may play a role in control of virus replication. The stimulus for IFN-alpha production, the cells that produce this cytokine, and the effectiveness of this IFN-alpha response for control of virus infection are not yet defined. Culture fluids from freshly isolated PBMC of HIV-1 seronegative donors contained high levels of IFN-alpha after exposure to 100 to 1000 infectious HIV-1 particles per culture. Levels of IFN-alpha induced by HIV-1 were directly dependent on the number of monocytes in cell preparations: No IFN-alpha was detected from T cell-enriched PBMC. In monocyte cultures, induction of IFN-alpha by HIV-1 was relatively specific: Levels of IL-1 beta, IL-6, IFN-gamma, and TNF-alpha remained at baseline. Capacity of HIV-1 virions to induce IFN-alpha was not dependent on virus replication. IFN-alpha was induced by (a) heat-inactivated HIV-1, (b) virions from 8E5 cells, a cell line that releases noninfectious HIV-1, (c) HIV-1-infected cells fixed in paraformaldehyde, and (d) T cell-tropic HIV-1 that binds to but does not infect monocytes. Capacity of HIV-1 virions and HIV-1 infected cells to induce IFN-alpha was completely inhibited by soluble rCD4 or mAb against CD4 or gp120. Antibodies against CD4, however, did not induce monocytes to produce IFN-alpha. HIV-1-induced IFN-alpha production was inhibited by antibodies against both V3 loop determinants and the CD4 binding site of gp120. Further, sera and purified immunoglobulin from HIV-1 infected patients also inhibited HIV-1-induced IFN-alpha production. These observations suggest that potentially protective antiviral responses associated with IFN-alpha production in HIV-1 infected patients are inhibited by the development of antibodies against gp120.

CD4 Antigens↗
PubMed1997

Protein 2A is not required for Theiler's virus replication.

Nonpolar mutations were introduced into all 12 regions of the genome of Theiler's murine encephalomyelitis virus. In agreement with data previously reported for other picornaviruses, mutations in regions 2B, 2C, 3A, 3B, 3C, and 3D totally abrogated viral RNA replication. Viruses with deletions in each of the capsid proteins retained RNA replication proficiency, although they were unable to propagate from cell to cell. As reported previously, mutations in the leader protein did not impair RNA replication or virus production in BHK-21 cells. Surprisingly, region 2A also appeared to be dispensable for the replication process. Indeed, up to 77 of the 133 amino acids of 2A could be deleted without significantly affecting RNA replication. 2A mutant viruses had only a slow cytopathic effect for BHK-21 cells and were totally avirulent for mice. As was the case for mutants lacking the leader protein, viruses with deletions in 2A propagated in BHK-21 cells, but their propagation was highly restricted in L929 cells.

Amino Acid Sequence↗
PubMedDate not supplied

Delta-infection and suppression of hepatitis B virus replication in chronic HBsAg carriers.

The presence of hepatitis B virus DNA and anti-delta was examined in a longitudinal study of 24 patients known to be delta-infected during the course from acute to chronic hepatitis B virus infection. Fifteen patients (63%) were hepatitis B virus DNA positive in the first serum sample. Eleven of 14 patients, who cleared hepatitis B virus DNA, did so following or at the same time as onset of delta-infection. Duration of hepatitis B virus DNA positivity in these 11 patients was shorter than in 11 anti-delta-negative controls matched according to duration of preceding hepatitis B virus DNA positivity, but the difference was not statistically significant. Considering only patients positive for IgM anti-delta in the last serum sample (eight patients), a statistically significant shorter duration of hepatitis B virus DNA positivity was found in delta-infected patients than in the controls (p less than 0.02). The study indicates that the delta-agent may have the capacity to inhibit hepatitis B virus replication and that a chronic delta-infection may lead to a termination of the period of active viral replication.

Adolescent↗
PubMed1985

Combined effects of amantadine and interferon on influenza virus replication in chicken and human embryo trachea organ culture.

Amantadine (greater than or equal to 100 micrograms/ml) treatment of chicken or human trachea organ cultures 6 h before infection inhibited influenza virus replication. Chicken or human leukocyte IFN evoked antiviral resistance in the cells of the homologous organ cultures only at a concentration of 100 U/ml or more. Treatment of organ cultures with combinations of the two substances resulted in an additive effect on influenza virus replication in both chicken and human tissues.

Amantadine↗
PubMed2002

Dengue virus replicative intermediate RNA detection by reverse transcription-PCR.

Dengue virus replication involves synthesis of a replicative intermediate RNA (RI-RNA), whose presence reveals an actual infection. We report on a simple and rapid reverse transcription-PCR for the detection of viral RI-RNA in infected cells. The product is demonstrated at 20 min postinfection. This method is useful for the study of virus-cell tropism.

Animals↗
PubMed2004

Effects of intrabodies specific for rotavirus NSP5 during the virus replicative cycle.

Intracellular antibodies or intrabodies (ICAbs) have great potential in protein knockout strategies for intracellular antigens. In this study, they have been used to investigate the role of the rotavirus non-structural protein NSP5 in the virus replication cycle. Intracellular antibody-capture technology was used to select single-chain Fv format (scFv) ICAbs against an NSP5 mutant. Five different specific ICAbs were selected and expressed in MA104 cells, in the scFv format, as cytoplasmic- and nuclear-tagged forms. By confocal microscopy, it was found that three of these ICAbs recognized the full-length wild-type NSP5 specifically, forming antigen-specific aggresomes in the cytoplasm of cotransfected cells. Expression of the ICAbs in rotavirus-infected cells largely reduced the assembly of viroplasms and cellular cytopathic effect. Replication of dsRNA was partially inhibited, despite there being no reduction in virus titre. These results demonstrate for the first time a key role for NSP5 during the virus replicative cycle.

Antibodies, Viral↗
PubMed1997

Hepatitis G virus replication in human cultured cells displaying susceptibility to hepatitis C virus infection.

We recently developed a hepatitis C virus (HCV) replication system using two cultured human cell lines: MT-2C, a human T-cell leukemia virus type I-infected cloned T cell line, and PH5CH, a non-neoplastic human hepatocyte line. In the course of the study, we found evidence that replication of hepatitis G virus (HGV), which has recently been identified, was supported in both MT-2C and PH5CH cells. When these cells were inoculated with serum 1B-3 containing both HCV and HGV obtained from a blood donor, the 5'-noncoding (5'-NC) regions of HCV RNA and HGV RNA were detected by RT-nested PCR in both cell lines more than 30 days postinoculation, and the 3'-noncoding region of HGV RNA was also detected in the both cell lines more than 30 days postinoculation. Sequence analysis of the 5'-NC region of HGV RNA revealed the quasispecies nature of HGV, although the 5'-NC region was highly conserved among HGV isolates. This HGV-infected culture system will be useful for various biological and virological studies of HGV.

Base Sequence↗
PubMed1988

Rubella virus replication: effect of interferons and actinomycin D.

The effect of alpha and gamma interferon (IFN alpha, IFN gamma) and actinomycin D on the expression of wild type rubella virus in African green monkey kidney cells (Vero 76) was studied. Viral protein synthesis in the infected cells was significantly reduced upon treatment of the cells with IFN alpha or IFN gamma, which is accompanied by the reduction in the level of both the (+) stranded and the (-) stranded viral RNAs. The residual rubella viral RNA from interferon-treated cells, however, was structurally intact as judged by Northern blot analysis and in vitro translation. These results suggest that the effect of IFN alpha and IFN gamma on rubella viral protein synthesis is both at the transcriptional and the translational level. The effect of actinomycin D on rubella virus replication was found to be time-dependent. It is much more pronounced during the eclipse phase of the viral growth (first 4 h) than after 8 h at which time actinomycin D had lesser effect. A similar effect on rubella virus replication was observed when alpha-amanitin was used instead of actinomycin D. These results were taken to indicate that during the viral infection, host cell DNA directs the synthesis of a cellular factor(s) which is essential for the viral replication. When the synthesis of this cellular factor(s) is terminated at an early stage of viral infection by actinomycin D or by alpha-amanitin, viral replication is impaired.

Amanitins↗
PubMed2003

Synergistic in vitro interactions between alpha interferon and ribavirin against bovine viral diarrhea virus and yellow fever virus as surrogate models of hepatitis C virus replication.

Monotherapy of hepatitis C virus infection with either alpha interferon or ribavirin alone is rather ineffective, while the use of the two antivirals together is much more efficacious. In vitro drug-drug combination analysis utilizing related members of the family Flaviviridae, bovine viral diarrhea virus and yellow fever virus, revealed significant direct synergistic interactions between these drugs' antiviral activities that might explain this clinical observation.

Animals↗
PubMed1985

Hepatitis B virus replication in acute glomerulonephritis with chronic active hepatitis.

A 3 year old boy who had chronic active hepatitis type B with features of ongoing liver damage and active virus replication, developed acute membranous glomerulonephritis two years after the clinical onset of liver disease, when both hepatitis B e antigen and antibody were detectable in serum. After withdrawal of short term steroid treatment and resolution of hepatitis B virus replication, both glomerulonephritis and chronic hepatitis went into remission. Some months later hepatitis B surface antigen was no longer found in serum.

Acute Disease↗
PubMed1991

Mutagenesis occurring following infection with herpes simplex virus does not require virus replication.

Infection of eukaryotic cells in culture with herpes simplex virus type-1 (HSV-1) or HSV-2 increased the mutation frequency of the supF gene carried on the shuttle vector pZ189 by around sixfold. The increase was apparent 2 hr postinfection and reached a peak after 8 hr. To investigate this mutagenesis, plasmids pCKRR1 and pCKRR2 were constructed to express the large and small subunits, respectively, of HSV-2 ribonucleotide reductase (RR) under the control of the inducible mouse metallothionein promoter. Expression from these plasmids, either singly or together, had no effect on the mutation frequency of pZ189 under conditions when virus RR activity was detected. The HSV-1 temperature sensitive (ts) mutant viruses ts 1207 and ts 1222, which have ts lesions in the genes encoding R1 and R2, respectively, were as mutagenic as wild-type HSV-1 at both the permissive and nonpermissive temperatures. These results indicate that expression of HSV RR is not mutagenic in this system. Experiments using other HSV-1 mutants and ultraviolet-inactivated virus localized the cause of the increased mutagenic frequency either to a component of the incoming virion or to an effect exerted by the virus DNA itself. The present study confirms previous reports that infection with HSV exerts a mutagenic effect. Further, virus replication and gene expression were not required for the mutagenic effect studied here. This may have implications for a role of HSV in cellular transformation, as a nonproductive infection could mutagenize cellular genes.

Cell Line↗
PubMed1995

Cytomegalovirus-mediated induction of antisense mRNA expression to UL44 inhibits virus replication in an astrocytoma cell line: identification of an essential gene.

We have used an antisense RNA approach in the analysis of gene function in human cytomegalovirus (HCMV). An astrocytoma cell line (U373-MG) that is permissive for virus replication was permanently transfected with a construct bearing sequence from HCMV UL44 (coding for the major late DNA-binding protein, ppUL44, also known as pp52 or ICP36) in an antisense orientation and under the control of the immediate-early enhancer-promoter element. Upon HCMV infection at a high multiplicity, we found a marked reduction in UL44 protein products (the ICP36 family of proteins) in established cell transfectants and a strong inhibition of virus yield in infected-cell supernatants at two weeks postinfection, while herpes simplex virus replication was not affected. In infected cells, viral DNA replication was strongly inhibited. While gene products such as pUS22 and pUL32 were also inhibited, pUL123 and pUL82 accumulated in the infected cells over time. Our data suggest an essential role for the UL44 family of proteins in HCMV replication and represent a model of virus inhibition by virus-induced antisense RNA synthesis in genetically modified cells.

Animals↗
PubMed2006

Exploring RNA virus replication in Xenopus oocytes.

Microinjection of poliovirus RNA in Xenopus oocytes initiates a complete and authentic viral replication cycle that yields newly synthesized infectious virus. This system can be used to study the molecular mechanism of the different steps involved in virus replication. Interestingly, viral replication only occurs if poliovirus RNA is coinjected with factors present in HeLa extracts. We have determined that two HeLa cell factors are required for viral replication in oocytes, one involved in initiation of translation (polio translation factor) and the other in RNA synthesis. Thus, microinjection in oocytes provides a strategy to identify and further analyze the function of these host cell factors and to biochemically dissect the mechanism of initiation of poliovirus translation and RNA synthesis. Here, we review protocols, approaches, and potential issues that can be addressed using the oocyte system.

Animals↗
PubMed1994

Porcine respiratory coronavirus-mediated interference against influenza virus replication in the respiratory tract of feeder pigs.

Effect of prior porcine respiratory coronavirus (PRCV) infection on replication of H1N1-influenza virus in the respiratory tract of swine was studied. In an initial experiment, 3 groups of 5 feeder pigs were studied. Pigs of 2 groups were inoculated sequentially with PRCV, followed by H1N1-influenza virus at 2- and 3-day intervals. Pigs of the other group were inoculated with H1N1-influenza virus only. Pigs were monitored clinically and examined for nasal excretion of influenza virus. In the singly influenza virus-inoculated group, 83% of nasal swab specimens were influenza virus-positive over a period of 6 days after inoculation. In the dually virus-inoculated groups, only 27% (2-day interval) and 53% (3-day interval) of nasal swab specimens were virus-positive over the same postinoculation period. However, clinical signs of infection in these dually inoculated pigs were more severe than those in the singly influenza virus-inoculated pigs. There were no significant differences in antibody responses against influenza virus among the 3 groups of pigs. In a second experiment, 2 groups of pigs were studied. One group of pigs was inoculated sequentially with PRCV, followed by H1N1-influenza virus 2 days later; the other group was inoculated with H1N1-influenza virus only. Pigs of both groups were serially euthanatized on postinoculation days (PID) 1, 2, 3, and 4 (after influenza virus). At necropsy, influenza virus titer and immunofluorescence in lung tissue were determined and gross lung lesions were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗