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Results for “Virus Replication”

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At least 235 records · Page 13Linked to original sources

PubMed1990

Hepatitis B virus replication in Chinese patients with hepatocellular carcinoma.

We studied the frequency of hepatitis B virus replication in Chinese patients with hepatocellular carcinoma. Hepatitis B e antigen and hepatitis B virus DNA could be detected in the sera of 28% and 47% of 116 HBsAg-positive patients, but not in the sera of 15 HBsAg-negative patients. Replicative forms of hepatitis B virus DNA were detected in the neoplastic and nonneoplastic liver tissues from 34% and 62% of 29 HBsAg-positive patients and 0% and 20% of five HBsAg-negative patients by Southern blot hybridization analysis. Of the 10 patients with chronic hepatitis B virus infection in whom hepatocellular carcinoma developed during follow-up, hepatitis B e antigen and hepatitis B virus DNA were detected in the sera of seven and eight patients, respectively, at presentation, 13 to 43 mo before the diagnosis of hepatocellular carcinoma. In nine patients, hepatitis B virus DNA was persistently or intermittently detected in the serum during follow-up. Five patients remained hepatitis B e antigen-positive and seven were detectable for hepatitis B virus DNA in serum when hepatocellular carcinoma was diagnosed. Four patients had one or more episodes of exacerbations before the diagnosis of hepatocellular carcinoma; in three, the exacerbations were associated with changes in level of hepatitis B virus replication. Our study demonstrated that despite the long interval between the onset of hepatitis B virus infection and the development of hepatocellular carcinoma, hepatitis B virus replication persisted in most patients with hepatocellular carcinoma, albeit at a low level.

Adolescent↗

PubMed1997

Mutations which alter the DNA binding properties of the herpes simplex virus type 1 transactivating protein Vmw175 also affect its ability to support virus replication.

The crucial role of herpes simplex virus type 1 immediate early protein Vmw175 (ICP4) in the regulation of all classes of viral genes has been established by extensive analysis of temperature-sensitive, insertion and deletion mutants. It has long been known that Vmw175 binds to selected DNA sequences, and recent studies have shown that it interacts with components of the basal transcription machinery. However, the role of DNA binding in its mechanism of action has been controversial. Despite the presence of Vmw175 recognition sites at numerous locations throughout the viral genome, it has proved difficult to establish that these sites are important for the activation of early and late promoters. In this study we have analysed the ability of a large number of insertion and single point mutant derivatives of Vmw175 to bind to DNA and to support virus replication. Vmw175 mutants which were unable to bind to DNA were also incapacitated in terms of their ability to activate gene expression in transfection assays and to complement the growth of a Vmw175 deletion mutant virus. These results strongly support the hypothesis that interaction with DNA is an essential feature of the mechanism of action of Vmw175.

Amino Acid Sequence↗

PubMed1995

Staphylococcal enterotoxin B-activated T cells can be redirected to inhibit multicycle virus replication.

Cell-mediated immunity is a crucial part of recovery from virus infections. Adoptive transfer of T cells into infected animals is restricted by the need for Ag-specific and MHC-restricted T cells. One way to overcome these limitations is to use bifunctional Abs to redirect the T cells against virus-infected cells. We have demonstrated that bifunctional Abs can inhibit virus replication in the presence of activated T cells. To generate a large number of activated T cells in a short time, we tested the ability of the superantigen, staphylococcal enterotoxin B (SEB), to activate T cells. We demonstrate that SEB-activated T cells are effective killers when bridged to Fc receptor-bearing target cells using anti-CD3 Abs. SEB T cells can lyse virus-infected target cells in the presence of HHA6, a bifunctional Ab specific for the V beta 8 TCR product and the H1 hemagglutinin of influenza A/PR/8/34 virus. In addition, bifunctional Ab and SEB T cells can inhibit multicycle virus replication in vitro. In a conventional 4-h chromium release assay, SEB-activated CD8 T cells are efficient killers, whereas CD4 T cells are not. Yet both subpopulations have the ability to inhibit multicycle replication in vitro. Superantigens may represent a potent method for generation of effector cells for use in redirected immunotherapy protocols.

Animals↗

PubMed1997

Human immunodeficiency virus type 1 coreceptors participate in postentry stages in the virus replication cycle and function in simian immunodeficiency virus infection.

Primate lentiviruses use chemokine coreceptors in addition to the CD4 receptor to initiate virus infection. Simian immunodeficiency virus (SIV) productively infects human cells expressing CD4 and the human allele of the chemokine coreceptor CCR-5 as efficiently as it infects macaque cells expressing human CD4, suggesting that SIV can function with either a simian or a human coreceptor in conjunction with human CD4. In the same macaque cells expressing human CD4, the replication of human immunodeficiency virus type 1 (HIV-1) is blocked at several stages of infection; some isolates are restricted prior to reverse transcription, while others, including some macrophage-tropic and primary isolates, are restricted at a step after reverse transcription but prior to migration of the preintegration complex to the nucleus. Both blocks in HIV-1 replication can be relieved by either expression of the appropriate human coreceptor (CCR-5 or CXCR-4) or expression of SIV gene products in cis with the HIV-1 envelope as a chimera between SIV and HIV-1 (SHIV). Thus, a virus with a SIV core and HIV-1 envelope can efficiently infect macaque cells expressing human CD4, presumably by interacting with the simian coreceptor, whereas a virus with an HIV-1 core and an HIV-1 envelope requires expression of the human allele of the coreceptor for productive infection of these cells. These studies suggest that there are interactions among the coreceptor, the viral envelope, and another viral gene product that govern postentry steps of virus replication. These data are consistent with the hypothesis that such interactions may be required for translocation of the virus core to the nucleus. Moreover, the differential abilities of SIV and HIV-1 to function in these processes with heterologous primate coreceptors may have implications for cross-species transmission.

Cell Line↗

PubMed1977

Respiration and ATP level in BHK21/13S cells during the earlist stages of rubella virus replication.

This study is concerned with the effect of virus infection on the energy balance of the cell and the possible involvement of mitochondria in virus replication. The process of rubella virus adsorption and penetration is immediately associated with a stimulation of O2 uptake. Shortly afterwards, ATP levels decline, possible because of increased ATP utilization. Virus infection appears to protect mitochondria against the uncoupling effect of dinitrophenol.

Adenosine Triphosphate↗

PubMed1998

The use of two immunosuppressive drugs, cyclosporin A and tacrolimus, to inhibit virus replication and apoptosis in cells infected with feline immunodeficiency virus.

An in vitro model of acute and chronic infections with feline immunodeficiency virus (FIV) was used to examine the effect of two immunosuppressive agents, cyclosporin A (CsA) and tacrolimus (also known as FK506), on the inhibition of the replication of the virus and of apoptosis. Both drugs significantly suppressed virus production in a dose-dependent manner in acutely and chronically infected cells. The ability of FK506 to inhibit virus replication was much lower than that of CsA, and was accompanied by marked antiproliferative activity. Treatment of infected cells with either CsA or FK506 did not affect the rise of free intracellular Ca2+ but did protect the cells against apoptosis. Thus, the antiviral activity of CsA and FK506 makes these compounds promising candidates for the development of drugs suitable for the treatment of AIDS.

Animals↗

PubMed1966

Virus replication and high-titered interferon production in human leukocyte cultures inoculated with Newcastle disease virus.

Wheelock, Frederick E. (Western Reserve University, Cleveland, Ohio). Virus replication and high-titered interferon production in human leukocyte cultures inoculated with Newcastle disease virus. J. Bacteriol. 92:1415-1421. 1966.-High titers of interferon (20,480 culture-protecting units per ml) are produced in freshly prepared human leukocyte cultures inoculated with a Newcastle disease virus (NDV)-cell multiplicity of 1:1. NDV replicates to low titers in these cultures. Incubation of leukocytes at 37 C for 24 hr prior to inoculation of NDV results in almost complete loss of detectable interferon production, but virus replicates to higher titers than in the freshly prepared cultures. In contrast, no diminution of interferon production in response to phytohemagglutinin (PHA) occurs on 24 hr of incubation of cultures prior to addition of PHA. Experiments with cultures of predominantly pure cell fractions of peripheral blood indicate that the lymphocyte fraction produces interferon in response to either NDV or PHA, and that polymorphonuclear leukocytes produce no interferon in response to these agents. These studies suggest a hitherto unsuspected ability of human lymphocytes to produce high titers of interferon in vivo.

Humans↗

PubMed1985

Quantitative analysis of visna virus replication in vivo.

Visna virus is the prototype of the lentivirus subfamily, a group of nontransforming retroviruses that cause slow infections in sheep and goats. In nature, virus is acquired primarily by the respiratory route and subsequently spreads to several organ systems. These viruses persist for years in their hosts despite a vigorous immune response because of a block in virus gene expression. This report continues the analysis of persistence in vivo, and specifically examines a gene dosage hypothesis that has been advanced as an explanation for the decrease in transcription and virus production in the cells in infected animals. For this analysis a new pulmonary model has been developed that, in conjunction with quantitative in situ hybridization, provides an opportunity to examine in animals the molecular events that occur in the course of the viral life cycle. We establish the feasibility of such a longitudinal analysis in vivo, document restriction in gene expression in alveolar macrophages and provide evidence that this restriction cannot be accounted for simply by gene dosage. The approach illustrated with visna should be of general applicability to other dynamic and molecular investigations of virus infection.

Animals↗

PubMed1966

Vesicular stomatitis virus replication in human leukocyte cultures: enhancement by phytohemagglutinin.

The replication of vesicular stomatitis virus in human leukocyte cultures shows that virus yields can be enhanced 6-to 180-fold by treating the leukocyte cultures with phytohemagglutinin prior to virus inoculation. Data suggest that a substance is produced in phytohemagglutinin-treated leukocyte cultures which is capable, on transfer to fresh leukocytes, of inducing blast cell formation and enhancing virus replication.

Adult↗

PubMed1991

Vaccinia virus DNA ligase is nonessential for virus replication: recovery of plasmids from virus-infected cells.

The essentiality of the vaccinia virus DNA ligase gene, SalF 15R, for virus growth was tested by insertional mutagenesis. A plasmid containing E. coli gpt inserted within a large deletion in the DNA ligase gene was transfected into vaccinia virus-infected cells and recombinant viruses selected by three cycles of plaque purification in the presence of mycophenolic acid (MPA). Surprisingly, in some isolates, which replicated in a manner indistinguishable from wild type (WT) virus, the WT gene was replaced by the gpt allele, demonstrating that the DNA ligase gene is nonessential for growth in cultured cells. In other isolates the entire plasmid was integrated into the virus genome by a single crossover event and a functional copy of the DNA ligase was retained. Southern blot analyses of the latter, drug-resistant viruses indicated extra DNA fragments, of sizes inconsistent with predicted viral structures, which represent the plasmid products of homologous recombination. Hirt extracts from cells infected with such multiply plaque purified virus isolates yielded plasmids that produced ampicillin-resistant colonies after transformation of E. coli. These plasmids were of two structures, representing either the original plasmid used for transfection, or a plasmid containing the WT ligase gene rescued by recombination with the virus genome. Similarly, insertional mutagenesis of the vaccinia virus thymidine kinase (TK) gene with gpt yielded plasmids containing mutant or wild type TK alleles when recombinant viruses were selected in MPA. Such plasmids were not isolated when TK minus viruses were selected in 5-bromodeoxyuridine (BUdR).

Animals↗

PubMed1992

HeLa cells grown continuously in protein-free medium: a novel model for the study of virus replication.

Human carcinoma of the cervix cell line HeLa, adapted to continuous growth in a protein-free chemically defined medium, was used as substrate for the replication of several human pathogenic viruses. Growth characteristics of the cells designated as HeLa-PF in protein-free 1:1 nutrient mixture of Dulbecco's modified MEM and Ham's F-12 supplemented with L-ascorbic acid 2-phosphate were similar to those of the cells grown in a serum-supplemented medium. After 30 months (135 subcultures) in the protein-free medium, HeLa-PF cells were infected with poliovirus types 1, 2 and 3; adenovirus types 2 and 5 and herpes simplex virus type 1. Both adenoviruses and polioviruses developed in HeLa-PF cells titers and showed cytopathic effects comparable to those obtained in conventionally grown and maintained cells; in contrast, significantly lower herpes simplex virus type 1 titers and changed characteristics of the cytopathic effects were observed in HeLa-PF cells. The results show that HeLa-PF cells grown continuously in protein-free medium provide a unique system for the study of virus replication.

Adenoviridae↗

PubMed1969

Effect of ultraviolet irradiation and actinomycin D on polyoma virus replication in mouse embryo cell cultures.

Ultraviolet irradiation and actinomycin D impair the capacity of mouse embryo (ME) cells to support the replication of polyoma virus, but not of encephalomyocarditis (EMC) virus. The loss in capacity for polyoma virus synthesis was an "all-or-none" effect and followed closely upon the loss in cellular capacity for clone formation. Cells treated with either agent produced polyoma "T" antigen, but did not synthesize polyoma structural protein. Infection of untreated ME cells with polyoma virus produced marked stimulation of both deoxyribonucleic acid (DNA) synthesis and ribonucleic acid (RNA) synthesis. ME cell cultures irradiated with ultraviolet for 30 sec at 60 muw/cm(2) or treated with actinomycin D at 0.1 mug/ml for 6 hr prior to infection were incapable of synthesizing DNA or RNA, even after infection with polyoma virus. Irradiation of cells during infection produced cessation of synthesis of both RNA and DNA. Addition of actinomycin D during infection did not inhibit DNA synthesis but abolished RNA synthesis and reduced the yield of polyoma virus to 10% of that in untreated infected cultures. Both agents lost the ability to prevent replication of a full yield of polyoma virus when administered 30 hr after infection or later. The period after which neither agent inhibited polyoma replication corresponded with the period at which maximal RNA synthesis in untreated infected cultures had subsided. It can be concluded on the basis of the data presented that the functional integrity of the mouse embryo cell genome is required for the replication of polyoma virus, but not for EMC virus. Whereas the requirement for cellular DNA-dependent RNA synthesis for polyoma virus replication has been demonstrated, the exact nature of the host-cell function remains to be elucidated.

Animals↗

PubMed1991

The topoisomerase I inhibitor, camptothecin, inhibits equine infectious anemia virus replication in chronically infected CF2Th cells.

Camptothecin (CPT), a topoisomerase I-specific inhibitor, was found in this study to inhibit the replication of equine infectious anemia virus (EIAV) in chronically infected CF2Th cells (designated CF2Th/EIAV). By measuring viral reverse transcriptase activity in the culture medium, we demonstrated that treatment for 1 h with noncytotoxic doses of this drug inhibited production by 32 to 52%, whereas continuous exposure to this drug resulted in an 85 to 92% inhibition. No effect on the viability or growth rate of the cells was detected in any of these treatments. Indirect immunofluorescence analysis of the CPT-treated CF2Th/EIAV cells with anti-p26 capsid protein antibodies showed 60 to 85% reduction in the immunofluorescence-positive cells following drug treatment, and radioimmunoprecipitation analysis of these cells showed a comparable decrease of the pr55gag precursor protein. These data suggest that CPT acts as an anti-EIAV agent to block virus replication in the chronically infected cells.

Animals↗

PubMed1999

Enhancement of hepatitis C virus replication by Epstein-Barr virus-encoded nuclear antigen 1.

Based on our recent observation that Epstein-Barr virus (EBV) is detected in 37% of the tissues of hepatocellular carcinoma, and especially frequently in cases with hepatitis C virus (HCV), the effect of EBV infection on the replication of HCV was investigated. EBV-infected cell clones and their EBV-uninfected counterparts in cell lines MT-2 (a human T-lymphotropic virus type I-infected T-cell line), HepG2 (a hepatoblastoma cell line) and Akata (a Burkitt's lymphoma cell line) were compared in terms of their permissiveness for HCV replication following inoculation of HCV derived from patients who were HCV carriers. The results indicated that EBV-infected cell clones, but not their EBV-uninfected counterparts, promoted HCV replication. EBV-encoded nuclear antigen 1 (EBNA1), which is invariably expressed in EBV-infected cells, supported HCV replication. Deletion analysis of the EBNA1 gene showed good correlation between transactivation activity and the activity supporting HCV replication. The present findings suggest that EBV acts as a helper virus for HCV replication.

Base Sequence↗

PubMed1989

Combined effects of acyclovir and human interferon-alpha on herpes simplex virus replication in cultured neural cells.

The combined effects of Acyclovir [9-(2'-hydroxyethoxymethyl)guanine; ACV] and human interferon-alpha (IFN-alpha) on replication of the herpes simplex virus type I (HSV-1) were determined in human neural cell lines, neuroblastoma (IMR), glioblastoma (118MGC), and glioma (U251MG). HSV-1 grew well in all these cells, with final yields of more than 1 x 10(6) PFU/ml. In terms of virus-yield reduction, ACV was found to be highly effective in IMR, moderately effective in U251MG, but ineffective in 118MGC. By contrast, IFN-alpha reduced the virus yield significantly in 118MGC and in U251MG, but did not in IMR. Combined application of ACV and IFN-alpha strongly inhibited the virus replication in all three cell lines with various degrees of synergism or additive effect. These results were also confirmed by immunofluorescent examinations. The sensitivity of HSV-1 to ACV or IFN-alpha was found to be different among the three different cell types. By combining the two agents, the virus growth was strongly suppressed in all the cells. These results suggest the importance of combination therapy for severe type of herpes simplex encephalitis in clinical practice.

Acyclovir↗

PubMed1992

The mechanism of inhibition of hepatitis B virus replication by the carbocyclic analog of 2'-deoxyguanosine.

The carbocyclic analog of deoxyguanosine inhibits hepatitis B virus replication by greater than 95% in the hepatitis B virus-producing cell line (2.2.15) as monitored by decreases of secreted hepatitis B virus DNA, hepatitis B virus polymerase activity and intracellular episomal hepatitis B virus DNA. Transcription of hepatitis B virus RNA from chromosomally integrated hepatitis B virus DNA was unaffected. Radioactive carbocyclic 2'-deoxyguanosine was directly phosphorylated within the 2.2.15 cells and was incorporated exclusively into DNA. In contrast, radioactive deoxyguanosine was presumably metabolized through the "salvage" pathway in which the guanine was primarily incorporated into cellular RNAs. The rate of incorporation of carbocyclic 2'-deoxyguanosine in 2.2.15 cells was similar to that in the parental cell line (HepG2), which does not contain hepatitis B virus sequences. Greater than 90% of the analog was present at internal sites within the DNA, indicating that the analog did not function as a DNA chain terminator. Kinetic analysis of the Km and Ki of dGTP and carbocyclic 2'-deoxyguanosine 5'-triphosphate, respectively, using both hepatitis B virus polymerase and DNA polymerase delta indicated that the analog is a competitive inhibitor for dGTP. Although both polymerases had similar Km's for dGTP, the Ki for carbocyclic 2'-deoxyguanosine 5'-triphosphate was about 6 times lower using the hepatitis B virus polymerase. This would indicate that, at low concentrations of intracellular carbocyclic 2'-deoxyguanosine 5'-triphosphate, the hepatitis B virus polymerase would be preferentially inhibited. We propose this to be the mechanism acting to inhibit preferentially hepatitis B virus replication in the tissue culture cells.

Antiviral Agents↗

PubMed1981

Bunyamwera virus replication in cultured Aedes albopictus (mosquito) cells: establishment of a persistent viral infection.

Bunyamwera virus replication was examined in Aedes albopictus (mosquito) cell cultures in which a persistent infection is established and in cytopathically infected BHK cells. During primary infection of A. albopictus cells, Bunyamwera virus reached relatively high titers ( approximately 10(7) PFU/ml), and autointerference was not observed. Three virus-specific RNAs (L, M, and S) and two virion proteins (N and G1) were detected in infected cells. Maximum rates of viral RNA synthesis and viral protein synthesis were extremely low, corresponding to <2% of the synthetic capacities of uninfected control cells. Viral protein synthesis was maximal at 12 h postinfection and was shut down to barely detectable levels at 24 h postinfection. Virus-specific RNA and nucleocapsid syntheses showed similar patterns of change, but later in infection. The proportions of cells able to release a single PFU at 3, 6, and 54 days postinfection were 100, 50, and 1.5%, respectively. Titers fell to 10(3) to 10(5) PFU/ml in carrier cultures. Persistently infected cultures were resistant to superinfection with homologous virus but not with heterologous virus. No changes in host cell protein synthesis or other cytopathic effects were observed at any stage of infection. Small-plaque variants of Bunyamwera virus appeared at approximately 7 days postinfection and increased gradually until they were 75 to 95% of the total infectious virus at 66 days postinfection. Temperature-sensitive mutants appeared between 23 and 49 days postinfection. No antiviral activity similar to that reported in A. albopictus cell cultures persistently infected with Sindbis virus (R. Riedel and D. T. Brown, J. Virol. 29: 51-60, 1979) was detected in culture fluids by 3 months after infection. Bunyamwera virus replicated more rapidly in BHK cells than in mosquito cells but reached lower titers. Autointerference occurred at multiplicities of infection of approximately 10. Virus-specific RNA and protein syntheses were at least 20% of the levels in uninfected control cells. Host cell protein synthesis was completely shut down, and nucleocapsid protein accumulated until it was 4% of the total cell protein. We discuss these results in relation to possible mechanisms involved in determining the outcome of arbovirus infection of vertebrate and mosquito cells.

Aedes↗

PubMed2003

Transcriptional inactivation of amphotropic murine leukemia virus replication in human cells.

Amphotropic murine leukemia virus (MLV) replicates in cells from various mammalian species including humans and is a potential contaminant in MLV vector preparations for human gene transfer studies. Because MLV replication proceeds through an RNA genome that is generated under the control of viral enhancer and promoter elements, vectors were developed that delete such elements during transduction to reduce the generation of replication-competent virus. It was shown recently that replication of amphotropic MLV in certain human cells is possible without the 75 bp transcription enhancers. It is now demonstrated that enhancer-independent replication requires functional elements within U3 and is repressed by an extended deletion in the U3 region comprising enhancers, promoter and flanking sequences. It is concluded that the transcriptional inactivation of amphotropic MLV in human cells requires the combined deletion of enhancers and of additional elements in U3.

Animals↗