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Results for “Virus Replication”

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At least 343 records · Page 19Linked to original sources

PubMed1999

Lassa and Mopeia virus replication in human monocytes/macrophages and in endothelial cells: different effects on IL-8 and TNF-alpha gene expression.

Cells of the mononuclear and endothelial lineages are targets for viruses which cause hemorrhagic fevers (HF) such as the filoviruses Marburg and Ebola, and the arenaviruses Lassa and Junin. A recent model of Marburg HF pathogenesis proposes that virus directly causes endothelial cell damage and macrophage release of TNF-alpha which increases the permeability of endothelial monolayers [Feldmann et al. , 1996]. We show that Lassa virus replicates in human monocytes/macrophages and endothelial cells without damaging them. Human endothelial cells (HUVEC) are highly susceptible to infection by both Lassa and Mopeia (a non-pathogenic Lassa-related arenavirus). Whereas monocytes must differentiate into macrophages before supporting even low level production of these viruses, the virus yields in the culture medium of infected HUVEC cells reach more than 7 log10 PFU/ml without cellular damage. In contrast to filovirus, Lassa virus replication in monocytes/macrophages fails to stimulate TNF-alpha gene expression and even down-regulates LPS-stimulated TNF-alpha mRNA synthesis. The expression of IL-8, a prototypic proinflammatory CXC chemokine, was also suppressed in Lassa virus infected monocytes/macrophages and HUVEC on both the protein and mRNA levels. This contrasts with Mopeia virus infection of HUVEC in which neither IL-8 mRNA nor protein are reduced. The cumulative down-regulation of TNF-alpha and IL-8 expression could explain the absence of inflammatory and effective immune responses in severe cases of Lassa HF.

Arenaviridae↗

PubMed2005

RNA interference of rotavirus segment 11 mRNA reveals the essential role of NSP5 in the virus replicative cycle.

Rotavirus genomes contain 11 double-stranded (ds) RNA segments. Genome segment 11 encodes the non-structural protein NSP5 and, in some strains, also NSP6. NSP5 is produced soon after viral infection and localizes in cytoplasmic viroplasms, where virus replication takes place. RNA interference by small interfering (si) RNAs targeted to genome segment 11 mRNA of two different strains blocked production of NSP5 in a strain-specific manner, with a strong effect on the overall replicative cycle: inhibition of viroplasm formation, decreased production of other structural and non-structural proteins, synthesis of viral genomic dsRNA and production of infectious particles. These effects were shown not to be due to inhibition of NSP6. The results obtained strengthen the importance of secondary transcription/translation in rotavirus replication and demonstrate that NSP5 is essential for the assembly of viroplasms and virus replication.

Genes, Essential↗

PubMed2001

Identification of a hepatic factor capable of supporting hepatitis C virus replication in a nonpermissive cell line.

Although hepatitis C virus E2 protein can bind to human cells by interacting with a putative viral receptor, CD81, the interaction alone is not sufficient to establish permissiveness for hepatitis C virus infection. Using an Epstein-Barr virus-based extrachromosomal replication system, we have screened through a human liver cDNA library and successfully identified a cDNA capable of supporting hepatitis C virus replication in an otherwise nonpermissive cell line. This cDNA encodes a protein exhibiting homology to a group of proteins derived from various evolutionarily distant species, including Oryza sativa submergence-induced protein 2A. The mRNAs encoding this factor are heterogeneous at the 5' ends and are ubiquitously expressed in multiple tissues, albeit in a very small amount. The longest mRNA contains an in-frame and upstream initiation codon and codes for a larger protein. This 5'-extended form of mRNA was detected in hepatocellular carcinoma, but not in normal liver tissue. Immunofluorescence analysis demonstrated that the hepatic factor was distributed evenly in cells, but occasionally formed aggregations in the peri- or intranuclear areas. In summary, we have identified a hepatic factor capable of supporting hepatitis C virus replication in an otherwise nonpermissive cell line. This factor belongs to a previously uncharacterized protein family. The physiological function of this protein awaits further study.

Amino Acid Sequence↗

PubMed1990

The regulatory mechanisms of human immunodeficiency virus replication predict multiple expression rates.

The qualitative nature of human immunodeficiency virus replication dynamics is examined by using the known action of regulatory proteins. The combination of activation of transcription by the Tat protein and the influence of the Rev protein on processing of RNA leads to a regulatory loop that can have multiple expression rates. In the lower state, the regulatory loop leads to low, or no, production of virus, which corresponds to its quiescent state. Conversely, when the regulatory loop is in the upper state, active production of virus is maintained over time. These features of the kinetic model have implications for both human immunodeficiency virus-related illness and therapeutics and predict testable experimental results in vitro.

Gene Products, tat↗

PubMed1981

Comparative inhibition of influenza and parainfluenza virus replication by ribavirin in MDCK cells.

Actinomycin D inhibited the yield of influenza virus hemagglutinin from MDCK cells infected at high multiplicity, but had little effect on the yield of parainfluenza virus hemagglutinin. In similar hemagglutinin yield experiments, ribavirin was only slightly more active (threefold) against influenza virus than against parainfluenza virus replication. In plaque inhibition experiments, ribavirin depressed influenza virus plaque formation by 50% at a concentration of approximately 3 micrograms/ml, whereas the corresponding figure for parainfluenza viruses was threefold higher. The concentration of ribavirin demonstrating anti-influenza activity was indistinguishable for that inhibiting host cell growth. It is concluded that, unlike actinomycin D, ribavirin is unlikely to have a major effect on the provision of host cell 5-germinal methylated cap structures and the subsequent priming of influenza messenger ribonucleic acid synthesis.

Animals↗

PubMed1996

Replicating viruses as selective cancer therapeutics.

Replication-competent viruses are used as selective cancer therapeutics and the mechanisms leading to tumor-specific replication and antitumoral efficacy are now becoming apparent. The specific viruses in development include tumor-targeting herpes simplex viruses, autonomous parvoviruses, Newcastle disease viruses and adenovirus. Information is also available on antiviral immunology and viral defenses against host-mediated immunity. This approach has many potential attributes, in addition to potential hurdles that must be overcome.

Adenoviruses, Human↗

PubMed1987

Inhibition of Rous sarcoma virus replication by antisense RNA.

Previous results have indicated that Rous sarcoma virus env gene expression is specifically inhibited by antisense RNA (L.-J. Chang and C. M. Stoltzfus, Mol. Cell. Biol. 5:2341-2348, 1985). In this study, we compare the extents of inhibition by antisense RNA derived from different parts of the Rous sarcoma virus genome, and we show that antisense constructs containing the 3'-end noncoding region inhibit env expression to a similar extent as those containing the 5'-end noncoding region or coding region. Furthermore, we show that antisense RNA inhibits virus replication at other levels in addition to translation.

Avian Sarcoma Viruses↗

PubMed1987

Friend virus replication as a function of age.

We have investigated the effect of age on the replication of Friend spleen focus-forming virus (SFFV). Recovery of SFFV from the spleens of four strains of mice was determined following intravenous infection with NB-tropic Friend virus (FV) complex at ages ranging from 6 to 134 weeks. In C57BL/6 mice, the virus did not replicate in adults up to 40 weeks of age, but beyond that there was a steep exponential increase with age in the amounts of SFFV recoverable. In C3H/He mice, which replicate the virus as young adults, the amount of SFFV recovered was 6-fold greater in old than in young mice. Recovery of virus was biphasic with age in SJL mice; in A strain mice no consistent change with age was noted. In C57BL/6 mice, reconstitution of lethally irradiated recipients with syngeneic marrow cells, followed by i.v. infection with FV, showed that the amounts of SFFV recovered depended on the age of the recipient. The present work shows that Friend SFFV replication is a sensitive indicator and can be used as a tool for the investigation of aging processes. The mechanisms responsible for the age-dependent change in regulation of virus replication and for the polymorphism remain to be determined.

Aging↗

PubMed1985

Effect of dimethyl sulfoxide on interaction of human cytomegalovirus with host cell: conversion of a nonproductive state of cell to a productive state for virus replication.

The effect of dimethyl sulfoxide (DMSO) on the interaction of human cytomegalovirus (HCMV) with host cell was studied. Confluent state of a human rhabdomyosarcoma cell line (A204) showed a much lower susceptibility to HCMV infection when compared to that in subconfluent actively growing cell cultures. Treatment of confluent cultures with DMSO, however, converted many nonproductive cells in these cultures to a productive state for virus replication. Infectious center assay revealed that approximately 100-fold more cells in the compound-treated cultures are able to produce infectious virus. The amount of infectious virus produced in DMSO-treated confluent cultures was enhanced by approximately 10,000-fold over production in untreated cultures and recovered to the level of that produced in subconfluent cultures productive state for virus replication. This cell physiology-dependent inhibition of HCMV replication and enhancement of virus growth by DMSO did not occur with herpes simplex virus type 2. Immunofluorescence staining, gel electrophoresis, and DNA analyses indicate that block of HCMV replication in confluent cultures probably occurs at the level of early transcription or translation of the viral genome. In contrast, in DMSO-treated confluent cultures appreciable amounts of HCMV DNA polymerase (an early virus function), viral DNA, and late antigens were synthesized. Pretreatment of confluent cultures with DMSO enabled the cells to support HCMV replication. In addition, the most effective enhancement by DMSO was found in cultures that had been treated with the compound up to 5 hr after infection. These results suggest that the enhancing effect by DMSO is primarily expressed through some host cellular function(s) and the early stages in virus growth cycle are most likely under control by DMSO action.

Antigens, Viral↗

PubMed1976

Homogenization-resistant and -susceptible components of tobacco mosaic virus replicative form RNA.

When prepared from tissue frozen with liquid nitrogen, tobacco mosaic virus replicative form RNA (TMV RF) was uniform in size but when prepared by high-speed homogenization, or when TMV RF prepared with liquid nitrogen was homogenized, 80 to 90% of the RF broke into relatively discrete pieces. The unbroken RF was not fragmented by additional homogenization. The TMV RF components susceptible and resistant to breakage, respectively, were synthesized with similar kinetics in relation to length of labelling period, but the slightly more resistant component was synthesized during the early infection period. Both components were produced by different strains of TMV but leaves infected with cowpea chlorotic mottle or southern bean mosaic viruses yielded only RF resistant to breakage. TMV replicative intermediate RNA was also broken by homogenization. The occurrence of the two RF components may be of significance in the replication of RNA viruses.

Nucleic Acid Denaturation↗

PubMed2003

Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2.

Growing evidence indicates that viral replication is regulated by the redox state of the host cell. We demonstrate that cells of different origins display differential permissivity for influenza A virus replication, depending on their intracellular redox power as reflected by Bcl-2 expression and glutathione (GSH) content. Bcl-2 expressing cells were found to have higher intracellular levels of GSH and to produce lower amounts of virus than Bcl-2 negative cells. Two different steps in the virus life-cycle were involved in Bcl-2/GSH mediated viral inhibition: 1) expression of late viral proteins (in particular hemagglutinin and matrix); and 2) nuclear-cytoplasmic translocation of viral ribonucleoproteins (vRNPs). Buthionine-sulfoximine-induced inhibition of GSH synthesis in Bcl-2 expressing cells caused an increase in the expression of late viral proteins but did not restore vRNP export to the cytoplasm. Collectively, our findings show that both Bcl-2 expression and GSH content contribute to the host cell's ability to down-regulate influenza virus replication, although their effects are exerted at different stages of the viral life-cycle. In certain cell populations, this form of down-regulation might conceivably favor the establishment of persistent viral infection.

Animals↗

PubMed1980

Inhibition of dengue virus replication by amantadine hydrochloride.

The effect of amantadine hydrochloride (1-adamantanamine hydrochloride) on dengue virus replication was examined in vitro. Amantadine decreased the titers of all four types of dengue viruses grown in LLC-MK2 cells by greater than 90% at concentrations of 50 micrograms/ml. There was no evidence for any cytopathic effect of the drug at concentrations less than 100 micrograms/ml. Studies of the time of addition showed that the antiviral effect was maximal when drug was added to virus cultures immediately after the viral adsorption period. In addition, amantadine caused a marked reduction in the growth of dengue virus type 2 in both human and rhesus peripheral blood leukocytes without affecting cell viabili ty. These findings demonstrate that amantadine significantly inhibits the replication of dengue viruses in vitro and indicate a need to determine the efficacy of this drug against dengue virus infections in vivo.

Amantadine↗

PubMed1990

Studies on adaptation of influenza virus replicated at low temperature.IV. Sensitivity of neuraminidase and hemagglutinin to some proteolytic enzymes, detergents and chemical agents.

Resistance against proteolysis enzymes, detergents and chemical group-specific reagents has been compared for the neuraminidase and hemagglutinin of influenza virus replicated at low temperature and original strain replicated at 37 degrees C before and after passage in the susceptible animal organism - cotton rat. Our study indicated great differences between strains and temperature conditions to resistance of the neuraminidase and hemaglutinin to proteolytic enzymes, detergens and chemical group specific reagents. No differences was found for sensitivity of influenza virus replicated at low temperature before and after passages for 3 strains -A/Pol/L/71, A/Phil/2/82, A/Pol/79/85 which are really cold adapted viruses. On the other hand neuraminidase of this strains was more resistance to these treatments.

Adaptation, Physiological↗

PubMed1979

Effect of passage history on dengue-2 virus replication in subpopulations of human leukocytes.

Three passage levels of dengue-2 virus strain PR-159, obtained during the course of deriving the attenuated S-1 vaccine, were tested for their ability to replicate in subpopulations of human peripheral blood leukocytes: (i) 6th primary African green monkey kidney (PGMK) cell passage (parent virus); (ii) 19th PGMK cell passage of a small-plaque-forming clone derived from the parent virus (S-1 PGMK virus); and (iii) virus derived by four additional passages of the S-1 PGMK virus in diploid fetal rhesus lung cells (S-1 vaccine virus). Replication of these PR-159 viruses and another strain of dengue-2 virus adapted to Raji cells (16681-Raji virus) was measured in adherent and nonadherent mononuclear cells. All viruses except the S-1 PGMK virus replicated in monocytes. Occasional replication of the S-1 PGMK virus was associated with reversion to parent virus. The addition to the monocyte cultures of low concentrations of homologous dengue-2 antibody or non-neutralizing heterologous antibody increased the yield of the parent virus as much as 400-fold. This phenomenon of immune enhancement usually enabled the S-1 PGMK virus to replicate slowly in monocytes, but the progeny virus produced large plaques similar to the parent virus. Replication of the S-1 vaccine virus in cultured monocytes did not result in the appearance of large plaques. We could not recover S-1 vaccine virus from monocytes harvested from infected volunteers in the same manner that monocytes from natural human infections yield wild virus. The three passage levels of PR-159 virus were tested for replication in lymphocytes in comparison with the 16681-Raji virus. Only the 16681-Raji virus replicated in human lymphocytes cultured with or without enhancing antibody.

Animals↗

PubMed2001

Inhibition of Mayaro virus replication by prostaglandin A(1) in Vero cells.

Prostaglandins exhibit antiviral activity against a wide variety of RNA and DNA viruses. In the present report, we describe the effect of cyclopentenone prostaglandin A(1) (PGA(1)) on Mayaro virus replication in Vero cells. Virus yield was significantly reduced at nontoxic concentrations which did not suppress DNA, RNA or protein synthesis in uninfected or infected cells. Antiviral action decreased if PGA(1) was added at later times after infection. In Mayaro virus-infected cells, PGA(1) inhibited the synthesis of virus proteins. This effect is accompanied by the induction of heat shock proteins (HSPs). Actinomycin D treatment not only inhibited the induction of HSPs but also partially prevented PGA(1) antiviral activity.

Alphavirus↗

PubMed1990

Chronic persistent hepatitis type B can be a progressive disease when associated with sustained virus replication.

In 44 hepatitis B virus (HBV) carriers with chronic persistent hepatitis (CPH), serial liver biopsies were available. At presentation 38 patients had HBV-DNA in their serum including 31 HBeAg positive and seven anti-HBe positive cases. The remaining six patients were anti-HBe positive and HBV-DNA negative. During a mean histologic follow-up of 4.2 years, 12 (32%) of the 38 HBV-DNA positive patients progressed to chronic active hepatitis (six cases) or to active cirrhosis (six cases), while 26 patients showed either unchanged features of CPH (21 cases), or histologic improvement to normal liver (five cases). Persistence of HBV-DNA in serum, independently of HBeAg/anti-HBe events, was significantly (p less than 0.01) associated with deterioration of liver disease, while termination of HBV replication correlated significantly (p less than 0.05) with spontaneous biochemical remission and with unchanged or improved histology. None of the six anti-HBe positive patients without serologic markers of hepatitis B virus replication showed histologic deterioration. These findings indicate that continuing HBV replication is a marker which predicts unfavourable evolution of chronic persistent hepatitis and frequent transition to chronic active hepatitis or cirrhosis.

Adolescent↗

PubMed1995

Bovine respiratory syncytial virus replicates minimally in bovine alveolar macrophages.

The interaction between two different bovine respiratory syncytial virus (BRSV) strains and bovine alveolar macrophages (BAMs) was studied in vitro. Bovine respiratory syncytial virus replicated minimally in BAMs and most of the virus produced remained cell-associated. Approximately 1 out of 1,000 BAMs produced infectious virus, a number that further declined during the 7 days of culture. In contrast, BAMs exposed to bovine parainfluenza 3 virus (PI3V) produced high amounts of infectious virus. The number of BAMs that contained BRSV antigen depended on the antigen load of the inoculum and not on the infectivity of the virus. Antibody mediated enhancement of infection was not detected. It is concluded that bovine alveolar macrophages exhibit a high intrinsic resistance to BRSV, but not to PI3V.

Animals↗

PubMed1995

High-level hepatitis B virus replication in transgenic mice.

Hepatitis B virus (HBV) transgenic mice whose hepatocytes replicate the virus at levels comparable to that in the infected livers of patients with chronic hepatitis have been produced, without any evidence of cytopathology. High-level viral gene expression was obtained in the liver and kidney tissues in three independent lineages. These animals were produced with a terminally redundant viral DNA construct (HBV 1.3) that starts just upstream of HBV enhancer I, extends completely around the circular viral genome, and ends just downstream of the unique polyadenylation site in HBV. In these animals, the viral mRNA is more abundant in centrilobular hepatocytes than elsewhere in the hepatic lobule. High-level viral DNA replication occurs inside viral nucleocapsid particles that preferentially form in the cytoplasm of these centrilobular hepatocytes, suggesting that an expression threshold must be reached for nucleocapsid assembly and viral replication to occur. Despite the restricted distribution of the viral replication machinery in centrilobular cytoplasmic nucleocapsids, nucleocapsid particles are detectable in the vast majority of hepatocyte nuclei throughout the hepatic lobule. The intranuclear nucleocapsid particles are empty, however, suggesting that viral nucleocapsid particle assembly occurs independently in the nucleus and the cytoplasm of the hepatocyte and implying that cytoplasmic nucleocapsid particles do not transport the viral genome across the nuclear membrane into the nucleus during the viral life cycle. This model creates the opportunity to examine the influence of viral and host factors on HBV pathogenesis and replication and to assess the antiviral potential of pharmacological agents and physiological processes, including the immune response.

Animals↗