Cellular Permissiveness
Mostrando 1-12 de 32 artigos, teses e dissertações.
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1. Human adenovírus serotype 41 interaction with hematopoietic cells: cellular permissiviness and viral gene expression analysis. / Interação do adenovírus humano, sorotipo 41, com células origem hematopoiética: análise da permissividade celular e da expressão gênica viral.
In order to verify the permissiveness of hematopoietic cells to HAdV-41 infection, PBMC and IEL from volunteers were infected. The infection assays were compared with infected HEK -293 cells. We analysed the E1A, E1B (55K), E3 (14K), VARNA, hexon and short fiber (SF) viral gene expression and GAPDH cellular gene expression. The mRNA were detected by real tim
Publicado em: 2008
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2. Regulating Intracellular Antiviral Defense and Permissiveness to Hepatitis C Virus RNA Replication through a Cellular RNA Helicase, RIG-I†
Virus-responsive signaling pathways that induce alpha/beta interferon production and engage intracellular immune defenses influence the outcome of many viral infections. The processes that trigger these defenses and their effect upon host permissiveness for specific viral pathogens are not well understood. We show that structured hepatitis C virus (HCV) geno
American Society for Microbiology.
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3. Replication of adeno-associated virus in cells irradiated with UV light at 254 nm.
Irradiation of simian virus 40 (ori mutant)-transformed Chinese hamster embryo cells (OD4 line) with UV light induced a cellular capacity which supported a full cycle of helper-independent adeno-associated virus replication. Monochromatic UV light at 254 nm was about 1,000-fold more effective than UV light at 313 nm, indicating that cellular nucleic acid is
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4. Transformation of human cells by oncogenic viruses supports permissiveness for parvovirus H-1 propagation.
Parvovirus H-1 has been shown to suppress spontaneous and chemically or virally induced tumorigenesis in hamsters. In human cell culture systems propagation of H-1 is restricted to transformed cells, which are killed by H-1 infection, in contrast to normal diploid cells, which are nonpermissive for H-1. By analyzing the permissiveness of a variety of human c
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5. Control of cytomegalovirus lytic gene expression by histone acetylation
Permissiveness for human cytomegalovirus (HCMV) infection is dependent on the state of cellular differentiation and has been linked to repression of the viral major immediate early promoter (MIEP). We have used conditionally permissive cells to analyze differential regulation of the MIEP and possible mechanisms involved in latency. Our data suggest that hist
Oxford University Press.
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6. Extracellular Vpr protein increases cellular permissiveness to human immunodeficiency virus replication and reactivates virus from latency.
The vpr gene product of human immunodeficiency virus (HIV) and simian immunodeficiency virus is a virion-associated regulatory protein that has been shown using vpr mutant viruses to increase virus replication, particularly in monocytes/macrophages. We have previously shown that vpr can directly inhibit cell proliferation and induce cell differentiation, eve
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7. Permissiveness of rabbit monocytes and macrophages for herpes simplex virus type 1.
The permissiveness of rabbit monocytes and macrophages for herpes simplex virus was examined. Peripheral blood monocytes, alveolar macrophages, and peritoneal exudate macrophages were studied for their ability to replicate herpes simplex virus strains RE and KOS. Results indicated different degrees of interaction with virus depending on the macrophage type.
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8. Relative permissiveness of macrophages from black and white people for virulent tubercle bacilli.
Epidemiological, clinical, and histopathological evidence suggests that black people are more susceptible to tuberculosis than are white people. The cellular basis of this putative susceptibility was investigated in vitro by comparing responses of blood-derived macrophages from black and white donors to experimental infection with virulent tubercle bacilli.
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9. Integrin αvβ3 mediates rotavirus cell entry
Rotavirus strains differ in their need for sialic acid (SA) for initial binding to the cell surface; however, the existence of a postattachment cell receptor, common to most, if not all, rotavirus strains, has been proposed. In the present study, antibodies to the αv and β3 integrin subunits, and the αvβ3 ligand, vitronectin, efficiently blocked th
The National Academy of Sciences.
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10. Mutational definition of the human immunodeficiency virus type 1 Rev activation domain.
Replication of human immunodeficiency virus type 1 requires the functional expression of the virally encoded Rev protein. The binding of this nuclear trans activator to its viral target sequence, the Rev-response element, induces the cytoplasmic expression of unspliced viral mRNAs. Mutation of the activation domain of Rev generates inactive proteins with nor
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11. Functional domains of the poliovirus receptor.
A number of mutant cDNAs of the human poliovirus receptor were constructed to identify essential regions of the molecule as the receptor. All mutant cDNAs carrying the sequence coding for the entire N-terminal immunoglobulin-like domain (domain I) confer permissiveness for poliovirus to mouse L cells, but a mutant cDNA lacking the sequence for domain I does
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12. Cell proteins bind to sites within the 3' noncoding region and the positive-strand leader sequence of measles virus RNA.
The genomic 3' noncoding region (NCR) of nonsegmented negative-strand RNA viruses contains recognition site(s) for the polymerase complex, while the RNA plus-strand leader sequence (LS) is probably involved in RNA encapsidation. It is known that host-encoded factors play a role in transcription and replication of some of this group of viruses. Here we report