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O Haller

Publications and source records attributed to O Haller.

At least 91 records · Page 5Linked to original sources
PubMed1985

Interferon-induced human protein with homology to protein Mx of influenza virus-resistant mice.

Polyclonal and monoclonal antibodies with specificity for protein Mx (a karyophilic 75,000-dalton protein induced by interferon [IFN] in mouse cells carrying the influenza virus resistance allele Mx+) detected an IFN-induced 80,000-dalton protein in peripheral blood lymphocytes and in fibroblasts of healthy human donors. The human protein, like protein Mx, was induced by IFN-alpha but not by IFN-gamma. Unlike the mouse protein, it was predominantly localized in the cell cytoplasm.

Alleles↗
PubMed1984

Mx-dependent resistance to influenza viruses is induced by mouse interferons alpha and beta but not gamma.

In cells derived from congenic BALB.A2G-Mx mice carrying the resistance gene Mx, but not in cells from BALB/c mice lacking Mx, mouse interferons alpha and beta induced the synthesis of a unique cellular protein that was associated with an efficient antiviral state with selectivity for influenza viruses. In contrast, native or recombinant mouse interferon gamma failed to efficiently protect Mx-bearing cells against influenza viruses and did not noticeably induce the synthesis of the Mx-associated protein, although interferon gamma was as effective as interferons alpha and beta in protecting BALB.A2G-Mx and BALB/c cells against the rhabdovirus VSV. These results demonstrate that different types of interferons differentially regulate the expression of the Mx gene and thereby induce distinct antiviral states.

Animals↗
PubMed1984

Genetic control of interferon action: mouse strain distribution and inheritance of an induced protein with guanylate-binding property.

Interferons (IFNs) induce in responsive cells the synthesis of various proteins including a set with high binding affinities to guanylates. These guanylate-binding proteins (GBPs) were analyzed in cells from 46 inbred mouse strains using GMP-agarose affinity chromatography. In cells of 11 strains, including A/J, BALB/cJ, and C3H/HeJ, type I and II IFNs induced the synthesis of a major GBP of Mr 65,000, designated here GBP-1, and of at least three minor GBPs. In contrast, cells of the remaining 35 strains, including DBA/2J, C57BL/6J, and A2G, failed to synthesize GBP-1 in response to both types of IFNs. Induction of the minor GBPs was comparable in cells of both groups of mice, confirming that they were all responsive to IFNs. Analysis of F1, F2, and BC1 offspring of crosses between GBP-1 inducible (A/J) and noninducible (DBA/2J or A2G) strains showed that inducibility of GBP-1 was inherited as a single autosomal gene. The symbol Gbp-1 is proposed for this locus, designated Gbp-1a for the allele causing inducibility and Gbp-1b for the other allele.

Alleles↗
PubMed1983

Interferon induces a unique protein in mouse cells bearing a gene for resistance to influenza virus.

Mouse cells carrying the dominant resistance gene Mx develop a more efficient antiviral state toward influenza viruses in response to interferon than do Mx-negative cells. We have identified an Mx gene-associated product by labeling cultured peritoneal macrophages and embryonic cells with [35S]methionine in the presence or absence of interferon. The radioactive proteins from unfractionated cytoplasmic extracts were separated electrophoretically in two dimensions and were revealed by fluorography. A protein with a Mr of 72,500 and an isoelectric point of 6.3 was induced by mouse interferon type I (a mixture of alpha and beta interferons) in cells carrying the gene Mx but not in cells lacking Mx. The induction of this protein could be blocked by actinomycin D. The maximal rate of synthesis was reached in embryonic cells 4-5 hr after treatment with 10(3) reference units of interferon per ml. When the allele Mx (present in the inbred mouse strain A2G) was repeatedly backcrossed on different genetic backgrounds (BALB/c, C57BL/6, A/J), a clear correlation between the inducibility by interferon of this protein and the presence of the allele Mx was observed. The results suggest that this protein induced by the interaction of interferon with Mx plays a role in the selective antiviral state against influenza viruses that is observed in interferon-treated Mx-bearing cells.

Animals↗
PubMed1983

Mx gene control of interferon action: different kinetics of the antiviral state against influenza virus and vesicular stomatitis virus.

The allele Mx regulates the extent to which interferon alpha/beta inhibits the growth of influenza viruses in mouse cells such as peritoneal macrophages. The time course of induction of the antiviral state against an influenza A virus is comparable in macrophages with and without Mx and is similar to that found with vesicular stomatitis virus. In contrast, the decay of the antiviral state against influenza virus is markedly slower in Mx-positive cells and slower than that against vesicular stomatitis virus observed in either Mx-positive or Mx-negative cells. Thus, after removal of interferon alpha/beta, Mx-positive cells remain protected against influenza virus at times when they have lost protection against vesicular stomatitis virus. These results suggest that interferon alpha/beta treatment activates different antiviral mechanisms, each acting against distinct groups of viruses and each independently controlled by host genes.

Animals↗
PubMed1982

Allelic forms of mouse transcobalamin 2.

Transcobalamin 2 is the only vitamin B12-binding protein found in mouse serum. Two allelic forms of mouse transcobalamin 2 are described. The two forms differ in their mobilities on polyacrylamide gel electrophoresis. The slowly migrating form has been found in serum from 25 inbred mouse strains. The more rapidly migrating form was detected in 3 inbred mouse strains (NZB, ST/bJ, and CPB-WV). Both parental variants were expressed in F1 progeny of appropriate interstrain crosses, showing codominant expression of the transcobalamin 2 alleles. In backcrosses between F1 and parental individuals, the two electrophoretic variants were inherited as single Mendelian traits. The strain distribution pattern of the two variants in recombinant inbred lines likewise suggested a single-gene mode of inheritance and indicated a lack of close linkage with a number of genetic loci on chromosomes 1, 2, 4, 5, 6, 7, 9, 12, 14, 15, and 17. We propose the symbol Tcn-2 for the polymorphic gene locus coding for transcobalamin 2 in the mouse and Tcn-2s and Tcn-2f for the two alleles.

Alleles↗
PubMed1982

Interferon independence of genetically controlled resistance to flaviviruses.

Flavivirus-resistant C3H/RV mice injected with sheep anti-interferon globulin and then infected with either West Nile or yellow fever virus survived and displayed no disease symptoms. Also, treatment of embryo fibroblast cultures prepared from C3H/RV or congenic susceptible C3H/HE mice with anti-interferon serum resulted in an increased yield of West Nile virus from both types of cultures, but the amount of infectious virus produced by resistant cultures remained 1 to 1.5 logs lower than that produced by susceptible cell cultures. These results indicate that the mode of expression of the flavivirus resistance gene differs significantly from that of the Mx gene conferring resistance to influenza virus-induced disease in A2G mice.

Animals↗
PubMed1982

Scoring rod-and-frame tests: quantitative and qualitative considerations.

An examination of current scoring procedures on the rod-and-frame test showed that these procedures depend on unrealistic assumptions about subjects' performance on the rod-and-frame test. A more general scoring procedure with more realistic assumptions was outlined and illustrated. Like the 1974 Nyborg procedure, this one (a) corrects for constant error, an error unrelated to current concepts of field dependence, (b) is sensitive to a subject's response strategy and choice of cues, i.e., a subject's qualitative aspects of rod-and-frame test performance, and (c) discriminates consistent from inconsistent responding. However, unlike Nyborg's procedure, this one also expresses field dependence relative to maximal field dependence given a subject's response strategy and choice of cue and utilizes all available information. This procedure is useful for the investigation of qualitative and quantitative aspects of rod-and-frame test performance and individual differences in laterality bias as defined by a constant error. Since this scoring procedure relies on computer scoring, a FORTRAN program has been made available.

Field Dependence-Independence↗
PubMed1981

Virus-specific interferon action. Protection of newborn Mx carriers against lethal infection with influenza virus.

The efficacy of interferon in antiviral protection of newborn mice differing at the Mx locus was investigated. Adult mice bearing the allele Mx exhibit a high degree of specific resistance toward lethal challenge with influenza viruses. In contrast, newborn Mx carriers are virtually as susceptible to influenza viruses as newborn mice devoid of Mx. Resistance can be abrogated by treating adult animals with anti-interferon serum. Here, we provide direct evidence of a virus-specific effect of interferon in vivo: newborn mice carrying the resistance gene Mx could be protected against lethal influenza virus infection with doses of interferon that were not protective in the absence of Mx. The efficacy of interferon towards a picornavirus (encephalomyocarditis virus) and a rhabdovirus (vesicular stomatitis virus) was independent of Mx.

Alleles↗
PubMed1981

Inborn resistance of mice to mouse hepatitis virus type 3 (MHV3): liver parenchymal cells express phenotype in culture.

Primary monolayer cultures of hepatocytes isolated from adult resistant A/J or partially resistant A/Sn or C3H/HeJ mice exhibited resistance to MHV3 as the respective macrophages do: Compared to susceptible C57BL/6 hepatocyte cultures, cytopathic effect occurred later and was restricted to small foci, coinciding with areas specifically labelled by immunofluorescence. Production of infectious particles was delayed, titers being 100 to 1000 fold lower at the moment of maximal yields in susceptible cultures. Pretreatment with interferon could reduce the titers in susceptible cultures to a level as seen in resistant cultures not treated with interferon. Nevertheless, interferon was not responsible for the genetic resistance of hepatocytes: it reduced virus titers in susceptible and resistant cultures to the same extent and the addition of specific antibodies to interferon after infection did not augment susceptibility of resistant cultures. We assume that intrinsic resistance of liver parenchymal cells is an important facet of inborn resistance of mice in vivo.

Animals↗
PubMed1981

Spontaneous reference systems in individuals.

In a series of five experiments the referencing function of spatial structures was investigated. The problem was (a) to determine whether subjects' effective frames of reference and their object figures could be experimentally identified, (b) to determine whether the analyses developed for this purpose were adequate, and (c) to determine some conditions of frames of reference. Graduate and undergraduate students were asked to reconstruct and to recall multiply-embedded figures viewed earlier. In these figures the spatial orientation of the figure elements was manipulated. Both reconstruction and recall errors were analyzed to identify subjects' effective frames of reference and their object figures. A single-subject design was used throughout. Frames of reference and their objects could be identified in Exp. 1. This experiment also showed the appropriateness of the analyses. Exp. 2 indicated that embedding figures provide one condition for identifying frames of reference. Exps. 3 to 5 demonstrated that changes in element figures, measurement, and reduction of trials and number of elements did not eliminate frames of reference. Differences in types of frames of reference were found. These differences were interpreted to indicate that some subjects use content, others formal schema (referents) to evaluate spatial orientation.

Adult↗
PubMed1980

Interferon-dependent genetic resistance to influenza virus in mice: virus replication in macrophages is inhibited at an early step.

Inborn resistance to orthomyxoviruses due to the allele Mx was investigated at the molecular level in macrophages from A2G mice. In the absence of interferon, Mx-bearing and control cells were equally permissive for M-TUR, a macrophage-adapted strain of influenza A virus. After treatment with various doses of mouse interferon type I, Mx-bearing cells were fully resistant to this virus whereas cells lacking Mx were only marginally protected. Virus attachment and penetration were equally efficient in Mx-carrying and control cells and were not influenced by interferon. However, virus protein synthesis was blocked in Mx-bearing macrophages expressing resistance. These findings indicate that the resistance mechanism specific for influenza viruses realized by Mx in cooperation with interferon inhibits influenza virus replication in macrophages at an early stage following attachment and penetration of the virus.

Alleles↗