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PubMed1987

Viral oncolysis in the A2G mouse revisited: monoclonal antibody-mediated tumor rejection.

A2G mice can be immunized against the Ehrlich ascites tumor (EAT) by influenza virus oncolysis or with influenza virus oncolysates. To facilitate studies of the cellular antigens immunopotentiated by viral oncolysis, monoclonal antibodies (mAbs) against EAT cells were produced from postoncolytic EAT-immune A2G mice. Reciprocal competitive binding on EAT cells was used to classify the mAbs into epitope-related groups. One mAb, 198.9, could fully protect A2G mice against EAT cell challenge, could rescue A2G mice from an established EAT, and could mediate lysis of EAT cells in vivo. mAb 198.9 provides a new tool for studying the biochemical characteristics and immunological properties of a cellular antigen centrally involved in this model.

Animals↗
PubMed1987

Interferons: from virus inhibitor to modulator of amino acid and lipid metabolism.

Purity of interferons has facilitated definition of pleiotropic biological effects. Alterations that might be suspect with use of impure interferons, such as those occurring in tryptophan and lipoprotein metabolism, have been defined both in vitro and in humans. Reduction in tryptophan contributes to antimicrobial effects for intracellular pathogens and may explain some clinical observations. Decreases in plasma lipoproteins occur rapidly and are of a magnitude similar to cholesterol-lowering drugs used clinically. Alteration in metabolism of amino acids and fats substantially extends the biological effects of a virus-inhibitory protein.

Amino Acids↗
PubMed1987

Do the interferons act singly or in combination?

Our views of interferon production and action have evolved from the simple to the complex. We review evidence that interferon-gamma (IFN-gamma) may induce a portion of its antiviral activity through the induction of another interferon. This is shown by demonstrating IFN-alpha in the supernatant fluids of IFN-gamma-treated mouse cells and showing that, under certain conditions, the antiviral activity of IFN-gamma in mouse and human cells can be reduced by antibody to IFN-alpha or IFN-beta, respectively. Induction of mouse spleen, bone marrow, and peritoneal exudate cells also results in their production of IFNs-alpha and/or -beta. In addition, new preliminary data indirectly suggests the presence of IFN-gamma in poly(IC):poly(LC)-treated mouse cells. In both of these systems, the maximal antiviral activity appears to develop as a consequence of the induction of a second interferon.

Animals↗
PubMed1987

Influenza virus resistance of wild mice: wild-type and mutant Mx alleles occur at comparable frequencies.

The laboratory-reared progeny of wild Mus musculus domesticus from several places in Europe and from California were tested for resistance to experimental infection with influenza viruses and for the ability of their explanted macrophages to synthesize Mx protein in response to type I interferon. About 75% of these mice were resistant to influenza viruses and were able to synthesize Mx protein, as expected for mice carrying the influenza virus resistance allele Mx+ in either homozygous or heterozygous form. Resistance of wild mice was inherited as a single autosomal dominant trait which cosegregated with the ability to synthesize Mx protein. About 25% of the randomly bred wild mice failed to synthesize Mx protein and died after infection with influenza virus, very much like inbred mice homozygous for the Mx- allele. We conclude that Mx+ and Mx- alleles occur at roughly equal frequencies in wild mice and that some selective advantage for heterozygous individuals exists in the wild. This finding raises new questions about the physiological role of the Mx locus.

Animals↗
PubMed1987

Transport of the murine Mx protein into the nucleus is dependent on a basic carboxy-terminal sequence.

Cytoplasmic microinjection of murine Mx mRNA synthesized in vitro or nuclear microinjection of Mx cDNA under the control of a constitutive promoter into murine Mx- cells led to the accumulation of Mx protein in the nucleus and inhibited the replication of influenza virus but not of vesicular stomatitis virus (VSV). Similar results were also found with dog, rat, chicken, and monkey cells. A human lung fibroblast cell line (A549) was exceptional in that Mx protein was located predominantly in the cytoplasm and showed antiviral activity. Truncation of the 19 last residues of murine Mx protein almost completely abolished accumulation of Mx protein in the nucleus; however the activity against influenza virus was at least partially retained. The truncated region contains a segment rich in basic amino acids, similar to that reported for several nuclear location signals.

Amino Acid Sequence↗
PubMed1988

The sensitivity of domestic animal cell lines to eight recombinant human interferons.

The biological activities of eight recombinant human interferons (IFNs) were tested on permanent cell lines and low-passage embryonic cultures from domestic animal tissues. Each titer was compared to its titer on Madin-Darby bovine kidney (MDBK) cells. Although different cells within a species had different sensitivities to different IFNs, the order of sensitivity, in general, was ox, sheep, pig, cat, horse, and dog, the latter being quite insensitive to most IFNs.

Animals↗
PubMed1988

Interferons-alpha/beta- and -gamma-resistant Friend cell variants exhibiting receptor sites for interferons but no induction of 2-5A synthetase and 67K protein kinase.

A number of Friend leukemia cell variants with a interferon-gamma (IFN-gamma)-resistant phenotype have been isolated. They appear resistant to the antiproliferative action of IFN-gamma and to the induction of the antiviral state assessed by Friend leukemia virus release and vesicular stomatitis virus yield. Selection was performed via a prolonged exposure to increasing amounts of highly purified recombinant IFN-gamma of wild-type Friend cells or of variant clones thereof already resistant to IFN-alpha/beta (Affabris et al., 1982, Virology 120, 441-452). Only the clones derived from IFN-alpha/beta-resistant variants showed a phenotype fully resistant to IFN-gamma treatment while keeping their previously acquired resistance to IFN-alpha/beta. These cells are not deficient in high-affinity receptors for IFN-gamma so that their resistant phenotype appears to be mediated by events distal to binding of IFN-gamma to its receptors. Furthermore, analysis of IFN-induced dsRNA-dependent 2-5A synthetase and 67K protein kinase enzymatic activities, biochemical markers for cellular responses to IFN, showed that both these activities were not induced in IFN-alpha/beta and IFN-gamma-resistant clones when treated with either type of IFN. Accordingly, no increased expression of 2-5A synthetase mRNA(s) could be detected by probing poly(A)+-enriched RNA from cells exposed to IFN-alpha/beta or IFN-gamma treatment with murine or human specific cDNAs. On the other hand, no major changes in restriction patterns of 2-5A synthetase gene(s) were observed in these variant cells by restriction endonuclease digestion and Southern blotting. In addition, analysis of 2-5A synthetase mRNA induction, performed on wild-type cells, showed that the kinetic of induction due to IFN-gamma treatment is slower than that obtained with IFN-alpha/beta.

2',5'-Oligoadenylate Synthetase↗
PubMed1988

Structure-function analysis of murine interferon-alpha: antiviral properties of novel hybrid interferons.

As described earlier the protein products of the murine interferon (IFN) genes MuIFN-alpha 1, -alpha 2, and -alpha 4 differ in their antiviral activity on hamster (CHO) and mouse (L929) cells. For structure-function analysis, hybrids were prepared between the three genes using common restriction enzyme sites. Natural and hybrid genes were transiently expressed in monkey COS cells. Under the conditions used IFN constituted 20-30% of the total amount of secreted proteins. Using a panel of hybrids either between alpha 1 and alpha 2 or between alpha 1, alpha 2, and alpha 4, the amino-terminal region of the protein, from amino acids 10 to 58, was found to determine its antiviral activity on hamster cells. On mouse cells, the antiviral activities of hybrids between alpha 4 and either alpha 1 or alpha 2 were compared. The high activity of alpha 4 (five to ten times that of alpha 1 or alpha 2) was not transmitted to hybrids having the amino-terminal part of alpha 4, but coincided with the presence of the alpha 4 carboxy-terminal region in all but one hybrid construct. The deletion of five amino acids (positions 103-107) located in this region of alpha 4 did not affect antiviral activity when introduced into MuIFN-alpha 2 and a MuIFN-alpha 42 hybrid by site-directed mutagenesis.

Animals↗
PubMed1989

Interferon production by the preimplantation sheep embryo.

Ovine trophoblast protein-1 (oTP-1), the major product secreted by the trophectoderm of the sheep conceptus between days 13 and 21 of pregnancy, is considered to mediate maternal recognition of pregnancy by maintaining the function of the corpus luteum. Its amino acid sequence has 40-55% identity with various mammalian interferons-alpha (IFN-alpha), and it has been shown to have antiviral activity. The present results confirm that oTP-1, which at days 15-17 of pregnancy is produced by a single embryo at more than 100 micrograms (greater than 1 million antiviral units) per day, is a functional IFN. A preparation of purified oTP-1 was made. Its amino-terminal sequence suggested that it consisted of a single homogeneous protein, so that its antiviral activity probably was not due to a contaminant. In a cytopathic effect inhibition assay with GBK-2 bovine cells challenged with vesicular stomatitis, its specific activity was 1.3 X 10(7) end point units/mg protein. It also protected GBK-2 cells against four other viruses, and A549 human cells against encephalomyocarditis virus. The antiviral activity was neutralized by an antiserum to human leukocyte IFN. Like human IFN-alpha, oTP-1 at concentrations as low as 10(-9) M inhibited the growth of GBK cells in culture and suppressed mitogen-stimulated incorporation of [3H]thymidine into ovine lymphocytes. Possible roles for oTP-1, functioning as an IFN-alpha during early pregnancy, are discussed.

Age Factors↗
PubMed1989

Significant differences in therapeutic responses to a human interferon-alpha B/D hybrid in Rauscher or Friend murine leukemia virus infections.

Treatment of mice infected with Rauscher (RMLV) or Friend (FMLV) murine leukemia viruses at an early stage of disease (beginning at day 0 and continuing every other day for 21 days) with 5 x 10(7) units/kg body weight of a cross-species-active recombinant human interferon-alpha B/D hybrid (rHuIFN-alpha B/D) was more effective in FMLV than in RMLV infections. In contrast, treatment with 5 x 10(7) units/kg body weight of IFN beginning as late as 15 days postinfection and continuing every other day for 21 days was more effective in RMLV than in FMLV infections. These differences were consistent with observed changes in circulating white blood cells, spleen weight, and reverse transcriptase levels. Additionally, biweekly long-term administration (beginning at day 0) of 5 x 10(6) units/kg of rHuIFN-alpha B/D (an ineffective treatment in short-term therapy) significantly prolonged the mean survival time of RMLV-infected mice, but only weakly prolonged that of FMLV-infected mice.

Animals↗
PubMed1989

Comparative susceptibility of respiratory viruses to recombinant interferons-alpha 2b and -beta.

Intranasal recombinant interferon-alpha 2b (rIFN-alpha 2b) protects against natural colds due to rhinoviruses, but apparently not against those caused by viruses. Because rIFN-beta serine17 (rIFN-beta ser) appears less active than rIFN-alpha 2b in preventing natural rhinovirus colds, we compared the two IFNs in two in vitro assays against selected respiratory viruses. In a yield reduction assay, both IFNs had comparable activity against rhinovirus types 39 and 1A and coronavirus 229E, which were inhibited by 90% or more at IFN concentrations of 10(-11) to 10(-10) gram of protein/ml (approximately 2-20 IU/ml). Similar activities were observed with rIFN-beta ser against rhinoviruses isolated from clinical specimens. At concentrations of 10(-9) gram protein/ml, both IFNs inhibited the growth of influenza A and parainfluenza viruses, but not of adenovirus or respiratory syncytial virus in the cell culture systems tested. Thus, the different clinical protection conferred by rIFN-alpha 2b and rIFN-beta ser in studies of natural rhinovirus colds are not accounted for by differences in their in vitro activity against these viruses, and other explanations must be found.

Biological Assay↗
PubMed1989

The role of interferon in the protection of ICR Swiss male mice by the nondiabetogenic variant of encephalomyocarditis virus against virus-induced diabetes mellitus.

The production of murine diabetes mellitus by the diabetogenic variant of encephalomyocarditis virus (EMCV-D) is prevented in mice preinfected for 24 h with nondiabetogenic virus (EMCV-B). It has been suggested that the protection of the animals is due to the induction of interferon (IFN) by EMCV-B. The present study was done to investigate further the role of IFN in the protection of male ICR Swiss mice against the diabetogenic effects of EMCV-D virus. The results show that this mouse strain is protected only by viable EMCV-B given by either the i.v. or i.p. route of inoculation and that the protection is not abrogated by anti-IFN gamma-globulin. Further, the animals were not protected by either IFN-alpha, IFN- beta, or IFN- alpha/beta at concentrations shown previously to protect mice against the lethal effects of other variants of EMCV. The data provide further evidence that, in the ICR Swiss mouse, IFN does not play a major role in protecting pancreatic beta-cells against infection by EMCV-D.

Animals↗
PubMed1987

Clonal analysis of the T-cell response of mice to herpes simplex virus: correlation between lymphokine production in vitro and the induction of delayed-type hypersensitivity and antiviral activity in vivo.

The properties of two morphologically distinct L3T4+, Lyt2- "helper" T-cell clones specific for herpes simplex virus were investigated. Both of the clones produced IL-3 and interferon, but neither produced IL-2. Clone D6.6 produced macrophage agglutinating factor, a fibronectin-like lymphokine, and also a delayed hypersensitivity (DH) response when injected locally into syngeneic mice. Despite the presence of a DH producing clone and a non-DH producing clone, both were able to reduce the local virus titre to an equivalent degree. It is suggested that this protective activity is associated with the production of interferon-gamma. The significance of these results to mechanisms of protection against herpes simplex virus in vivo is discussed.

Animals↗