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PubMed1973

Enhancement of Sendai virus-mediated cell fusion by cupric ions.

The effect of divalent cations on cell fusion by concentrated Sendai virus, inactivated by beta-propiolactone, was investigated using Vero and mouse L-929 cells in monolayers. With both cell lines, which are normally resistant to exogenous viral fusion, Cu(2+) in sublethal concentrations was found to promote polykaryon formation to a marked degree. The simultaneous presence of Cu(2+) and virus was required for this effect, which was thought to be related to the cytotoxic action of Cu(2+) on the cell membrane. Accordingly, under standard conditions and in the absence of virus, leakage of isotopically labeled intracellular protein was shown to bear a quantitative relationship to Cu(2+) concentration. Concomitant changes in the membrane were seen electron microscopically to consist of loss of microvilli and the appearance of numerous vesicles on, or adjacent to, the membrane. The relationship of enhanced fusibility to these toxic changes was not further elucidated. The fusion-promoting effect of Cu(2+) far exceeded that of Ca(2+); and other cations tested had no effect.

Amnion↗
PubMed1973

The linkage of genes for the human interferon-induced antiviral protein and indophenol oxidase-B traits to chromosome G-21.

13 independent mouse-human somatic cell hybrid clones derived from beta-propiolactone-inactivated Sendai stimulated cell fusion of human cells with mouse cells were tested for their sensitivities to human and mouse interferon. All of them were protected by mouse interferon and only six of the clones were protected by both human and mouse interferon. Only the six that were protected by human interferon were shown to express the human dimeric form of indophenol oxidase. Complete chromosomal analysis of the clones indicated human chromosome G-21 to be the only human chromosome in common for the six clones which had both phenotypes present. Nine subclones were derived from one of the clones expressing both phenotypes. Eight of the nine subclones were shown to retain both phenotypes, whereas one subclone lost both. Chromosomal analysis of the subclones indicated the loss of chromosome G-21 from the subclone which lost both phenotypes. It is apparent from these findings that the gene(s) for indophenol oxidase (IPO-B) and the gene(s) for the antiviral protein are syntenic and that they are linked to human chromosome G-21.

Animals↗
PubMed1997

Anti-major histocompatibility complex antibody responses to simian B cells do not protect macaques against SIVmac infection.

Macaques have been protected against infection with human cell-grown SIVmac by immunization with antigens encoded by the human major histocompatibility complex (MHC). Here, we investigated the efficacy of alloimmunization with simian B cells expressing high levels of MHC class I and class II molecules to confer protection against systemic challenge with simian-grown SIVmac. Eight rhesus macaques were vaccinated with glutaraldehyde-fixed and beta-propiolactone-inactivated herpesvirus papio-transformed B cells. Four of the macaques received 5 doses, the others 10. Animals were challenged with rhesus macaque spleen-derived cell-free SIVmac. Allogeneic B cells elicited antibody responses to rhesus MHC class I and II but failed to protect animals against infection. Anti-MHC class I antibodies were restricted in specificity and failed to recognize MHC class I from some B lymphoblastoid cell lines (B-LCLs) including a B-LCL from the animal in whose cells the challenge virus was grown. Vaccinated animals responded to self-MHC class I antigens but not to self-MHC class II antigens from peripheral blood mononuclear cells (PBMCs). Animals that underwent the shorter immunization regimen had transiently enhanced PBMC-associated virus loads after challenge, whereas the average virus-infected cell load was reduced in animals that underwent the more extensive immunization. These results suggest that antibody responses to allogeneic MHC molecules do not protect against infection with immunodeficiency lentiviruses.

Adoptive Transfer↗
PubMed1985

Carcinogen specificity in the activation of transforming genes by direct-acting alkylating agents.

DNAs from rat nasal and mouse skin carcinomas and fibrosarcomas induced by the alkylating agents methylmethane sulfonate (MMS), beta-propiolactone (BPL), and dimethylcarbamyl chloride (DMCC) were tested for their ability to transform NIH3T3 cells by DNA transfection. Each of eight MMS-induced rat nasal carcinomas and two of five BPL-induced mouse skin tumors were positive in the transfection assay while all of four fibrosarcomas and six carcinomas induced by DMCC were negative. Anchorage independent growth, tumorigenicity in nude mice, and secondary transfection confirmed the transformed phenotype of the positive transfectants. The transfectants from MMS-induced tumor DNAs did not contain restriction fragments homologous to rat H-, K- or N-ras oncogenes although exogenous (rat) tumor-derived DNA sequences were detected in transfectant genomes by Southern analysis. In contrast a BPL-induced mouse skin tumor showed evidence of containing activated H-ras. These results suggest specificity among causal chemical carcinogens for activation of transforming genes in experimental tumors.

Alkylating Agents↗
PubMed1974

Lack of chemically induced mutation in repair-deficient mutants of yeast.

Two genes, rad6 and rad9, that confer radiation sensitivity in the yeast Saccharomyces cerevisiae also greatly reduce the frequency of chemically-induced reversions of a tester mutant cyc1-131, which is a chain initiation mutant in the structural gene determining iso-1-cytochrome c. Mutations induced by ethyl methanesulfonate (EMS), diethyl sulfate (DES), methyl methanesulfonate (MMS), dimethyl sulfate (DMS), nitroquinoline oxide (NQO), nitrosoguanidine (NTG), nitrogen mustard (HN2), beta-propiolactone, and tritiated uridine, as well as mutations induced by ultraviolet light (UV) and ionizing radiation were greatly diminished in strains homozygous for either the rad6 or rad9 gene. Nitrous acid and nitrosoimidazolidone (NIL), on the other hand, were highly mutagenic in these repair-deficient mutants, and at low doses, these mutagens acted with about the same efficiency as in the normal RAD strain. At high doses of either nitrous acid or NIL, however, reversion frequencies were significantly reduced in the two rad mutants compared to normal strains. Although both rad mutants are immutable to about the same extent, the rad9 strains tend to be less sensitive to the lethal effect of chemical mutagens than rad6 strains. It is concluded that yeast requires a functional repair system for mutation induction by chemical agents.

Cytochrome c Group↗
PubMed1985

Rhesus diploid rabies vaccine (adsorbed): a new rabies vaccine using FRhL-2 cells.

The FRhL-2 cell line, a diploid line derived from the lung of a fetal rhesus monkey, was used to prepare a potent rabies vaccine by adapting the Kissling strain of rabies virus to FRhL-2 cells, growing the virus in quantity, inactivating the virus with beta-propiolactone, and concentrating the virus by adsorption to aluminum phosphate. High levels of antibody to rabies virus, induced by the vaccine in both guinea pigs and humans at 14 days after immunization, were determined to be IgG. Data from postexposure protocols with guinea pigs and simulated postexposure protocols in humans showed protection and antibody response even when rabies immune globulin was administered at the time of vaccination.

Animals↗
PubMed1992

Infectious respiratory syncytial virus (RSV) effectively inhibits the proliferative T cell response to inactivated RSV in vitro.

The effect of respiratory syncytial virus (RSV) on the cellular immune response of human mononuclear cells in vitro was examined. Inhibition by RSV of the lymphocyte response to phytohemagglutinin in vitro was confirmed using cells from human umbilical cord blood. In addition, RSV significantly inhibited both the proliferative and T cell colony responses of human mononuclear cells to Epstein-Barr virus. An RSV-specific cellular immune response was induced in vitro by stimulation of mononuclear cells from RSV-seropositive donors with beta-propiolactone-inactivated RSV. This RSV-specific response was significantly inhibited by infectious RSV itself, and the inhibition was mediated by an extracellular factor produced by RSV-infected mononuclear cells. A similar inhibition in vivo of the RSV-induced cellular immune response may contribute significantly to delayed recovery from primary infection and to reduced resistance to subsequent infections.

Antigens, CD↗
PubMed1977

Chromosome aberrations and sister chromatid exchanges in Chinese hamster cells exposed to various chemicals.

To evaluate its usefulness for detection of mutagenicity and oncogenicity of chemicals, the frequency of chromosome aberrations and sister chromatid exchanges (SCE) was examined in cultured Chinese hamster cells exposed to 33 kinds of chemical agents, including 2 aromatic hydrocarbons, 7 amine derivatives, 3 phenols, 6 carboxylic acid derivatives, 4 azo compounds, 7 heterocyclic compounds, and 4 other types of agents. Among them, 7 chemicals, including 5 known oncogens (N-n-butyl-N-nitrosourethan, N-methyl-N-nitrosourea, beta-propiolacton, methylazoxymethanol acetate, and propane sultone) and 2 non-oncogens (potassium sorbate and sodium benzoate) were inducers of aberrations and/or SCE, although the effective doses for the last two agents were considerably higher. The mutagenic activities estimated by chromosome aberrations were not necessarily the same for a given chemical when estimated by SCE. Slightly to moderately increased rates of SCE or aberrations were noticed among the other 26 chemicals. However, these values were usually without a clear dose relationship.

Amines↗
PubMed1994

Validation of the in vivo CD1 mouse splenocyte micronucleus test.

In order to validate the in vivo micronucleus test in mouse splenocytes using the cytokinesis block method, 14 compounds with various mechanisms of action were tested: three direct alkylating agents (mitomycin C, ethylnitrosourea, beta-propiolactone), seven indirect alkylating agents (cyclophosphamide, benzo[a]pyrene, diethylnitrosamine, dimethylnitrosamine, 4-aminophenol, 4-aminobiphenyl, 1,1-dimethylhydrazine), two intercalating agents (acridine orange, ethidium bromide) and two spindle poisons (vincristine, colchicine). Male mice were dosed once with the compound, and spleen samples were taken 2 or 14 days after treatment. A significant increase in the binucleated micronucleated splenocyte rate was observed with all the alkylating and intercalating agents at at least one sampling time. In contrast, no increase in the binucleated micronucleated splenocyte rate was observed with the spindle poisons. In conclusion, under these experimental conditions, this in vivo test seems appropriate for the detection of clastogenic compounds including compounds that cannot be detected in the bone marrow micronucleus test. The limit of this test, as expected, is the lack of detection of aneugenic compounds.

Alkylating Agents↗
PubMed1991

Antibody-dependent cellular cytotoxicity against HIV-1 in sera of immunized chimpanzees.

After immunization of chimpanzees against HIV antigens, antibodies that mediate antibody-dependent cellular cytotoxicity (ADCC) were evaluated and compared with anti-HIV-antibody levels detected by enzyme-linked immunosorbent assay (ELISA) and neutralizing antibody titers. Adult chimpanzees were immunized with different HIV-1 (LAV-BRU) antigen preparations: recombinant vaccinia virus (rVV) expressing gp160, p25 or p27nef; formalin- and beta-propiolactone-inactivated whole virus (inHIV); soluble recombinant gp160 either associated or not associated with other HIV proteins; a 25-mer peptide from the V3 region of gp120 coupled with KLH (V3-KLH). Immunization with the various rVV mixtures induced no or borderline ADCC increase above preimmune serum levels. Stronger and more sustained reactivity was elicited by inHIV. Purified HIV antigens elicited ADCC activity when the chimpanzees were naive; ADCC increased or remained at the same level when the animals had been preimmunized with rVV and/or inHIV. This type of reactivity apparently did not depend on whether gp160 alone or mixed with other proteins was used for immunization. The injection of V3-KLH resulted in only little, if any, recall ADCC response. ELISA antibody titers significantly correlated with ADCC and neutralizing antibody titers, but serum ADCC was independent of neutralizing antibody titers, an indication that the two latter serum activities are mediated by independent antibodies. Therefore, ADCC is elicited in the same manner as other antibody activities by the immunization of chimpanzees with inHIV or with purified recombinant HIV antigen preparations. The results obtained from the three chimpanzees of this series, which were subsequently challenged with infectious virus through the intravenous route, suggest that serum ADCC may be considered for vaccination purposes.

Amino Acid Sequence↗
PubMed1981

Entry of rabies virus into the peripheral nerves of mice.

Young adult mice were inoculated in the hind limb with rabies virus or Sindbis virus. Rabies 1820B virus antigen was detected in leg sections by immuno-fluorescence at 1 h post-inoculation at sites comparable in form and distribution to cholinesterase-positive sites, which represent motor end-plates (MEPs). Sites which were rabies virus antigen-positive by immunofluorescence were also cholinesterase- positive on double-stained slides. Rabies CVS virus detected by autoradiography was similarly distributed at 6 h post-inoculation. Uptake of rabies virus at motor nerve endings was confirmed by the detection of rabies antigen by immunofluorescence in ventral horn cells in the spinal cord at 20 h post-inoculation before involvement of dorsal root ganglia. Rabies virus antigen could not be detected at MEPs if the virus had been inactivated by beta propiolactone or mixed with antibody prior to injection or if the sciatic nerve had been cut 7 days earlier, similarly treated groups of mice survived for the observation period of 6 weeks. Rabies virus antigen was found at MEPs in mice given antibody 24 h before virus injection, but virus antigen was not found in the spinal cord, and mice similarly treated survived. Sindbis virus strain Ar86, which like rabies virus is neurotropic in adult mice, was also found at MEPs and in peripheral nerves by autoradiography at 6 h post-inoculation. In contrast to results with rabies virus-infected mice, stimulation of the sciatic nerve for the first hour post-inoculation prevented mortality. Sindbis virus strain Ar339, which is not neurotropic in adult mice, could not be detected at MEP's by immunofluorescence or autoradiography and mice injected with virus survived. The results presented here suggest that rabies virus and perhaps other neurotropic viruses can use the motor axon terminal at the neuromuscular junction as a site of entry into the nervous system.

Animals↗
PubMed1986

Chromosome damage induced by herpes simplex virus type 1 in early infection.

The chromosome damage induced by herpes simplex virus type 1 (HSV-1) in vitro was examined up to 6 h after infection using HT-1080 cells. Initial damage occurring within 3 h was specific, involving uncoiling of chromosome 1q12-21 and to a lesser extent the pericentric regions of chromosomes 9, 16 and satellited chromosomes. For the initial unwinding, synthesis of the immediate early class of HSV proteins needed to occur as was demonstrated using HSV-1 temperature-sensitive mutants tsK and tsB7 and two viral inhibitors, beta-propiolactone and psoralen plus long wavelength u.v. light. Later damage included chromatid breaks, acentric fragments and pulverization which did not take place until synthesis of delayed early proteins had begun.

Cell Line↗
PubMed1986

Coronavirus IBV: virus retaining spike glycopolypeptide S2 but not S1 is unable to induce virus-neutralizing or haemagglutination-inhibiting antibody, or induce chicken tracheal protection.

Avian infectious bronchitis coronavirus (IBV) inactivated by beta-propiolactone induced partial protection of the trachea in up to 40% of chickens following one intramuscular inoculation 4 to 6 weeks prior to challenge. Retention of an intact tracheal ciliated epithelium 4 days after challenge was the criterion of protection. There was no correlation between protection and serum titres of virus-neutralizing (VN) and haemagglutination-inhibiting (HI) antibody, which were maximal at about 4 weeks after inoculation. Virus from which the S1 but not the S2 (spike-anchoring) spike glycopolypeptide had been removed by urea did not induce protection or VN or HI antibody. Four intramuscular inoculations of monomeric S1 induced VN and HI antibody in two and four chickens respectively. These results indicate that VN and HI antibodies are induced primarily by S1, that intact spikes are a major requirement for the induction of protective immunity and that this property is probably associated with S1.

Animals↗
PubMed1988

Alphaherpesvirus saimiri in rabbits: a model for human encephalitis?

One (KM91) of a series of isolates of alphaherpesvirus saimiri (alpha HVS) produced rapidly fatal encephalitis in rabbits following intradermal infection, whereas the others (KM180, KM322 and KM338) were non-lethal and produced ganglionitis and prolonged latency. Alphaherpesvirus saimiri KM91 initially produced ganglionitis but quickly ascended the spinal cord to the brain causing death 10 days post-infection. Prior infection with any of the three benign isolates or inoculation with beta-propiolactone (beta PL)-inactivated alpha HVS KM91 protected rabbits from lethal encephalitis when they were subsequently challenged with a lethal dose of alpha HVS KM91. Each of 20 rabbits co-inoculated in the same site with a lethal dose of alpha HVS KM91 and either alpha HVS KM322 (1.5 X 10(3) to 1.5 X 10(5) p.f.u.) or beta PL-inactivated alpha HVS KM322 (1 X 10(7) p.f.u. equivalents) survived. In contrast only half of those co-inoculated with alpha HVS KM91 and beta PL-inactivated alpha HVS KM91 (1 X 10(7) p.f.u. equivalents) survived. Co-inoculation of lethal alpha HVS KM91 (75 p.f.u.) and benign alpha HVS KM322 (1.5 X 10(3) p.f.u.) into opposite flanks resulted in protection from encephalitis in one of four rabbits. Alphaherpesvirus saimiri KM91 was shown to have the capacity to become latent in dorsal root ganglia if the rabbit did not die.

Animals↗
PubMed1989

Protection of mice from lethal influenza by adoptive transfer of non-neutralizing haemagglutination-inhibiting IgG obtained from the lungs of infected animals treated with defective interfering virus.

The lungs of C3H/HeMg mice infected with a lethal dose of the influenza virus A/WSN (H1N1) contained antibody to the viral neuraminidase glycoprotein but not to the haemagglutinin (HA). When coinoculated with a life-saving amount of defective interfering (DI) WSN, lungs were found to contain both anti-neuraminidase and haemagglutination-inhibiting (HI) antibodies which peaked at 3 and 5 days post-infection (p.i.), respectively. Mice coinoculated with WSN and beta-propiolactone-inactivated DI WSN had only anti-neuraminidase antibody in the lungs. The HI activity was unusual in that there was no detectable neutralizing activity. The HI activity has been affinity-purified by adsorption to and elution from WSN HA and consisted entirely of IgG, comprising isotypes IgG1, IgG2a and IgG2b. The antibody was specific for WSN HA, of low activity and had disappeared from the lungs by 20 days p.i. Transfer of affinity-purified HA-specific, non-neutralizing antibody to mice 24 h before infection with WSN alone protected 60% from death. We conclude that the antibody contributes significantly to the life-saving activity of DI WSN virus and that the ability to stimulate such antibody represents a novel property of this DI virus.

Animals↗
PubMed2006

Comparative evaluation of two severe acute respiratory syndrome (SARS) vaccine candidates in mice challenged with SARS coronavirus.

Two different severe acute respiratory syndrome (SARS) vaccine strategies were evaluated for their ability to protect against live SARS coronavirus (CoV) challenge in a murine model of infection. A whole killed (inactivated by beta-propiolactone) SARS-CoV vaccine and a combination of two adenovirus-based vectors, one expressing the nucleocapsid (N) and the other expressing the spike (S) protein (collectively designated Ad S/N), were evaluated for the induction of serum neutralizing antibodies and cellular immune responses and their ability to protect against pulmonary SARS-CoV replication. The whole killed virus (WKV) vaccine given subcutaneously to 129S6/SvEv mice was more effective than the Ad S/N vaccine administered either intranasally or intramuscularly in inhibiting SARS-CoV replication in the murine respiratory tract. This protective ability of the WKV vaccine correlated with the induction of high serum neutralizing-antibody titres, but not with cellular immune responses as measured by gamma interferon secretion by mouse splenocytes. Titres of serum neutralizing antibodies induced by the Ad S/N vaccine administered intranasally or intramuscularly were significantly lower than those induced by the WKV vaccine. However, Ad S/N administered intranasally, but not intramuscularly, significantly limited SARS-CoV replication in the lungs. Among the vaccine groups, SARS-CoV-specific IgA was found only in the sera of mice immunized intranasally with Ad S/N, suggesting that mucosal immunity may play a role in protection for the intranasal Ad S/N delivery system. Finally, the sera of vaccinated mice contained antibodies to S, further suggesting a role for this protein in conferring protective immunity against SARS-CoV infection.

Administration, Intranasal↗
PubMed1978

Physico-chemical properties of mouse hepatitis virus (MHV-2) grown on DBT cell culture.

Some properties of a strain of mouse hepatitis virus, MHV-2, grown on DBT cells were determined using a plaque assay on the cells. Viral growth was not inhibited by the presence of actinomycin D or 5-iodo-2-deoxyuridine. MHV-2 was completely inactivated by ether, chloroform, sodium deoxycholate or beta-propiolactone, but showed a moderate resistance to trypsin. Heating at 56 C for 30 min did not completely abolish the virus infectivity. The virus was stable after heating at 50 C for 15 min in 1M-MgCl2 or 1M-MgSO4 as well as at 37 C for 60 min at pH 3.0 to 9.0. Infectivity was decreased to 1/100 and 1/400 after storing at 4 C for 30 days and 37 C for 24 hr, respectively. The virus passed through a 200-nm but not a 50-nm Sartorius membrane filter. The buoyant density of MHV-2 was 1.183 g/cm3 in sucrose gradient, and the fraction contained coronavirus-like particles measuring 70 to 130 nm in diameter. Survival rate was 10% after exposure to ultraviolet at 150 ergs/mm2. Freezing and thawing or sonication at 20 kc for 3 min did not affect the virus titer. No hemagglutinin was demonstrable with red blood cells of the chicken, Japanese quail, mouse, rat, hamster, guinea pig, sheep, bovine or human.

Cell Line↗
PubMed1981

Essential Role of T cells in the postexposure prophylaxis of rabies in mice.

Athymic nude mice injected intramuscularly with a street stain of rabies virus were not protected against rabies by postexposure administration of beta-propiolactone-inactivated rabies vaccine. In contrast, their normal littermates were completely protected from death by the same vaccination regimens. Nude mice did not produce IgG antibody as a result of the vaccine during the test period of 15 days, whereas normal littermates produced IgG antibody from day 5 after vaccination. However, passive immunization with antirabies hyperimmune mouse ascites showed that antibody was completely ineffective in protecting either nude mice or their normal littermates against rabies when given later than 2 days after infection. No significant difference in the induction of circulating interferon by the vaccination was noted in these mice. Passive transfer of immune spleen cells to nude mice immediately after infection resulted in 30 to 37.5% protection of the mice. Passively transferred spleen cells did not produce detectable amounts of neutralizing antibody in the recipient mice except on day 2 after the transfer, when a low level of antibody was detected. These observations demonstrate the essential role of T cells in the postexposure prophylaxis of rabies in mice. The mechanisms of the failure of postexposure vaccination in nude mice are discussed.

Animals↗