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Biomedical subjects

A Brown

Publications and source records attributed to A Brown.

At least 649 records · Page 36Linked to original sources
PubMed1976

Early events in the lytic infection of primary mouse kidney cell culture with polyoma virus. The effect of various input multiplicities.

Early polyoma (Py) virus-specific RNA synthesis was examined in cells infected with different concentrations of Py-virus. The effect of various multiplicities of infection (m.o.i.) on the rate of Py-RNA synthesis is different at 30 hr as compared to 65 hr. Thirty hours after infection at 27degrees, in the presence of 5-fluoro-2-deoxyuridine (FdU), an increase in input multiplicity was not associated with a quantitatively commensurate increase in the amount of virus-specific RNA synthesized. At 65 hr, the amount of viral RNA synthesized was roughly proportional to the number of infecting virus particles.

Cells, Cultured↗
PubMed1975

Hydrogen-deuterium exchange in nucleosides and nucleotides. A mechanism for exchange of the exocyclic amino hydrogens of adenosine.

The pH dependence of the apparent first-order rate constant for the exchange of the exocyclic amino hydrogens of adenosine with deuterium from the solvent was measured by stopped-flow ultraviolet spectroscopy. This dependence shows acid catalysis, base catalysis, and spontaneous exchange at neutral pH values. A study of the effect of several buffers on the rates of exchange reveals both general acid and general base catalytic behavior for the exchange process. We propose a general mechanism for the exchange which requires N-1 protonated adenosine as an intermediate for the acid-catalyzed exchange and amidine anion for the base-catalyzed exchange. In both cases the rate-limiting step is the base-catalyzed abstraction of a proton from the exocyclic amino moiety. Evaluation of the rate constants predicts the equilibrium for the exocyclic amino/imino tautomers to be 6.3 times 10(3):1.

Adenosine↗
PubMed1975

An attenuated variant of Eastern encephalitis virus: biological properties and protection induced in mice.

Wild type Eastern equine encephalitis virus (E) was compared with a mutant (Em) derived from it. The latter was tested as an attenuated vaccine in mice. They differed in the following properties: Em formed smaller plaques on chick embryo (CE) cell monolayers and, unlike E, did not plaque on mouse embryo (ME) monolayers. Futher, Em had a longer latent period and attained a lower peak titer than E after infection of CE cells, was more senssitive than E to chick interferon, and was less virulent for mice (SC and IP routes) and hamsters (IP route) than E. Both viruses were similar in several other properties tested. The mutant was found to induce a gradient in the specificity of protection in mice against challenge by selected viruses after a single subcutaneous injection of living virus. The protection was best against autologous (Em) challenge, was next best against challenge by the virulent parent (E) virus, but was not demonstrable against cross challenge by Venezuelan encephalitis (V) virus. Conventional hemagglutination-inhibiting (HI), complement-fixing (F), and neutralizing (N) antibodies could not be detected in Em-immunized mice even when fresh monkey or guinea pig serum was included in Ntests to provide complement and/or accessory factor(s). However, N antibodies were detected in protected mice by an indirect antiglobulin test. Passive protection by serum or ascites fluids (a.f.) was characterized by a lower but otherwise similar protection gradient like that found after active immunization with virus as described above. Interferon was not detected in the a.f. used for passive protection, nor was heterologous interference evident in Em immunized mice challenged 18 days later with vaccinia or vesicular stomatitis virus. Immunized mice that survived autologous (Em) challenge showed broadened protection against a second challenge by parent E virus, and cross protection against V virus. This typical protection was associated with the presence of HI and conventional N antibodies, except for V which showed no detectable neutralizing antibodies by either a standard or antiglobulin technique.

Animals↗
PubMed1975

Attenuation and immunogenicity of ts mutants of Eastern encephalitis virus for mice.

Preliminary experiments were intiated to test the attenuation for mice of chemically induced temperature-sensitive (Ets) mutants of a virulents strain of Eastern encephalitis (E) virus, and the potential of such mutants as live virus vaccines for mice. The reversion frequencies of eight mutants to temperature insensitivity were measured and the defects in their biosynthesis at the non-permissive temperature were studied. All eight mutants were less virulent for mice, but the extent of avirulence varied with the mutant and route of injection. The mutants selected as potential vaccines protected mice against subsequent challenge at 10 to 21 days by the virulent virus of strain E. Neutralizing antibody activity was detected in almost all the mutant-infected mice after 10 days, and was found in all infected mice at 21 days. Immunization by two doses of virus induced a very high protection against intracerebral challenge by virus strain E.

Animals↗
PubMed1975

Preliminary evidence for cell-mediated immunity in cross-protection among group A arboviruses.

Unfractionated and T cell-enriched populations from spleens of mice immunized with Sinbdis virus confer cross-protection against Semliki forest virus challenge in recipient mice. Both Group A viruses are serologically related, but not by tests for cross-neutralizing antibody. The protection in mice persisted for three consecutive cell passages in uninfected mice. The results suggest that cell-mediated immunity accounts for cross-protection.

Animals↗
PubMed1974

Reciprocal inhibition of mouse leukemia virus infection by Fv-1 allele cell extracts.

Soluble extracts of mouse cells with Fv-1(n) or Fv-1(b) gene alleles specifically and reciprocally inhibit infection of B- or N-tropic mouse leukemia viruses in permissive cell cultures. NB-tropic virus infection was not inhibited by either cell extract. Extracts from Fv-1(-) cells did not inhibit infection by the three virus host-range types, but N- or B-tropic virus infection of Fv-1(-) cells was inhibited by extracts of the nonpermissive cells, and Fv-1(nb) cell extracts inhibited both viruses. The maximum degree of inhibition was 50-80% as determined by immunofluorescent or plaque assays, with extracts containing up to 500 mug/ml of nonpermissive cell protein. The inhibitor(s) is relatively unstable since activity is lost after 2 hr at 37 degrees or 30 min at 56 degrees . The inhibitor(s) was most effective if added 2 hr before or within 2 hr after infection, did not react with the virus directly, inhibit virus attachment, or inhibit the normal cell functions tested. These results indicate that nonpermissive mouse cells contain a product, possibly determined by the Fv-1 gene, which inhibits some early postpenetration event(s) in leukemia virus infection.

Alleles↗