PubMed Health⌕ Search

Biomedical subjects

E Zebovitz

Publications and source records attributed to E Zebovitz.

9 recordsLinked to original sources
PubMed1977

A spontaneous temperature sensitive mutant of Japanese encephalitis virus: preliminary characterization.

A spontaneously arising temperature sensitive (ts) mutant of Japanese encephalitis virus (JEV), ts104, was isolated from chick fibroblast (CF) cell cultures of JEV strain M 1/311. Strain ts104 was plaque purified and characterized to ascertain its potential as a candidate for a live vaccine. Parameters of its growth, temperature lability, immunogenicity and virulence were examined. Ts104 has been shown to be stable ts JEV strain, multiplying as well as the parent strain in CF cultures at 35 degrees C, but not mutiplying at 39 degrees C. It was avirulent for embryonated chicken eggs incubated at 39 degrees C and of reduced virulence for intracerebrally (i.c.) inoculated mice as measured by LD50 in weanling mice and average day of death in weanling and suckling mice. Intraperitoneal injection of adult mice with either parent or ts strain resulted in similar levels of protection against challenge with either strain. The potential of ts104 as a candidate live JEV vaccine strain is discussed.

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↗
PubMed1974

Involvement of the host cell nuclear envelope membranes in the replication of Japanese encephalitis virus.

The distribution of viral ribonucleic acid (RNA) on various cell membrane fractions derived from a porcine kidney cell line infected with Japanese encephalitis virus was investigated. At 40 h postinfection, after virus growth had reached its peak, three viral RNAs, 45S, 27S, and 20S, were associated with the cytoplasmic membranes and intact nuclei. The amount of each RNA associated with the nucleus was two- to fivefold greater than that present with the cytoplasmic membranes. Treatment of washed infected nuclei with 1.0% Triton X-100, which removed the outer nuclear envelope membrane, also removed the viral RNA. When the nucleus was fractionated into nuclear envelope membranes and a large particle fraction which sedimented at 600 x g, nearly all of the viral RNA remained associated with the envelope membranes. The nuclear envelope membranes contained higher viral RNA polymerase activity than the cytoplasmic membranes derived from the same cells. These data suggest that major sites for Japanese encephalitis virus RNA synthesis may be localized on or in very close association with the nuclear envelope membranes.

Animals↗
PubMed1973

System for studying uninfected and virus-infected cell cultures in hyperbaric chambers.

Equipment and techniques previously used to investigate the effect of hyperbaric gases on bacteria were modified to permit comparable investigations with uninfected and virus-infected tissue cell cultures. This report describes the modified equipment and related methodology. Use of the system is illustrated with findings on the effect of oxygen-helium mixtures at 68 atm on cell physiology and virus growth in two cell types. Our results suggested that, under those experimental conditions, several synthetic processes in chick fibroblast monolayers are inhibited but that Sindbis virus growth in the cells is increased. Growth of Japanese encephalitis virus in porcine kidney cells was found to be unaffected by oxygen-helium gas at partial pressures of oxygen between 0 and 700 mm Hg, but morphological alterations in the cells occurred at low and high pO(2) levels.

Amino Acids↗
PubMed1968

Interference among group A arboviruses.

Interference among group A arboviruses is described which does not involve the mediation of interferon. Interference was observed only if the interfering virus had an advantage over the challenge virus, either in time or in multiplicity of infection. Adsorption, penetration, and uncoating of challenge virus did not appear to be inhibited, but the synthesis of infectious viral ribonucleic acid of the challenge virus was significantly retarded. It was shown with temperature-sensitive viruses or mutants that the replication of viral ribonucleic acid by the interfering virus was required to establish interference. A mechanism of interference based on a competition for replication sites or substrates is compared with other possible explanations.

Arboviruses↗
PubMed1967

Temperature-sensitive steps in the biosynthesis of Venezuelan equine encephalitis virus.

In contrast to Eastern equine encephalitis virus, the replication of Venezuelan equine encephalitis (VEE) virus was strongly inhibited at 44 C in chick embryo cells. The inhibited steps were analyzed by shifting the incubating temperatures up or down, and by determining during the shifts the rate and extent of infectious ribonucleic acid (RNA) synthesis, intact virus synthesis, and formation of complement-fixing antigen or of antigen detectable by a direct fluorescent-antibody technique. The inhibition appeared to be due to two temperature-sensitive steps involved in the synthesis of VEE virus in chick embryo cells. The first step of inhibition at 44 C occurred early in virus replication and could be completely reversed simply by transferring cultures to 37 C. The inhibition appeared to take place at some point between the time when the virus entered the cell and was uncoated and the beginning of viral RNA synthesis. The second temperature-sensitive step in VEE virus synthesis was irreversible; it occurred at a point after the synthesis of viral RNA, and before the formation of virus protein measured as complement-fixing antigen or as antigen that could be stained with fluorescent antibody.

Animals↗