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COLORADO TICK FEVER VIRUS IN CELL CULTURE. I. CELL-TYPE SUSCEPTIBILITY AND INTERACTION WITH L CELLS.

Trent, Dennis W. (University of Oklahoma School of Medicine, Oklahoma City) and L. Vernon Scott. Colorado tick fever virus in cell culture. I. Cell-type susceptibility and interaction with L cells. J. Bacteriol. 88:702-708. 1964.-Colorado tick fever (CTF) virus was serially propagated in monolayer cultures of L and FL cells. Early passages of virus in FL cells yielded viral titers 10(4)-fold greater than did the corresponding L-cell passages. During L-cell passage number 4, there was a 10(3)-fold increase in the amount of infectious virus produced as compared with virus cultured earlier in this cell line. Viruses from L-cell passages 8 and 12 were identified with specific immune serum to be CTF viruses which were antigenically similar, if not identical, to the mouse-adapted virus. Parallel titrations of mouse-, L cell-, and FL cell-adapted viruses were performed in mice and replicate monolayers of L, FL, HeLa, KB, chick embryo, and cotton rat kidney cells. Cytopathic effects and viral replication were noted in all cultures except HeLa and cotton rat kidney. Cultures of L, FL, and chick embryo cells were as sensitive to infection as were suckling or weanling mice. KB cells were the least susceptible of those cell types examined. In L-cell cultures, 90% of the input virus was adsorbed to the cells during the first 30 min of incubation. The latent period lasted 10 to 12 hr, and was followed by rapid viral synthesis for the next 10 to 24 hr, depending upon the multiplicity of infection. Curves describing exponential increase in cell-associated and cell-released virus were separated by 4 hr. When the maximal total virus titers were reached, 80 to 90% of the virus was released from the cell.

Adsorption↗

REPLICATION OF A DEOXYRIBONUCLEIC ACID VIRUS IN THYMINE-DEFICIENT MAMMALIAN CELLS.

Gentry, Glenn A. (University of Mississippi School of Medicine, Jackson), Lucy A. Lawson, and Charles C. Randall. Replication of a deoxyribonucleic acid virus in thymine-deficient mammalian cells. J. Bacteriol. 88:1324-1328. 1964.-Equine abortion virus (EAV), a deoxyribonucleic acid (DNA) virus, causes the degradation of host cell DNA to acid-soluble components in the L-M cell. It was hypothesized that inhibitors of DNA synthesis such as 5-fluorodeoxyuridine (FUdR) and amethopterin, which act by causing a deficiency in thymidine (TdR) nucleotides, would not block virus replication because the breakdown of the host cell DNA would supply sufficient TdR nucleotides for synthesis of viral DNA. The drugs were added 24 hr prior to the virus, amethopterin at 10(-6)m with adenosine included as a purine source, or FUdR at 10(-5)m. In either case, control experiments indicated that the thymineless state was achieved in the host cells. When EAV was added, neither FUdR nor amethopterin had any effect on the production of infectious virus, as determined by plaque assay, thus supporting the hypothesis.

Animals↗

INHIBITION BY EXOGENOUS INTERFERON OF REPLICATION OF POLIOVIRUS RIBONUCLEIC ACID IN CHICK BRAIN.

Youngner, Julius S. (University of Pittsburgh, Pittsburgh, Pa.), and Marion E. Kelly. Inhibition by exogenous interferon of replication of poliovirus ribonucleic acid in chick brain. J. Bacteriol. 90:443-445. 1965.-The replication of poliovirus was studied after the intracerebral inoculation of infectious ribonucleic acid (RNA) into the brains of 2-day-old chicks; these animals are not susceptible to intact virus. Single-cycle replication of virus, which reached a peak in about 12 hr, was completely inhibited by prior intraperitoneal injection of interferon prepared from the allantoic fluid of chick embryos infected with influenza virus. A single dose of as little as 500 units of interferon, measured by a plaque-reduction method, completely suppressed viral replication when injected 24 hr prior to infectious RNA. This system provides a model for the study of the protection of target organs by passively transferred interferon injected at a distance.

Allergy and Immunology↗