PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “VIRUS CULTIVATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed1964

DENSITY GRADIENT CENTRIFUGATION OF A MURINE LEUKEMIA VIRUS.

The Rauscher leukemia virus separated as a single band upon density gradient centrifugation in cesium chloride, rubidium chloride, sucrose, potassium citrate, or potassium tartrate. Prolonged exposure to concentrated potassium citrate or potassium tartrate solutions caused lysis of the virus; the resulting products, having different densities, separated on the density gradients.

Animals↗
PubMed1964

RUBELLA VIRUS: INHIBITION IN VITRO BY AMANTADINE HYDROCHLORIDE.

Amantadine (or 1-adamantanamine) hydrochloride, a compound reported to be active against influenza viruses and Sendai virus, inhibited the growth of rubella virus in tissue culture. The antiviral activity appears at an early phase of the infection and is not due to direct inactivation of the virus.

Amantadine↗
PubMed1964

EFFECTS OF POLYCYCLIC AROMATIC CARCINOGENS ON VIRAL REPLICATION: SIMILARITY TO ACTINOMYCIN D.

When incorporated into a nutrient overlay, the carcinogenic hydrocarbons benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene inhibit plaque formation by herpes virus and vaccinia virus, DNA viruses, but not by Sindbis virus, an RNA virus. These carcinogens also decrease herpes and vaccinia virus yields in liquid medium, without affecting Sindbis virus yields. Four structurally related, but noncarcinogenic polycyclic hydrocarbons, namely benzo[e]pyrene, pyrene, benz[a]anthracene and anthracene, have no inhibitory effect on DNA virus replication. Taken together with the known inhibition of interferon production, these effects on virus growth resemble the action of actinomycin D and hence provide evidence for a selective interaction of these carcinogens with DNA.

Anthracenes↗
PubMed1965

CONDITIONAL-LETHAL MUTANTS OF AN ANIMAL VIRUS: IDENTIFICATION OF TWO CISTRONS.

Two different temperature-sensitive conditional-lethal mutants of Sindbis virus, an animal virus that contains RNA, have been isolated. When cultured in chick fibroblast monolayers at 42 degrees C, these mutants yield less than 0.05 percent as much virus as does the wild type, whereas at 27 degrees C they grow normally. One mutant appears to be altered in the synthesis of a protein that is produced early in the infection and is required for viral RNA synthesis. The other mutant produces as much infectious RNA as the wild type at 42 degrees C and appears to be altered in the synthesis of a protein produced late in the infection.

Animals↗
PubMed1963

QUANTITATION OF VIRUSES BY THE PLAQUE TECNHIQUE.

Berg, Gerald (Robert A. Taft Sanitary Engineering Center, Cincinnati, Ohio), Eugene K. Harris, Shih L. Chang, and Kenneth A. Busch. Quantitation of viruses by the plaque technique. J. Bacteriol. 85:691-700. 1963.-This paper presents the results of a study on overcrowding as it occurred with several strains of enteroviruses on monkey kidney cell layers. Each cell sheet area was 4,500 mm(2). Dispersion analysis of all plaque counts in the study revealed that the percentage error, in the absence of overcrowding, fluctuated within a range of 7 to 36% about a mean value of about 17%, which is close to what is expected from purely statistical variation in sampling. Overcrowding with Mahoney virus, a mixture of particles producing either rapidly or slowly expanding plaques, resulted primarily from the obscuring effect produced as rapidly expanding plaques obliterated infected foci produced by virus particles responsible for slow-forming plaques. Overcrowding occurred at plaque levels in excess of 35 to 40 per cell sheet. Overcrowding with Mahoney LP virus, a strain derived from a rapidly expanding Mahoney plaque which produced uniformly expanding plaques, did not occur until counts in excess of 60 to 70 per cell sheet were reached. Plaque obscuring was again responsible. Apparent overcrowding with Coxsackie A9 virus, when plaques were not permanently marked from the first day of counting, resulted from coalescence at levels above about 40 to 50 plaques per cell sheet. When plaques were permanently marked, overcrowding resulted from plaque obscuring which did not occur until levels in excess of about 120 per cell sheet were reached.

Enterovirus↗
PubMed1963

INTERACTION OF AN INTERFERON WITH L CELLS.

Lockart, Royce Z., Jr. (The University of Texas, Austin) and Barbara Horn. Interaction of an interferon with L cells. J. Bacteriol. 85:996-1002. 1963.-Data were presented on the effect of time of exposure and concentration of an interferon in provoking viral inhibition in L cells. Populations of L cells which made reduced amounts of Western equine encephalomyelitis virus as a result of treatment with interferon did so at reduced rates proportional to the concentration of interferon used. Virus yields were maximal, however, 25 hr after challenge regardless of the amount of virus produced. Such populations of cells contained a proportion of cells no longer able to produce infective virus, while the average maximal yield of the remainder of the cell population was reduced. It was suggested that only cells which made new virus underwent cytopathic effects. The rate of viral inhibition in monolayers of L cells was dependent on the concentration of interferon added, but inhibition was nearly maximal at 8 hr, regardless of the interferon concentration. Viral inhibition was shown to persist in multiplying cells, but it gradually diminished. The amount of inhibition after either one or two cell divisions was greater in those cultures treated with greater amounts of interferon. Viral inhibition could be passed through cell division with no loss when cells were incubated with a sufficient concentration of interferon. A model of interferon action based on the preceding data was presented.

Animals↗
PubMed1963

CHIMPANZEE KIDNEY TISSUE CULTURES FOR GROWTH AND ISOLATION OF VIRUSES.

Dick, Elliot C. (University of Wisconsin, Madison). Chimpanzee kidney tissue cultures for growth and isolation of viruses. J. Bacteriol. 86:573-576. 1963.-Chimpanzee kidney tissue cultures were employed for propagation of several laboratory strains of viruses that commonly inhabit the respiratory and intestinal tracts, or both, and for isolation of viruses from throat washings of persons with common colds and tonsillitis-pharyngitis. This tissue culture host was found to support the growth of approximately the same viruses as do Rhesus monkey kidney tissue cultures, with two exceptions: (i) chimpanzee kidney tissue culture was much more susceptible to herpes simplex infection, and (ii) cytopathic effects were not produced by either "M" or "H" strains of muriviruses (common cold viruses). The presence of adventitious viruses in some uninoculated chimpanzee kidney tissue cultures is suspected.

Animals↗
PubMed1964

INFECTIOUS BOVINE RHINOTRACHEITIS VIRUS REPLICATION, CYTOPATHOLOGY, AND PLAQUE FORMATION IN THE PRESENCE AND ABSENCE OF NUCLEIC ACID ANALOGUES.

Stevens, Jack G. (University of Washington, Seattle), and Neal B. Groman. Infectious bovine rhinotracheitis virus replication, cytopathology, and plaque formation in the presence and absence of nucleic acid analogues. J. Bacteriol. 87:446-453. 1964.-Cytopathology induced by infectious bovine rhinotracheitis (IBR) virus was correlated with the one-step growth cycle. Nuclear alterations, including the development of inclusion bodies, preceded the appearance of virus. It was found that similar effects occurred in the presence of 5-bromodeoxyuridine (BUDR) and 5-fluorodeoxyuridine (FUDR), compounds which depress the yield of "standard" virus from a range of 116 to 500 to less than 0.5 plaque-forming units per cell. As with known members of the herpesvirus group, IBR virus plaques developed and enlarged indefinitely in the presence of specific antibody. An analysis of the mechanism operative in this process was undertaken. The evidence suggested that neither viral nor subviral particles capable of replicating "standard" virus passed between cells during the first 8 hr of infection. This is the time preceding the release of extracellular virus from initially infected cells. With BUDR and FUDR, it was shown that plaques also developed in this system in the virtual absence of production of "standard" infectious virus. However, a class of analogue-dependent virus was found which may have been at least partly responsible for plaque formation in the analogue-treated system. The relative contributions of subviral particles or of a self-sustaining molecular disorganization to the process have not been completely assessed as yet.

Animals↗