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Published on: July 11, 2015
PRODUCTION OF AN INTERFERON BY L CELLS INFECTED WITH WESTERN EQUINE ENCEPHALOMYELITIS VIRUS
Lockart, Royce Z., Jr. (The University of Texas, Austin). Production of an interferon by L cells infected with Western equine encephalomyelitis virus. J. Bacteriol. 85:556-566. 1963.-Two strains of Western equine encephalomyelitis virus (WEE), WEE (L+) and WEE (L-), which differed with respect to their cytopathogenicity for L cells were isolated. Both strains reproduced in L cells, and both induced the production of an interferon distinct from virus particles. L-cell monolayers were protected from degeneration by prior addition of interferon. By use of the absence of cytopathic effects (CPE) as an end point, interferon content was assayed. Monolayers failing to show CPE consistently produced less than 2% as much virus as control monolayers, indicating that virus synthesis was also inhibited. The use of this assay method was facilitated by the use of horse serum that appeared to contain antibodies against WEE and that permitted interferon to act selectively in the presence of active virus. It was found that interferon was produced during the time in which active virus was produced, and not significantly later. No interferon could be found in fluids from cells treated with inactive virus, although these are known to act as interfering agents. Interferon production was inhibited by pretreatment of L cells with sufficient amounts of interferon. It is concluded that interferon production is closely connected with WEE virus synthesis in L cells. The question is raised as to whether interferon need be a necessary intermediate for interference in L cells.
Lockart, Royce Z., Jr. (The University of Texas, Austin). Production of an interferon by L cells infected with Western equine encephalomyelitis virus. J. Bacteriol. 85:556-566. 1963.-Two strains of Western equine encephalomyelitis virus (WEE), WEE (L+) and WEE (L-), which differed with respect to their cytopathogenicity for L cells were isolated. Both strains reproduced in L cells, and both induced the production of an interferon distinct from virus particles. L-cell monolayers were protected from degeneration by prior addition of interferon. By use of the absence of cytopathic effects (CPE) as an end point, interferon content was assayed. Monolayers failing to show CPE consistently produced less than 2% as much virus as control monolayers, indicating that virus synthesis was also inhibited. The use of this assay method was facilitated by the use of horse serum that appeared to contain antibodies against WEE and that permitted interferon to act selectively in the presence of active virus. It was found that interferon was produced during the time in which active virus was produced, and not significantly later. No interferon could be found in fluids from cells treated with inactive virus, although these are known to act as interfering agents. Interferon production was inhibited by pretreatment of L cells with sufficient amounts of interferon. It is concluded that interferon production is closely connected with WEE virus synthesis in L cells. The question is raised as to whether interferon need be a necessary intermediate for interference in L cells.
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