Temin, Howard M. (1960) The interaction of Rous sarcoma virus and cells in vitro. Dissertation (Ph.D.), California Institute of Technology. http://resolver.caltech.edu/CaltechETD:etd-10222002-093114
By the use of new methods for assaying in vitro Rous sarcoma virus (RSV) and Rous sarcoma cells and for isolating the progeny of single particles of RSV, it has been found that the morphology of Rous sarcoma cells is partially controlled by genetic factors in the virus. The influence of the state of the cell before infection, operating directly on the virus-cell complex has been demonstrated. A single particle of RSV is able to initiate infection, but viral genetic factors and genetic and physiological factors in the cell determine whether or not a cell does become infected. Host range mutants of the virus are described. It was shown that there exists a state in which resistant cells become competent to support the growth of RSV. RSV rapidly adsorbs and penetrates into cells. After a 12 hour period new virus appears. The final rate of virus release of 10 focus-forming units per cell per 10 hours is reached about 40 hours after infection. The ability of a cell to produce RSV is transmitted to its progeny as an intracellular event, the number of Rous sarcoma cells doubling every 15 - 20 hours. Immediately after infection the X-ray resistance of the capacity of a cell to release virus is the same as its capacity to divide. By 15 - 20 hours after infection, the resistance of the capacity of the cells to release virus increases about 30 times. Direct observation of isolated cells in microdrops shows that a cell can release virus and then divide. Interference caused by one particle of inactive virus, operating on some intracellular process after penetration of the virus into the cell was found. The relationship between RSV and temperate bacteriophage, the relevance of the findings to the cancer problem, and the relationship between RSV and other animal viruses are discussed.
|Item Type:||Thesis (Dissertation (Ph.D.))|
|Degree Grantor:||California Institute of Technology|
|Awards:||The Nobel Prize in Physiology or Medicine 1975.|
|Thesis Availability:||Public (worldwide access)|
|Defense Date:||1 January 1960|
|Default Usage Policy:||No commercial reproduction, distribution, display or performance rights in this work are provided.|
|Deposited By:||Imported from ETD-db|
|Deposited On:||22 Oct 2002|
|Last Modified:||29 Nov 2016 21:24|
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