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Baluda, Marcel Albert (1957-01-01) Homological interference by ultraviolet inactivated virus in Newcastle disease virus. http://resolver.caltech.edu/CaltechETD:etd-06292004-111411


Type of Document Dissertation
Author Baluda, Marcel Albert
URN etd-06292004-111411
Persistent URL http://resolver.caltech.edu/CaltechETD:etd-06292004-111411
Title Homological interference by ultraviolet inactivated virus in Newcastle disease virus
Degree PhD
Option Biology
Advisory Committee
Advisor Name Title
Renato Dulbecco Committee Chair
Keywords
  • none
Date of Defense 1957-01-01
Availability unrestricted
Abstract
The present study concerns a quantitative analysis of the interference between the irradiated and the active Newcastle disease virus.

The inactivated particles adsorb to the surface of the cells and do not proceed any further. This union induces surface changes which make it impossible for a superinfecting active particle to penetrate into the host cell and to initiate the production of new virus. The more UVI particles that are adsorbed, the faster the interfering reaction occurs.

In 50 per cent of the cells, however, interference is not complete; these cells can be superinfected provided the multiplicity of the superinfecting virus is high. The effect is equivalent to having on the average four per cent of the total surface of the cell unaffected by the changes induced by the inactivated virus.

The interfering reaction is dependent at all times upon the presence of the unmodified UYI particles at the critical sites - exposure of the interfered cells to specific anti-NDV serum eliminates interference. However, in 50 per cent of the cells interference becomes irreversible 30 minutes after the attachment of UVI virus. Whether this irreversible interference involves more profound cellular changes or depends upon the physiological state of the cells at the time of infection is at present unknown.

Eventually, the union between UVI virus and cellular site is broken with the subsequent return of the cell to susceptibility to infection. This loss of resistance occurs spontaneously from 26 to 60 hours after exclusion has been induced.

The superinfecting virus which does not initiate infection is destroyed after its adsorption to the lung cell. A cell where interference has been removed after superinfection with active virus must be infected a second time in order to yield progeny virus.

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