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,¶
* Departments of Bacteriology
Pathology, Medical School, Foresterhill, Aberdeen AB9 2ZD
Division of Immunology and Experimental Biology, National Institute for Medical Research, Mill Hill, London NW7
CBA mice, inoculated intravenously with large doses of adenovirus type 5, showed raised levels of serum aspartate aminotransferase (SAAT; EC 2.6.1.1 [EC] ) and died within a few days from histologically demonstrable hepatic necrosis. After inoculation of 1 LD50, virus was rapidly taken up by the tissues where infectivity then declined greatly. Organ titres then increased about 100-fold by 48 h p.i. but, in the liver, which showed intranuclear inclusion bodies, and by electron microscopy, scattered intranuclear and intracytoplasmic adenovirions, the increase was 10000- to 100000-fold. P antigen was detected by single radial diffusion in liver extracts, and by immunofluorescence in 80% of liver cells at 36 h p.i. Hexon, penton base and fibre antigens appeared later and in fewer cells. The maximum amount of hexon, of demonstrable type 5 specificity, was shown by radioimmunoassay to be equivalent to up to 5 x 1011 whole adenovirions/g liver. It is concluded that human adenovirus type 5 undergoes an abortive but lytic infection in most liver cells but that replication may proceed to completion in a few.
Present address: Pollards Wood Research Station, Nightingale Lane, Chalfont St Giles, Buckinghamshire, HP8 4SP.
< |Present address: Department of Medical Microbiology, Flinders Medical Centre, Bedford Park, South Australia 5042.
¶ Present address: Department of Anatomy, Medical School, University of Newcastle upon Tyne.
Received 1 December 1977;
accepted 10 January 1978.
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