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1 Department of Medicine, Rochester General Hospital and University of Rochester School of Medicine and Dentistry, 1425 Portland Avenue, Rochester, New York 14621
2 Division of Metabolism and Endocrinology, Washington University School of Medicine, Box 8127, St Louis, Missouri
3 Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110-1093
4 Department of Molecular Microbiology and Immunology, St Louis University School of Medicine, 1402 South Grand Avenue, St Louis, Missouri 63110-0250, USA
Serial passage of yellow fever virus (YF17D) in mouse brain enhances neurovirulence, causing a reduction in survival time after intracerebral inoculation of adult mice. To study the biological and genetic basis for this phenomenon, we compared neurovirulence properties of the neuroadapted Porterfield strain (PYF) to a YF17D strain generated from a full-length YF cDNA template (YF5.2iv). Adult mice were infected by olfactory bulb inoculation, which results in widespread distribution of virus throughout the central nervous system. Although PYF and YF5.2iv spread rapidly throughout the neuraxis, maximal titres of PYF in the brain and spinal cord were 1000- to 10000-fold higher than those of YF5.2iv. Paralysis and death occurred earlier with the PYF strain. Several cDNA clones of the E/NS1 region of the PYF strain were sequenced. Three predicted amino acid changes were consistently observed in the envelope protein of the PYF strain compared to YF5.2iv. Common substitutions were also identified in NS1 and NS2A. The potential contribution of these genetic differences to neurovirulence was evaluated by generating recombinant, intertypic PYF/YF5.2iv viruses. Physical signs of disease and mean spinal cord titres after inoculation of one recombinant were not different from the YF5.2iv parent. Our data indicate that PYF and YF5.2iv differ significantly in their virulence properties, however, common amino acid substitutions in the E/NS1 region of the PYF strain do not determine its enhanced neurovirulence. Other regions of the viral genome may contribute dominant effects on the virulence properties of the PYF strain.
* Author for correspondence. Fax +1 314 773 3403.
Received 4 August 1995;
accepted 23 January 1996.
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