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U.S. Department of Health, Education and Welfare, Public Health Service, National Institute of Health, National Institute of Allergy and Infectious Diseases Rocky Mountain Laboratory, Hamilton, Montana 59840
The* Wistar Institute of Anatomy and Biology, 36th Street at Spruce, Philadelphia, Pennsylvania 19104, U.S.A.
We have shown previously that a non-fatal outcome of infection with street rabies virus occurs more often when mice are exposed to a high ambient temperature (HAT = 35 °C) early in the course of the infection. To determine what influence the virus strain had on this protective effect of HAT, we have extended these observations to studies of a fixed rabies strain, CVS and several substrains of CVS virus derived from temperature-sensitive (ts) mutants. In all cases, mortality was reduced to some extent by exposure of the animals to HAT; however, dramatic strain-specific differences in the extent of the effect were noted. Although each of the virus substrains tested was revertant in the ts character (as tested in vitro using a non-permissive temperature of 40.5 °C), several substrains (ts 1, ts 4, RT51) caused disease that was sensitive (> 90% reduction in mortality) to HAT. Mortality induced by the parental CVS virus was reduced approx. 50% at HAT. A single CVS virus substrain, VSW89, caused disease that was less affected by HAT than was disease induced by the parental strain. As in previous studies with street virus, the incubation periods for infection with CVS virus substrains were consistently prolonged at HAT.
Received 17 January 1977;
accepted 5 April 1977.
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