Kaschka-Dierich C, Thomssen R
J Gen Virol. 1979 Nov;45(2):253-61. doi: 10.1099/0022-1317-45-2-253.
The development of cytopathogenic changes in chicken embryo fibroblasts infected with the herpesvirus of the turkey, strain PB-THVI, and the release of virus particles into the supernatant of infected cultures is accelerated at temperatures higher than 37 degrees C and is fastest at 41 degrees C, the normal body temperature of chickens. The growth rate of HVT in CEF cultures was followed by determination of the number of virus genome equivalents within infected cells at various time intervals p.i. A temperature-dependent increase in the amount of virus DNA per infected cell could be detected, which is highest at 41 degrees C. At all temperatures tested (34, 36, 41 and 43 degrees C) the number of virus genome equivalents per infected cell ultimately reaches the same level. In the course of infection, virus DNA in CEF cultures at 37 and 41 degrees C becomes associated with the cellular DNA, as determined by neutral CsCl gradients of the total cellular DNA and hybridization of each fraction with 32P-labelled virus-specific complementary RNA. Association of virus to cellular DNA occurs earlier at 41 than at 37 degrees C. However, the same proportion (45%) of the total virus DNA appears ultimately to be associated with cellular DNA at both temperatures. A temperature-shift of CEF cultures infected with PB-THVI from 41 to 37 degrees C 24 h p.i. resulted in the same replication kinetics of virus DNA as was found at 41 degrees C.