Giesendorf B, Bosch F X, Orlich M, Scholtissek C, Rott R
Virus Res. 1986 Jul;5(1):27-42. doi: 10.1016/0168-1702(86)90063-8.
Influenza A virus reassortants which are nonpathogenic for chickens are like mammalian influenza A viruses in that they are temperature sensitive for growth at 41 degrees C. We have investigated the mechanism of this temperature sensitivity using reassortants between the two highly pathogenic strains A/FPV/Rostock/34 (FPV, H7N1) and A/turkey/England/63 (TE, H7N3). These reassortants show a strict correlation between the pathogenicity for chickens and the constellation of the genes coding for the ribonucleoprotein complex, RNP. Evidence is presented which shows that all viral components are synthesized in sufficient amounts and that the block in the viral replication cycle at the nonpermissive temperature is a late one affecting virus maturation. It is suggested that the RNP, although still enzymatically functional, may lose its ability to interact normally with viral surface components, thus interfering with the process of virus maturation. Some of the nonpathogenic reassortants which possessed the neuraminidase of TE showed an interesting temperature-dependent phenomenon: the haemagglutinin synthesized at the elevated temperature could only agglutinate erythrocytes at 20 degrees C, when the neuraminidase was inhibited or the infected cells vigorously disrupted by ultrasonication. This phenomenon is possibly not directly related to the temperature-sensitive block.
