Studies on the host-cell range of influenza and Newcastle disease viruses.

It is well known that some strains of the influenza virus are rendered to be neurotropic, and this expression means that these neurotropic strains cause death to mice with cerebral symptomes and multiply in the brain if inoculated intracerebrally. The histopathological changes in mice infected with a neurotropic variant of influenza virus were described by Stuart-Harris(1), according to whom the most prevailing features in the brain were a congestion of vessels without perivascular cuffing, a mononuclear cell infiltration of the meninges and changes in the neurones, particularly of Ammon's horn. Francis and Moore(2) also succeeded to obtain neurotropic variants from several strains of influenza virus and described the histopathological findings as hyperemia and lymphocytic meningitis with little or no involvement of the brain parenchyma. On the other hand, Henle and Henle(3) studied the neurotropic effect of non-neurotropic strains of influenza virus and revealed that the histopathological lesions consists mainly of the destruction of the ependymal lining of the ventricles, and there was only slight evidence of meningeal involvement with essentially unaffected brain parenchyma. It seems to be very curious that there is an entire difference between the lesions produced by a neurotropic variant on one hand, and by a non-neurotropic original strain on the other hand, in spite of their common ancestor. From our virological common sence, it might be expected that some common features could be found between those pathological changes produced by a variant and its original strain of a virus. In the case of influenza virus, for example, the manifestation of neurotropism may involve several steps of reaction and non-neurotropic strains may be able to manifest only parts of them so that they produce toxic lesions in a massive inoculation but do not multiply in the same cell group, that is attacked by the toxic action, while the neurotropic variant steps further in the same reaction series and that results in its multiplication. In this respect it may be of interest to take into consideration a fact described by McKee(4) that a non-toxic influenza virus variant, which is unable to produce toxic lesions to mouse brain or lungs, has never been produced from mouse-adapted virus capable of multiplying in mouse lung epitheliums.