- Volume 50, Issue 1, 1980

Inborn resistance to orthomyxoviruses due to the allele Mx was investigated at the molecular level in macrophages from A2G mice. In the absence of interferon, Mx-bearing and control cells were equally permissive for M-TUR, a macrophage-adapted strain of influenza A virus. After treatment with various doses of mouse interferon type I, Mx-bearing cells were fully resistant to this virus whereas cells lacking Mx were only marginally protected. Virus attachment and penetration were equally efficient in Mx-carrying and control cells and were not influenced by interferon. However, virus protein synthesis was blocked in Mx-bearing macrophages expressing resistance. These findings indicate that the resistance mechanism specific for influenza viruses realized by Mx in cooperation with interferon inhibits influenza virus replication in macrophages at an early stage following attachment and penetration of the virus.

Simultaneous injection of newborn rabbits with the Schmidt-Ruppin and Prague strains of Rous sarcoma virus regularly induces antibodies which not only recognize the pp60src of both strains but also give positive kinase reaction with extracts of cells infected with either strain.

An antiserum to immune T-type mouse interferon was prepared in rabbits by repeated injections of interferon, induced by phytohaemagglutinin (PHA) in mouse spleen cells and purified to 1 × 105 units/mg protein. The antiserum neutralized mouse interferons synthesized in vitro in response to several T mitogens and Brucella organisms, and also the type II interferon present in the serum of BCG-sensitized mice after an injection of the specific antigen, tuberculin. All these interferons are thus antigenically related; they are also all unstable at pH 2. In contrast, the antiserum did not neutralize interferons induced by West Nile virus (WNV) and Newcastle disease virus (NDV) in vitro, or by lipopolysaccharide and Brucella organisms in vivo; all these interferons are stable at pH 2. It also failed to neutralize a non-glycosylated virus interferon prepared in the presence of tunicamycin.

Electron microscopy of root and leaf cells of Beta vulgaris, Spinacia oleracea, Chenopodium quinoa and Stellaria media infected with beet necrotic yellow vein virus revealed individual rod-shaped particles, sometimes scattered throughout the cytoplasm, but more often loosely associated within angled-layer aggregates. These particles were restricted to a few cells of the host tissues and not associated with any cell constituents.

The Tm-1 gene in tomato inhibits development of mosaic symptoms and multiplication of tobacco mosaic virus (strain o isolates). A virus isolate of strain 1 type caused mosaic symptoms on Tm-1 hosts almost as severe as those it caused on susceptible hosts. However, multiplication of strain 1 virus (measured as accumulation of virus RNA or coat protein) was still partly inhibited in Tm-1 hosts. Thus the two end effects of the Tm-1 gene were to some extent separable.