In influenza the combined virus-bacterial pneumonia is approximately three times more common than primary viral pneumonia. The bacteria most commonly involved are Staphylococcus aureus, Streptococcus pneumoniae and Haemophilus influenzae. S. aureus co-infection is reported to have a fatality rate of up to 42% (ref. 2). It is thought that virus infection in the respiratory tract favours growth conditions for bacteria. In this letter data are presented which show that some S. aureus strains secrete a protease which exerts a decisive influence on the outcome of influenza virus infection in mice by cleavage activation of the virus haemagglutinin.

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[The nature of the influenza C virus receptor and the specificity of the receptor-destroying enzyme].

Bacterial neuraminidases destroy influenza C virus receptors of chick erythrocytes and inactivate hemagglutination inhibitors: rat alpha 1-macroglobulin (RMG) and bovine submaxillary mucin (BSM). These data indicate that neuraminic acid may be a component of influenza C virus receptor. The inhibiting activity of RMG and BSM is also eliminated by the receptor-destroying enzyme (RDE) of influenza C virus. After inactivation, the inhibitors (RMG and BSM) contain a reduced amount of N-acetyl-9-0-acetylneuraminic acid (Neu5, 9Ac2) and a larger amount of N-acetylneuraminic acid (Neu5 Ac). Transformation of Neu5, 9Ac2 into Neu5 Ac may also occur upon incubation of free neuraminic acid with influenza C virus. These data indicate that the RDE of influenza C virus is neuraminate-O-acetylesterase (N-acyl-9 4-O-acetylneuraminate O-acetylhydrolase (EC 3.1.1.53). It was shown that inhibition of influenza C virus hemagglutination by RMG and BSM and, apparently, adhesion of the virus to the cell surface involves binding of influenza C virus with Neu5, 9Ac2.

Acetylesterase↗

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On the receptor of influenza viruses. 1. Artificial receptor for influenza virus.

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Adsorption↗

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[Influenza, a special form of zoonosis].

Findings based on molecular genetics and phylogeny indicate that avian species represent an important reservoir for influenza viruses and that virus strains of man and different mammals originated from avian influenza virus ancestors. In contrast to infectious agents causing classical zoonoses, influenza viruses have to alter their genetic make up in order to change their host range. The special, segmented structure of the viral RNA allows an exchange of gene(s) between two different influenza viruses (reassortment) resulting in viruses with different combinations of genome segments and thereby creating new biological properties. Under the selective pressure of the new host the most adapted virus variants will succeed which arose from a genetically heterogeneous virus population with additional mutations. In particular mutations of the genes encoding the polymerase complex (mutator mutations) would be advantageous for rapid adaptation in a hostile environment. The generation of influenza viruses capable of overcoming the species barrier is a rare event since only virus variants will succeed which are genetically stable and transmissible and which replicate efficiently in the new host. It is considered likely that pigs act as intermediate hosts for adaptation of avian viruses to man.

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