Structure and Replication

All influenza viruses show the same structure (see Fig. 7.3, p. 380) and a pronounced pleomorphism. In human tissues and fresh isolates, some filamentous forms several micrometers long are found, with increasingly round forms dominating after several laboratory passages. The genome of the influenza viruses is segmented and comprises eight separate antisense RNA strands, each of which codes for one specific protein. Together with the nucleoprotein, they form the helical nu-cleocapsid. Closely association with this structure is the RNA polymerase complex, which consists of three high-molecular-weight proteins with different functions. The nucleocapsid itself is embedded in a protein (so-called membrane or matrix protein). The virus is enclosed by an envelope made of cell membrane lipids with viral protein inclusions (hemagglutinin and neuraminidase, responsible for infectivity and viral progeny release). Both proteins are seen under the electron microscope as protrusions ("spikes") on the virus surface.

Replication of the influenza viruses proceeds as described on p. 385 for the antisense-strand viruses, whereby the cap of the viral mRNA is acquired by way of a unique mechanism. First, a protein of the polymerase complex separates the cap, together with 10-13 nucleotides, from the cellular RNA molecules by cleavage. This short, cap-bearing sequence serves as the primer in the synthesis of viral mRNA, which therefore begins with a cellular cap and a small piece of cellular RNA. "

Continued: Structure and Replication

The close association of cellular and viral transcription is also reflected in the fact that RNA synthesis in the myxoviruses takes place in the nucleus of the host cell and not, as in other RNA viruses, in the cytoplasm.

Pathogenesis and clinical picture. The aerogenically transmitted influenza viruses normally replicate in the mucosa of the nasopharynx, resulting in a pharyngitis or at most a tracheobronchitis, after an incubation period of 24-72 hours. Pulmonary dissemination of the infection can result from an upper respiratory infection or manifest without one, whereby the prognosis in the latter case is less favorable. Pneumonia caused solely by the influenza virus is rare. As a rule, bacterial superinfections with staphylococci, streptococci, pneumococci, or Haemophilus bacteria are responsible. These infections, which used to be the normal cause of influenza deaths (Haemophilus influenzae in the "Spanish flu" of 1918), can be controlled with antibiotics.

Diagnosis. Influenza viruses can be grown and isolated in cell cultures if the diagnostic specimen is obtained very early, i.e., in the first one or two days of the infection. Throat lavages and swabs provide suitable material. The latter must be placed in a suitable transport medium without delay to prevent them from drying out. Identification of the cultured viruses is achieved based on the hemagglutinating properties of the myxoviruses in the hemagglutination inhibition test or by means of immunofluorescence.

If the specimen was obtained too late for virus isolation, a diagnosis can be arrived at by serological means, whereby a rise in the antibody titer of patient serum proves infection.

Table 8.5 Classification and Antigen Structure of Influenza A Viruses

Viral prototype Predominance Antigen formula

Hemagglutinin Neuraminidase (H) (N)

A/Cambridge/46 A/F/M1/47


A/Hong Kong/68







H2 H3 H1

N2 N2 N1

Epidemiology. Influenza A viruses are genetically variable. Slight antigenic changes are the general rule (antigenic drift, quasispecies, p. 391) and are explained by selection of point mutants in the hemagglutinin under immunological pressure. More profound changes (antigenic shifts) explain the periodic occurrence of influenza A epidemics and pandemics (Table 8.5).

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