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The evolution of influenza viruses is increasingly pursued by molecular analyses that complement classical methods. The analyses focus on the two surface proteins hemagglutinin (HA) and neuraminidase (NA) which determine the viral antigenic profile. Influenza A(H3N2) viruses are exceptionally variable, so that usually at least two virus variants cocirculate at the same time. Together with influenza B viruses they caused approximately 90% of influenza virus infections in Germany during the last 12 seasons, while influenza A(H1N1) viruses only played a subordinate part. Unexpectedly, reassorted viruses of subtype A(H1N2) appeared during the seasons 2001/02 and 2002/03, but were isolated only rarely and gained no epidemiological significance. Furthermore, during the season 2001/02 influenza B viruses of the Victoria-lineage reappeared in Germany and other countries of the northern hemisphere after 10 years of absence. These viruses reassorted with the cocirculating Yamagata-like influenza B viruses, as could be seen by the appearance of viruses with a Victoria-like HA and a Yamagata-like NA.

In addition to acute viral diseases, persistent infections have attained considerable interest in recent years. Such persistent infections are characterized by extended time periods in which the infecting virus remains within the organism before the eventual appearance of manifest symptoms. These infections may be evoked by a variety of virus species resulting in a diversity of pathogenic reactions and clinical manifestations. The mechanisms of viral persistence, where known, also appear to be quite diverse. As far as space permits, some examples of persistent infections will be presented and the mechanisms of the pathogenesis of the resulting diseases will be discussed.