In conclusion, the results of this study illustrates that, despite being given information, respondents had no detailed understanding of avian influenza, had a great perceived risk of experiencing avian influenza, and had a low compliance with precautions behaviors. These observations raise concerns about a clear need to find the optimal way of correcting these deficiencies by developing and implementing public health policy regarding priorities for tailored educational and promotion strategies and in particular more attention should be given on using preventive approaches in these population. Nevertheless, it is important to consider that dissemination and widespread adoption of preventive measures require education. Encouragingly, respondent's interest in learning more about avian influenza was high in our survey. Therefore, designing and implementing avian influenza educational programs and measuring their effectiveness should be priorities to incentive the population to take a more active role. The evolution of human influenza A viruses from 1999 to 2006: A complete genome study BACKGROUND: Knowledge about the complete genome constellation of seasonal influenza A viruses from different countries is valuable for monitoring and understanding of the evolution and migration of strains. Few complete genome sequences of influenza A viruses from Europe are publicly available at the present time and there have been few longitudinal genome studies of human influenza A viruses. We have studied the evolution of circulating human H3N2, H1N1 and H1N2 influenza A viruses from 1999 to 2006, we analysed 234 Danish human influenza A viruses and characterised 24 complete genomes. RESULTS: H3N2 was the prevalent strain in Denmark during the study period, but H1N1 dominated the 2000–2001 season. H1N2 viruses were first observed in Denmark in 2002–2003. After years of little genetic change in the H1N1 viruses the 2005–2006 season presented H1N1 of greater variability than before. This indicates that H1N1 viruses are evolving and that H1N1 soon is likely to be the prevalent strain again. Generally, the influenza A haemagglutinin (HA) of H3N2 viruses formed seasonal phylogenetic clusters. Different lineages co-circulating within the same season were also observed. The evolution has been stochastic, influenced by small "jumps" in genetic distance rather than constant drift, especially with the introduction of the Fujian-like viruses in 2002–2003. Also evolutionary stasis-periods were observed which might indicate well fit viruses. The evolution of H3N2 viruses have also been influenced by gene reassortments between lineages from different seasons. None of the influenza genes were influenced by strong positive selection pressure. The antigenic site B in H3N2 HA was the preferred site for genetic change during the study period probably because the site A has been masked by glycosylations. Substitutions at CTL-epitopes in the genes coding for the neuraminidase (NA), polymerase acidic protein (PA), matrix protein 1 (M1), non-structural protein 1 (NS1) and especially the nucleoprotein (NP) were observed. The N-linked glycosylation pattern varied during the study period and the H3N2 isolates from 2004 to 2006 were highly glycosylated with ten predicted sequons in HA, the highest amount of glycosylations observed in this study period. CONCLUSION: The present study is the first to our knowledge to characterise the evolution of complete genomes of influenza A H3N2, H1N1 and H1N2 isolates from Europe over a time period of seven years from 1999 to 2006. More precise knowledge about the circulating strains may have implications for predicting the following season strains and thereby better matching the vaccine composition. Every year the influenza A virus causes human infection with varying severity depending on the host acquired immunity against the particular virus strain. Three to five million people experience severe illness and 0.25 to 0.5 million people die of influenza yearly worldwide (WHO EB111/10). The influenza virus evades host immunity by accumulation of point mutations (drift) in the major surface glycoproteins, haemagglutinin (HA) and neuraminidase (NA) or by reassortment of segments from different viruses co-infecting the same cell leading to a new stain with a HA (and NA) not seen in the population before (shift). In the worst case, shifts may cause pandemics. There have been three pandemics the last hundred years, the Spanish flu in 1918 (H1N1), the Asian flu in 1957 (H2N2) and the Hong Kong flu in 1968 (H3N2). It is believed that new pandemics emerge through shifts with strains from the avian reservoir, as was the case of the pandemics of 1957 and 1968, or by direct introduction of an avian strain into the human population as suggested for the 1918 pandemic [1] . At present only two of the 16 possible HA subtypes (H1 and H3), and two of the nine possible NA subtypes (N1 and N2) are circulating in man. H3N2 and H1N1 influenza A viruses have co-circulated in the human population since the re-emergence of H1N1 in 1977, increasing the possibility for genetic reassortments. The prevalence of the different subtype combinations may vary from season to season. The H3N2 has been the predominant influenza A strain during the last 20 years, with the exception of the 1988-1989 and 2000-2001 seasons where H1N1 infections dominated [2] . In the 2000-2001 season a new reassorted human strain, H1N2, emerged in Europe and became established in the autumn 2001 [3, 4] . The new H1N2 subtype was covered by the 2002-2003 H1 and N2 trivalent vaccine components and because both H1 and N2 viruses had circulated the previous years some degree of herd immunity against the new strain was expected. The H1N2 viruses were not associated with severe influenza illness that season. In 2002, a new lineage A/Fujian/411/02(H3N2)-like emerged in Asia and caused significant outbreaks on every continent [5, 6] .