A simple but likely explanation for the sudden interruption of the spread of influenza could thus be the increase in the spread of above all rhinoviruses. It is well known that a major rhinovirus epidemic always occurs soon after school has started [7]. The virus is spread mainly by contaminated hands [8], and has not been reported to be climate-dependent. Thus the spread of rhinoviruses may have had an advantage over influenza due to the mild and moist climate. Once a rhinovirus infection has become established, infected cells start producing interferon and other cytokines, similar to those produced by influenza [9]. This immune reaction causes the cells to enter an antiviral state. Though double infections occur, they are probably not common enough to maintain high level spread of both rhino and influenza viruses in the population.
Influenza surveillance with sentinel reporting normally does not start until week 40, and respiratory sampling for viral diagnostics is usually scarce during early autumn. For week 40, most Swedish sentinel doctors usually report zero cases of influenza-like illness (ILI), and we do not know whether we the early autumn rhinovirus peak would have been reported as ILI in previous years even if reporting had been in place then. The reason for the large number of rhinovirus infections diagnosed in 2009 was most likely that people who got respiratory tract infections, who would not normally have visited a doctor, did so due to the fear of the pandemic influenza.
In conclusion, we hypothesise that a rhinovirus epidemic that occurred after the end of the summer holidays may have interfered with the spread of pandemic influenza during a period with warm and humid climate that decreases spread of influenza by aerosol. Although the laboratory data supporting this hypothesis are limited, it may stimulate research into the possibility that the interaction between different circulating viruses may affect influenza epidemiology.