Re: Why the United States?
I just came across the following which tentatively suggests that the common cold may have delayed the progress of swine flu in Europe.
Does viral interference affect spread of influenza?
EXTRACT - Full report at
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19354
Eurosurveillance, Volume 14, Issue 40, 08 October 2009
Rapid communications
Does viral interference affect spread of influenza?
A Linde ()1, M Rotz?n-?stlund2, B Zweygberg-Wirgart2, S Rubinova1, M Brytting3
1. Department of Epidemiology, Swedish Institute for Infectious Disease Control, Solna, Sweden
2. Department of Clinical Microbiology, Karolinska University Hospital, Solna, Sweden
3. Department of Virology, Swedish Institute for Infectious Disease Control, Solna, Sweden
Citation style for this article: Linde A, Rotz?n-?stlund M, Zweygberg-Wirgart B, Rubinova S, Brytting M. Does viral interference affect spread of influenza?. Euro Surveill. 2009;14(40)

ii=19354. Available online:
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19354
Date of submission: 07 October 2009
This short communication hypothesises that rhinovirus epidemics occurring after start of school may interfere with the spread of influenza during the period when warm and humid climate decreases the influenza spread by aerosol. Limited laboratory data supporting this hypothesis are included in the article, but the report is written mainly to stimulate interest and research concerning the possibility that viral interaction may affect influenza epidemiology.
...
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.
We therefore suggest the following:
1. The epidemiology of influenza should be related to that of other respiratory viruses for improved understanding of the true epidemiological situation.
2. Surveillance of respiratory infections should be conducted throughout the year to create reliable baselines for ILI and acute respiratory infections, which are useful when a pandemic virus occurs that does not follow the usual pattern of spread.