Influenza 2010–2011: Lessons from the 2009 pandemic

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ABSTRACTMuch was learned about the diagnosis, management, and pathogenesis of influenza from the 2009 pandemic of influenza A (H1N1). This knowledge can be applied to the management of people affected by seasonal infection and to future pandemics.


  • In the H1N1 pandemic, proportionally more children and younger adults were infected and had serious disease than in the seasonal epidemic. Older people were relatively spared from infection, but if infected they had high rates of serious disease as well.
  • Groups at risk of serious complications from seasonal or pandemic influenza include the very young, the very old, pregnant women, and those with chronic medical conditions.
  • Currently available rapid antigen detection tests have limitations; molecular tests such as polymerase chain reaction are the optimal diagnostic method and are now more widely available.
  • Early diagnosis and treatment are associated with better outcomes in influenza-infected patients, particularly those needing hospitalization.
  • It is critical to continue aggressive vaccination and diligence in diagnosing and treating influenza to mitigate the continued threat of this important infection.



Fortunately, the 2009 pandemic of influenza A (H1N1) was less severe than some earlier pandemics, in part thanks to advances in our ability to diagnose influenza, to treat it, and to quickly activate the public health and industry infrastructures to mitigate such a pandemic.

In this article, we present lessons learned from the 2009 pandemic, which may allow clinicians to better prepare for the upcoming influenza seasons.


Influenza causes annual epidemics of varied severity and risk of death. In the United States, these seasonal epidemics are estimated to account for more than 200,000 hospitalizations1 and 1.4 to 16.7 deaths per 100,000 persons (3,349 to 48,614 deaths) each year, mostly in the elderly.2

The past 100 years have seen four influenza pandemics3,4: H1N1 in 1918, H2N2 in 1957, H3N2 in 1962, and H1N1 in 2009. With each pandemic came a spike in hospitalization and death rates in addition to a higher proportion of deaths in people under the age of 65,3 although the relative impact varied widely with the different viruses.3,5

After the 1918, 1957, and 1962 pandemics, the rates of hospitalization and death decreased, although still varying from year to year, and the pattern of who developed serious disease returned to normal, with the very young, those with underlying medical conditions, pregnant women, and those age 65 and older being at risk.3,5,6 Whether the situation in the current postpandemic period will evolve similarly remains uncertain; however, it is believed that the 2009 H1N1 virus will continue to circulate among other established viruses in the community.


In the late winter and early spring of 2009, H1N1, a novel strain of influenza A, was recognized to have caused outbreaks of respiratory illness in Mexico and southern California. 7,8 The virus spread rapidly, and with the aid of global air travel it reached nearly every country in the world within several weeks.4,9

The virus was of swine origin, having six genes of North American swine virus lineage and two genes of Eurasian swine virus lineage. 10 Although classic teaching suggested that pandemics were caused by “new” viruses, typically of avian origin,11 antigen mapping has clearly shown that swine viruses are antigenically significantly divergent from human viruses,14 but are more adapted than avian viruses for human transmission.10,12,13

Little antigenic drift has occurred since the beginning of the outbreak. Nearly all isolates seen to date are antigenically similar to the A/California/7/2009 strain that was selected for pandemic influenza vaccines worldwide and that is now included in the vaccine for seasonal influenza for 2010–2011.4,6,15

The virus appears to replicate more efficiently in the lungs and lower airways than seasonal H1N1 and H3N2 viruses, but generally lacks many of the mutations associated with greater pathogenicity in other influenza viruses.4,10,16


Most infections caused by the 2009 influenza A (H1N1) pandemic virus were acute and self-limited, similar to seasonal influenza.4 Asymptomatic infection has been demonstrated from serologic surveys.17,18

Notably, many older people had preexisting antibodies that cross-reacted with the novel 2009 pandemic virus, which is antigenically related to but highly divergent from the 1918 pandemic H1N1 virus.14 This phenomenon may explain why older people were relatively protected against contracting the virus, while younger people, who lacked these antibodies, were more likely to be infected.

A number of studies, using various methods, suggest that each person infected goes on to infect 1.3 to 1.7 other people, a rate called the basic reproduction number or R0. This rate is comparable to that for seasonal influenza and is higher in more crowded settings.4,19 Seroprevalence studies suggest that there was significant geographic variability in the proportion of the population affected during the first and second waves of the pandemic.4,20,21

Risk factors for complications or severe illness include age younger than 5 years, pregnancy, morbid obesity, and chronic medical conditions. Interestingly, although people 65 years of age and older had the lowest rate of infection, they had high case-fatality rates if they became sick.4,22–25 However, in up to 50% of patients with severe disease, no conventional risk factor could be identified.4,22

Hospitalization rates varied widely by country but were generally highest in those under the age of 5; 9% to 31% of hospitalized patients required intensive care, and 14% to 46% of those receiving intensive care died.4

Overall, the case-fatality rate was less than 0.5%, but ranged from 0.0004% to 1.47%.4 The lowest case-fatality rates were in Japan, where early diagnosis and treatment are credited, in large part, for such exceptional outcomes.26

The incubation period of pandemic H1N1 influenza is 1.5 to 3 days but may be as long as 7 days.4 This virus causes a spectrum of clinical syndromes that range from afebrile upper respiratory illness to fulminant viral pneumonia. 4 As with seasonal influenza, most patients present with fever, sore throat, and cough. Gastrointestinal symptoms including nausea, vomiting, and diarrhea are more common than with seasonal influenza.4,27,28

The viral kinetics of H1N1 are similar to those of seasonal influenza in ambulatory patients, although some reports suggest that the duration of viral shedding may be slightly longer.28

Most patients who needed to be hospitalized presented late after symptom onset with viral pneumonia, which was sometimes may be accompanied by severe hypoxemia, acute respiratory distress syndrome, shock, and renal failure.29,30 Viral loads were very high in those needing intensive care, and virus shedding longer than 5 days, particularly in the lower respiratory tract, was documented despite antiviral therapy.29 Fewer patients were hospitalized for other indications, including exacerbation of underlying medical conditions (especially asthma or chronic obstructive pulmonary disease) and bacterial pneumonia, which might be explained by the different profiles of patients with pandemic vs seasonal influenza.4,31–33

In severe cases, a number of laboratory abnormalities were common at presentation, including lymphopenia and elevations in levels of serum aminotransferases, lactate dehydrogenase, creatine kinase, and creatinine.4

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