While certain comparisons can be drawn to the H1N1 outbreak in 2009, it is important to remember key distinctions between H1N1 and SARS-CoV-2. Certainly, the public health measures implemented to prevent COVID-19 have been far more widespread and disruptive to normal life than the H1N1 outbreak. To understand why these measures have been different, a short background on H1N1 is needed.
A novel influenza A (H1N1) virus emerged in the spring of 2009. This virus, designated as (H1N1)pdm09 (colloquially called the 2009 swine flu), was very different from other H1N1 strains circulating at the time. Very few young people had pre-existing immunity to the virus, but nearly ⅓ of people over age 60 had antibodies against (H1N1)pdm09, suggesting exposure to an older H1N1 earlier in their lives. The CDC estimates that, in the United States, from April 12, 2009 to April 10, 2010, the (H1N1)pdm09 virus led to:
60.8 million cases
The CDC estimates that 151,700 to 575,400 people around the globe died from infection in its first year of circulation (0.001-0.007% of the world’s population). While these numbers are staggering, the impact of the (H1N1)pdm09 virus on the global population was less severe than previous influenza pandemics. In comparison, pandemic influenza mortality rate was estimated to be 0.03% of the world’s population during the 1968 H2N2 pandemic, while the mortality rate for the 1918 H1N1 pandemic was estimated to be 1-3% of the world’s population.
The case fatality rate for (H1N1)pdm09 was approximately 0.02% in the U.S. from April 2009-April 2010. A monovalent (H1N1)pdm09 vaccine was produced and available in large quantities in November 2009. This rapid response was possible because the similarity to other influenza strains allowed the use of established biological and regulatory practices. In August 2010, the WHO declared the end of the global 2009 H1N1 influenza pandemic. While the numbers are still evolving for the COVID-19 outbreak, according to the CDC’s initial report on the first COVID-19 cases in the United States, the case fatality rate for COVID-19 is estimated to be 1.8-3.4% in the U.S.
The H1N1 flu was also less contagious than COVID-19. In a 2014 BMC Infectious Diseases article, Biggerstaff et al. estimated the R0 value for (H1N1)pdm09 to be 1.46. As of March 25th, the R0 for COVID-19 is considered to be between 2-4, as discussed earlier in the module. Finally, while people over age 60 did have some immune protection against the (H1N1)pdm09 virus, there is no pre-existing immunity to SARS-CoV-2, as this virus has never been experienced before by a global population.
The beginning of both the H1N1 and COVID-19 outbreaks appeared similar in terms of major turning points. At the beginning of both H1N1 and COVID-19 pandemics, the genetic sequences of both viruses were released online to enable scientists to begin development of diagnostic tests, vaccines, and antiviral treatments. Just nine days after (H1N1)pdm09 was detected, on April 24, 2009, the CDC uploaded genetic sequences of the virus to a public database and work began on developing a vaccine. Five days after SARS-CoV-2 was detected, on January 12, 2020, Chinese scientists published the viral genetic sequence, and scientists around the globe catapulted into action. The U.S. declared H1N1 to be a public health emergency just 11 days after the first confirmed U.S. case in 2009. The U.S. Department of Health and Human Services also declared COVID-19 a public health emergency 11 days after the first U.S. case was detected.
Despite these initial similarities, the response to COVID-19 has not been as smooth as it was to H1N1 following the initial weeks of detection. Four weeks after H1N1 was detected, the CDC released health supplies from their stockpiles that could prevent and treat influenza. By this time, most U.S. labs had diagnostic tests that could detect H1N1 without verification by the CDC.
In contrast, the CDC began sending diagnostic kits for SARS-CoV-2 to 100 public health laboratories around the U.S. on February 5, 2020. However, most of the labs received defective kits, which caused significant delays in detecting and combating the virus. Testing could only be performed at the CDC headquarters until they could send replacement kits. This constraint allowed the virus to spread undetected for weeks. By March 10, seven weeks after the first U.S. confirmed case, only 79 state and local health labs could test for COVID-19--many of whom were already running out of supplies to run the tests. Moreover, since SARS-CoV-2 was a novel virus, there were no medications, let alone stockpiles that could be used to prevent or treat COVID-19. (For the latest on testing and treatment, see (For the latest on testing and treatment, see Module 1, sections on Diagnostics and Investigational Therapeutics and Vaccine Development.)
According to Dr. Steffanie Strathdee, the Associate Dean of Global Health Sciences at the University of California San Diego’s Department of Medicine, “The 2009 H1N1 pandemic should have been a warning sign. It didn’t end up being a pandemic that killed millions of people as we feared it would, but it should have been a wake-up call. By all serious estimates, COVID-19 is going to be a major killer.”
The key differences between the H1N1 and COVID-19 outbreaks include case fatality rate, R0, pre-existing immunity in the population, testing capability, and preexistence of antiviral treatments. The response to the COVID-19 outbreak has been unprecedented in this century because of the cumulative impact of many of these factors.
CORE TEXT: Baird, R. What Went Wrong with Coronavirus Testing in the U.S. New Yorker, 3.16.20
[5.1.20] Diane posts a wistful thought on Twitter: “6 wks since I last hugged my friends at church. The H1N1 pandemic didn't seem like such a big deal. How did COVID get to be so much worse?” What might you tweet back?
[3.27.20] Brian has just posted on Facebook: “Swine flu was a pandemic, but no one called for us to turn our lives upside down. Why are we freaking out about COVID-19?” What would you write?