Recombinomics: Swine H1N1 Fatality in Washington

Commentary

Recombinomics Commentary 07:46
May 10, 2009

The Snohomish County man, who officials said was in his 30s, had an underlying heart condition. He became sick on April 30 and died Wednesday from what appears to be complications of swine-origin influenza (H1N1), officials with the state Department of Health said.

The above comments describe the first reported H1N1 swine influenza death in Washington state. The death follows two deaths in Texas and one in Canada. These deaths highlight concerns that H1N1 deaths in the United States will parallel the deaths in Mexico when the number of cases increase.

The virus is rapidly spreading in the United States (see updated map), but the vast majority of reported cases are in children or young adults and most of these cases have been mild and did not require hospitalization. However, as the number of deaths in the United States increase, the similarities with Mexico will become clearer.

These similarities are most easily seen in the sequences of the swine H1N1 from patients in Mexico and the United States (see list here), which are virtually identical. Moreover the same sequences had been identified in isolates worldwide, strongly suggesting that differences in mortality are largely due to testing and detection frequencies.

The H1N1 in Mexico was recently confirmed by labs in the United States and Canada. Prior to the lab confirmation, the reports out of Mexico were mixed. It was clear that patients between the ages of 25-44 were dying from atypical pneumonia, but the etiological agent was unclear. The identification of swine H1N1 that matches the virus circumnavigating the globe provides a tight association between prior events in Mexico and future events in countries with more recent introductions.

However, the timing of these introductions remains uncertain. The mild nature of the vast majority of case allows for silent spread. The first two cases in the United States were identified through a border surveillance system. Other infections would go undiagnosed or misdiagnosed because of similarities with seasonal flu. Most infected patients would not seek medical attention, and those that did would be positive for influenza A and treated as seasonal flu patients.

This silent spread will likely continue because of decisions to limit testing of patients by state labs. Many have indicated that they will concentrate on more severe cases. Although an influenza A positive at this time of the year in the northern hemisphere will be increasingly likely to be H1N1 swine flu, a lab confirmation is the best tracking data.

The deaths of the young adults in Texas and Washington highlights the similarities between the H1N1 swine flu pandemic of 2009 and the 1918 outbreak, which also began with mild influenza due to efficient swine H1N1 transmission in a human population.

The rapid spread in the human population increases the likelihood of co-infrection with H1N1 seasonal flu and the acquisition of key polymorphisms linked to adaptation in human hosts. Two likely acquisitions are NA H274Y and PB2 E627K, which are fixed in human H1N1.

Close monitoring of sequences, including those from the southern hemisphere in the near term, will allow for detection of key changes that will drive swine H1N1 infections in the northern hemisphere in the fall.
The key acquisitions were recently demonstrated in the fixing of oseltamivir (Tamiflu) fixing in H1N1 seasonal flu, and acquisition of key polymorphisms via homologous recombination remains a cause for concern.

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