|Home||Founder||What's New||In The News||Contact Us|
|Paradigm Shift Intervention Monitoring||Audio: Sep22 Nov10 Jan19 Mar23
Human Spread of Swine H1N1 in Southern California
The above ProMED comments on the two swine flu isolates from children in southern California may be accurate for transmission in swine, but the symptomatic family members described in the MMWR dispatch provides information that transmission in humans is efficient, which is also supported by the fact that these two clusters are 100 miles apart (see updated map).
The family members had even milder courses than the two confirmed cases, so no samples were collected and the spread was both efficient and silent. There is no indication that the four symptomatic family members sought treatment, and in most instances medical assistance would have just led to an influenza A diagnosis and treatment.
The two cases were identified because they were linked to surveillance program that sero-typed the virus. The sero-typing failure led to further testing which identified the H1N1 serotype as swine. A more routine visit would have just determined that the patient had influenza A.
The lack of any connection between the two confirmed cases, other than age (9F and 10M) and location in southern California suggests that there are many undetected cases in the area, which likely includes Mexico, where some contacts were located. Therefore, an international survey would gain additional information on the spread of the H1N1.
These two clusters differ from prior swine detections because the two outbreaks are separated by a large distance and involve the same virus with the unusual constellation of swine flu genes that has not previosult been reported in swine.
The CDC has promptly released the HA (EPI176470), NA(EPI176472), and M(EPI176471) gene sequences of A/California/04/2009 from 10M (at GISAID). These sequences confirm that the NA and M gene have a Eurasian swine origin, while the HA sequences is North American swine. The presence of S31N in the M gene, which is common in European swine, confers resistance to amantadine and rimantadine. Release of the sequences from the other isolate would be useful to determine how long these viruses have been in human populations.
The efficient transmission of swine H1N1 in a human population raises concerns of further evolution and adaptation through the exchange of genetic information with human seasonal flu via reassortment and recombination (including H274Y).
Recombination between swine H1N1 and seasonal H1N1 generated the 1918 pandemic strain, which is cause for concern.