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Commentary
Absence
of Phylogenetic Analysis On Swine H3N2 Cases
Recombinomics
Commentary 06:20
November 13, 2010
The above comments on the two recent swine H3N2 cases indicate the isolates are not due to direct clonal expansion, but they fail to address transmission of swine H3N2 in humans. Although there have only been five documented cases of H3N2 in humans in the United States, all have been in 2009 and 2010, and four of the five were reported in 2010. Detection of such case through routine sub-type is difficult because the H3 has a human origin, as does the N2. It is likely that most cases are found by routine sequencing, which involves a small subset of tested samples.
The case in Wisconsin was infected in September, prior to the official start of the flu season. The Pennsylvania case developed symptoms on October 24, which is in week 43 when only 7 samples from the entire country were sero-typed as H3. In spite of this low level of seasonal H3 cases, two H3N2 swine flu cases were identified.
The recent increase in such cases raises concerns that the virus is spreading at low levels within the human population. Two cases in the same reporting week is without precedent, which contributed to the pager alert. Moreover, a link between swine H3N2 cases and ill swine has not been established for any of the five cases.
The CDC comments do not address the relationship between the five cases reported to date. Sequences from Kansas, A/Kansas/13/2009, have been released. However, all other human sequences have been withheld. If swine H3N2 is transmitting in humans, phylogenetic analysis would place multiple sequences on the same branch. However, such phylogenetic analysis has not been described, and the withholding of the sequences prevents independent analysis.
The spread of swine H3N2 in humans, even at low levels is cause for concern. The child from Wisconsin required hospitalization. Since the H on the virus is from the 1990’s, children would have limited immunity. Moreover, circulation in swine since the mid 90’s leads to additional changes. The same is true for N, which traces back to human sequences circulating in 2003.
In addition to the linkage to earlier sequences, the genes evolve in swine, which involves polymorphisms that are not common in contemporary human flu sequences. These differences can lead to increased virulence in humans of all ages.
Moreover, the jump to humans allows for adaptations that increase transmission efficiencies that can create rapid spread, as was seen in pandemic H1N1.
Thus, the sequences on the cases reported in 2010 should be released, and sequencing of influenza A positive samples should be increased.
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