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Co-circulation of H5N1 Strains in Indonesia Causes Concern
Recombinomics Commentary
September 30, 2005
According to Nidom one of the compiler's amino acids (Deoxyribo Nucleic Acid) DNA the A virus of type influenza with sub the type H5N1 that attacked the Indonesian poultry experienced the change. The change like this according to him was mentioned as 'point mutation' or 'antigenic drift'.
"That happened was 'point mutation' or 'antigenic drift', not yet 'antigenic shift'," he explained.
The change in the amino acid composition in DNA this virus according to him caused the occurrence of the change in the character of this virus, both to antigenitas him and spesifitas the virus personally.
Was based on the change that happened to DNA this virus of Nidom grouped the sub-type of the virus H5N1 to the poultry in Indonesia became two groups. "We could not say this group by the name of certain but that clear this has become the special branch," he explained.
The above machine translation provides further evidence for recombination in H5N1 in Indonesia. This recombination has created a second group, which is co-circulating with the group previously described for Indonesian poultry.
WHO has indicated that sequence data from the first two confirmed cases indicated there was no reassortment and the sequences were most closely related to H5N1 sequences from Indonesian poultry. However, the above data indicates that the recombination has generated two distinct groups.
Publication of these sequences would be useful. The co-circulation of two distinct groups will likely lead to additional recombination and identification of parental strains will help define additional recombination. The recombination between closely related strains can be misinterpreted as point mutations. However, new mutations are extremely rare. Most changes in polymporphisms are actually generated via recombination.
These recombinations can lead to the acquisition of mammalian polymorphisms, which was seen in isolates from Vietnam and Thailand as well as wild bird sequences in H5N1 at Qinghai Lake. It would be useful to see if the new Indonesian sequences have the virulence change in PB2, E627K. This polymorphism is usually limited to mammalian isolates, but was present in all 16 H5N1 isolates from the birds at Qinghai Lake. Recombination between the wild bird sequences and various H5N1 emdemic regions in Asia, like Indonesia, was expected.
These changes would explain the increase efficiency of H5N1 infections of humans. There are more familial clusters as well as more clusters of clusters. The number of patients linked to Rangunan Zoo is an example of casual transmission. Moreover, the H5N1 infected birds at the zoo were asymptomatic. In contrast, there have been several reports of recent poultry deaths in Indonesia, which again supports the co-circulation of H5N1 bird flu groups.
The sequences difference between bird and human H5N1 sequences is minimal and the number of human H5N1 sequences in Indonesia is limited because H5N1 can be most easily be isolated from the nose and throat at the early stages of infection. However, initial cases are admitted to primary care facilities which do not collect samples. By the time the patient is transferred to infectious disease hospitals, the H5N1 has moved to the lings and the nose and throat swabs are negative.
Thus, the sequences from the birds will be useful in determining the parental strains which can be used to predict additional recombination. The above comments demonstrate once again that H5N1 evolves via recombination, not reassortment with human genes.
The acquisition of mammalian polymorphisms by recombination is the key driver of H5N1 evolution and expansion of its host range, which now clearly involves humans, as demonstrated by human-to-human transmission and infections via casual contact.
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