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Vaccine Driven Recombination of H5N1 in Indonesia?
Recombinomics Commentary
September 29, 2005
According to Nidom, the virus H5N1 that the discovery to the poultry and the pig experienced the mutation took the form of the RNA change (ribo nucleic acid) and had the difference of the character, but did not yet become the new virus. "I mentioned him two subgroups, but still was H5N1," he stated.
Added by him, with this mutation, as a result the effectiveness of the vaccination will against the poultry decrease, if this vaccine did not agree with the virus subgroup H5N1.
Nevertheless, he appealed to the community in order to not panic because this mutation just happened to the animal body and was not yet found to the human body. "I did not yet find the mutation of this virus to humankind." His sample was just sent from the Department of the Health was thorough, he said.
Nidom also stated that the mutation was the natural matter for the virus to maintain the life. Nidom expected the use of the vaccine that at random to the poultry to Triger That sped up this mutation.
As far as this is concerned Nidom and his team were continuing the monitoring towards this mutation to try prevented so that the virus not bermutasi became cruel.
The above machine translation indicates novel combinations of polymorphisms have been found in isolates from H5N1 in Indonesia. These changes are discussed in the context of swine sequences and mismatched vaccines. Both areas are cause for concern and may explain why H5N1 has become more efficient at infecting humans.
The acquisition of mammalian polymorphisms by various H5N1 has been noted. These polymorphisms are easily seen in H5N1 isolates from Vietnam and Thailand and have been call human / swine signatures previously.
Although WHO was notified of these changes in July of 2004, they continued to maintain that H5N1 was not in swine and continued to look for reassortment with human genes, which they continue to cite in press releases. H5N1 has never been reported to have human genes and mixing experiment with the 1997 H5N1 and human influenza failed to identify such changes. However, the lack of reassortment has been used repeatedly to offer reassurances, but is not reassuring because H5N1 has broadened its host range without reassortment with human genes. Such arguments are scientifically flawed, because the human receptor binding domain is on H and reassortment with a human H would not produce an H5 serotype.
Instead H5N1 evolves by recombination, and acquires mammalian polymorphisms to expand its host range to more mammals. These changes can be driven by selection, and a mismatched vaccine can drive such changes. Indonesia has been using a vaccination approach to control H5N1, but the program is not effective. H5N1 has become endemic in Indonesia and recent data indicates that the endemic H5N1 also is in asymptomatic, swine and birds. Mild cases in humans suggest it may also be silently spreading in human populations also.
This expansion of host range seeds new populations with H5N1, leading to further recombination. These changes would explain the "mutations" described above. Much of this change can be seen in H5N1 sequences from birds, but Indonesia has yet to make any H5N1 sequences from 2005 public. So far WHO has only issued general statements on the irrelevant lack of reassortment.
In Vietnam and Thailand, the human sequences are virtually identical to the bird sequences, and deposit of the Indonesian sequences in a public databank such as GenBank or the Los Alamos influenza database is long overdue.
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