Announcement

**sharon sanders** · November 3, 2011, 11:24 AM

Re: Indonesia - 2011 H5N1 Bird Flu Sequence from Fatal Case - 2 Year Old Male

It appears it could be this case:

"Avian influenza – situation in Indonesia - update

14 MARCH 2011 - The Ministry of Health of Indonesia has announced 2 new but unrelated confirmed cases of human infection with avian influenza A (H5N1) virus.

The first case is a 2 year old male from Depok City, West Java Province. He developed symptoms on 3 February, was admitted to a private clinic on 5 February and referred to a hospital on 6 February. He died on 6 February. Prior to his illness, sick and dead poultry were reported in his neighborhood."

more....

404

http://www.who.int/csr/don/2011_03_14/en/index.html

Erreur 404

**sharon sanders** · November 5, 2011, 10:52 AM

Re: Indonesia - 2011 H5N1 Bird Flu Sequence from Fatal Case - 2 Year Old Male

There has been some speculation about the identity of the deceased person whose tissue was submitted for analysis.

I believe it is most probably the 2 year old listed in the above WHO report for the simple reason that in the past few years Indonesia has not been publicly releasing much information about bird flu - H5N1 cases. It makes sense that the government would release a sequence that matches a publicly known case to forestall releasing new information.

We ask that all information pertaining to influenza be released by all governments so that a thorough world wide investigation can be performed by all interested parties.

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**sharon sanders** · November 7, 2011, 11:03 AM

Re: Indonesia - 2011 H5N1 Bird Flu Sequence from Fatal Case - 2 Year Old Male - February 2011

In this sample HA 226 was indicated. This means that the receptor binding site is higher up the throat than found in previous isolate analysis which showed the binding sites to be deep in the lung.

Also, the presence of HA 193 may indicate drug resistance.

**Giuseppe** · November 7, 2011, 12:45 PM

Re: Indonesia - 2011 H5N1 Bird Flu Sequence from Fatal Case - 2 Year Old Male - February 2011

Originally posted by sharon sanders View Post

In this sample HA 226 was indicated. This means that the receptor binding site is higher up the throat than found in previous isolate analysis which showed the binding sites to be deep in the lung.

Also, the presence of HA 193 may indicate drug resistance.

For the hemagglutinin mutation at 226 position see this paper just cited by CIDRAP:

Virology, via CIDRAP: http://www.sciencedirect.com/science...42682211004752

<TABLE width="100%"><TBODY><TR><TD style="PADDING-BOTTOM: 0px; PADDING-LEFT: 0px; PADDING-RIGHT: 0px; FONT-SIZE: 0.85em; PADDING-TOP: 9px" align=left>doi:10.1016/j.virol.2011.10.006</TD></TR><TR><TD style="FONT-SIZE: 0.9em"></TD></TR></TBODY></TABLE>
In vitro evolution of H5N1 avian influenza virus toward human-type receptor specificity

Li-Mei Chen<SUP>a</SUP><SUP>, </SUP><SUP>1</SUP>, Ola Blixt<SUP>b</SUP><SUP>, </SUP><SUP>d</SUP><SUP>, </SUP><SUP>1</SUP><SUP>, </SUP><SUP>2</SUP>, James Stevens<SUP>a</SUP><SUP>, </SUP><SUP>c</SUP>, Aleksandr S. Lipatov<SUP>a</SUP>, Charles T. Davis<SUP>a</SUP>, Brian E. Collins<SUP>b</SUP><SUP>, </SUP><SUP>d</SUP>, Nancy J. Cox<SUP>a</SUP>, James C. Paulson<SUP>b</SUP><SUP>, </SUP><SUP>d</SUP><SUP>, </SUP><SUP>1</SUP>, Ruben O. Donis<SUP>a</SUP><SUP>, </SUP><A href="http://www.sciencedirect.com/science/article/pii/S0042682211004752#cr0005" name=bcr0005><SUP>, </SUP><SUP>1</SUP><SUP>, </SUP><SUP></SUP>

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<TABLE><TBODY><TR><TD class=authorSup><SUP>a</SUP></TD><TD class=authorAddr>Influenza Division, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, United States</TD></TR></TBODY></TABLE>
<TABLE><TBODY><TR><TD class=authorSup><SUP>b</SUP></TD><TD class=authorAddr>Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, United States</TD></TR></TBODY></TABLE>
<TABLE><TBODY><TR><TD class=authorSup><SUP>c</SUP></TD><TD class=authorAddr>Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, United States</TD></TR></TBODY></TABLE>
<TABLE><TBODY><TR><TD class=authorSup><SUP>d</SUP></TD><TD class=authorAddr>Glycan Array Synthesis Core-D, Consortium for Functional Glycomics, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, United States</TD></TR></TBODY></TABLE>
Received 27 August 2011; revised 26 September 2011; Accepted 10 October 2011. Available online 5 November 2011.

Abstract

Acquisition of α2-6 sialoside receptor specificity by α2-3 specific highly-pathogenic avian influenza viruses (H5N1) is thought to be a prerequisite for efficient transmission in humans. By in vitro selection for binding α2-6 sialosides, we identified four variant viruses with amino acid substitutions in the hemagglutinin (S227N, D187G, E190G, and Q196R) that revealed modestly increased α2-6 and minimally decreased α2-3 binding by glycan array analysis. However, a mutant virus combining Q196R with mutations from previous pandemic viruses (Q226L and G228S) revealed predominantly α2-6 binding. Unlike the wild type H5N1, this mutant virus was transmitted by direct contact in the ferret model although not by airborne respiratory droplets. However, a reassortant virus with the mutant hemagglutinin, a human N2 neuraminidase and internal genes from an H5N1 virus was partially transmitted via respiratory droplets. The complex changes required for airborne transmissibility in ferrets suggest that extensive evolution is needed for H5N1 transmissibility in humans.

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<SCRIPT language=javascript xmlns=""> Loader.feature('lp_embed').qCode("loadEmbedContent (EMBED_APC, 'embedAPCModule');") </SCRIPT>Keywords: Highly pathogenic avian influenza virus; Hemagglutinin; Host cell receptor; Virus attachment; H5N1; Sialoglycan; Host range; Pandemic virus emergence

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**Giuseppe** · November 7, 2011, 12:49 PM

Re: Indonesia - 2011 H5N1 Bird Flu Sequence from Fatal Case - 2 Year Old Male - February 2011

For the other hemagglutinin mutation at position 193 alleged in connection with oseltamivir resistance, it is worth to note that - relatively to the old human seasonal strain A(H1N1), not current A(H1N1)pdm09 - the mutation is not causing alone the possible treatment failure (because it is needed the mutation in neuraminidase protein, H274Y) but it is possibly involved in the worldwide spread of the H1N1 oseltamivir-resistant strain - via an hitchhiking like mechanism.

If this mechanism would be viable for transporting other oseltamivir resistant influenza viruses (such as A(H1N1)pdm09 or A(H5N1)) it remains to be established.(IOH)