1918 Flu - 90 years of immunity

Antibodies isolated from survivors of the 1918 pandemic influenza virus can protect mice from lethal infection. Summaries of newsworthy papers include New susceptibility gene for type 2 diabetes, Ion channels implicated in bipolar disorder and Cancer taking the Myc


For papers that will be published online on 17 August 2008

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Nature: 1918 Flu - 90 years of immunity

Genetics: New susceptibility gene for type 2 diabetes

Genetics: Ion channels implicated in bipolar disorder

Nature: Cancer taking the Myc

· Mention of papers to be published at the same time with the same embargo

· Geographical listing of authors

PDFs of all the papers mentioned on this release can be found in the relevant journal’s section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.

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[1] Nature: 1918 Flu - 90 years of immunity
DOI: 10.1038/nature07231

Antibodies isolated from survivors of the 1918 pandemic influenza virus can protect mice from lethal infection, according to research published online in Nature this week. The finding proves that the immune system in these individuals still 'remembers' the virus nearly 90 years after the initial infection.

James Crowe and colleagues found that all 32 individuals tested, born in or before 1915, had antibodies that recognised the 1918 strain of the flu virus. Several of the individuals also had circulating B cells that were still produced these specific antibodies. Importantly, the antibodies were still functional and were able to protect mice from experimental infection with the 1918 viral strain.

The team went on to identify the area on the virus where the antibodies bound to stop infection. The authors suggest that these antibodies could act as useful therapeutics, should another virus similar to the 1918 flu strain ever emerge.

Author contact:
James Crowe (Vanderbilt University Medical Center, Nashville, TN, USA)
Tel: +1 615 343 8064; E-mail: [email protected]

[2] & [3] Genetics: New susceptibility gene for type 2 diabetes
DOI: 10.1038/ng.207
DOI: 10.1038/ng.208

Scientists have identified variants that increase risk of type 2 diabetes in populations of both East Asian and European origin. Each copy of one of these risk variants increases an individual’s odds of getting the disease by 30–40%, an effect that exceeds all of the other susceptibility genes identified to date, with the exception of TCF7L2.

Online in Nature Genetics this week two groups report genome-wide association studies of Japanese individuals with type 2 diabetes. Masato Kasuga and colleagues found variants in KCNQ1 to be associated with increased risk of the disease, which they subsequently replicated in populations from Korea, China and Sweden. Shiro Maeda also identified risk variants in KCNQ1 in Japanese, and replicated the associations in affected individuals from Singapore and Denmark. KCNQ1 encodes a potassium channel subunit, and although KCNQ1 mutations have most prominently been associated with life-threatening cardiac arrhythmias, the gene has also been reported to regulate insulin secretion in the pancreas.

The risk variants have a similar effect in both East Asian and European populations, but they are much less frequent in Europeans, which may explain why they were not previously identified in the European-based large-scale studies of type 2 diabetes. As such, these results add to the growing body of evidence that the frequency of disease susceptibility variants may differ depending on ancestry, and underscore the importance of carrying out genome-wide association studies of individuals of non-European descent.

Author contacts:
Masato Kasuga (Kobe University Graduate School of Medicine, Kobe, Japan) Author paper [2]
Tel: +81 78 382 5861; E-mail: [email protected]

Shiro Maeda (Center for Genomic Medicine, RIKEN, Yokohama, Japan) Author paper [3]
Tel: +81 45 503 9595; E-mail: [email protected]

Additional contact for comment on papers:
Mark McCarthy (University of Oxford, UK)
Tel: +44 1865 857298; E-mail: [email protected]

[4] Genetics: Ion channels implicated in bipolar disorder
DOI: 10.1038/ng.209

Variants in two genes are associated with increased risk of bipolar disorder, according to a study published online this week in Nature Genetics. Bipolar disorder is a common mood disorder formerly known as manic depression, and is characterized by alternating episodes of mania and depression.

Previously published genome-wide association studies have generated suggestive evidence for genetic risk factors, although with little agreement from study to study. Pamela Sklar, Nick Craddock and Shaun Purcell led a collaborative effort to re-analyze the published results in combination with a genome scan of an additional group of individuals with the disease.

The strongest evidence for genetic risk factors was for variants in ANK3 and CACNA1C. The gene ANK3 encodes a protein called ankyrin G, which has been reported to regulate the assembly of sodium channels. The gene CACNA1C, encoding a calcium channel subunit, provides support for an association that had previously been suggested. Some of the authors had also previously shown that both these genes are down-regulated in the mouse brain in response to lithium, which is one of the most effective therapies for bipolar disorder. The data raise the possibility that bipolar disorder is, in part, a result of altered ion channel function.

Author contacts:
Pamela Sklar (Massachusetts General Hospital, Boston, MA, USA)
Tel: +1 617 726 0475; E-mail: [email protected]

Nick Craddock (Cardiff University, UK)
Tel: +44 2920 744 663; E-mail: [email protected]

Shaun Purcell (Massachusetts General Hospital, Boston, MA, USA)
Tel: +1 617 726 7642; E-mail: [email protected]

[5] Nature: Cancer taking the Myc
DOI: 10.1038/nature07260

Therapies that block the action of a gene called Myc may prove useful against cancer, suggest results from a mouse study in this week’s Nature.

Myc is a regulatory gene found in normal, healthy cells. However, it is commonly overexpressed in tumours, making it a possible target for anti-cancer therapies. Gerard Evan and colleagues now show that when Myc is inhibited in a mouse model of lung cancer, early and established tumours quickly regress. Importantly, in this model Myc was not overexpressed, demonstrating that Myc might be a more general therapy target.

Critics warn that cancer therapies that block Myc could cause devastating side effects because the gene helps regenerative tissues, such as those found in skin and bone marrow, to replenish themselves. Although the mice in this study showed no overt signs of ill health or distress, bone marrow proliferation and white blood cell count were reduced, and the animals also became anaemic. However, the side effects were short lived and disappeared after two weeks, suggesting that Myc may be a viable anti-cancer target after all.

Author contact:
Gerard Evan (University of California, San Francisco, CA, USA)
Tel: +1 415 514 0438; E-mail: [email protected]

Items from other Nature journals to be published online at the same time and with the same embargo:

Nature (http://www.nature.com/nature)

[6] Replication fork movement sets chromatin loop size and origin choice in mammalian cells
DOI: 10.1038/nature07233

[7] An intrinsic mechanism of corticogenesis from embryonic stem cells
DOI: 10.1038/nature07287

[8] Heterochromatin links to centromeric protection by recruiting shugoshin
DOI: 10.1038/nature07217

NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)

[9] Network-based prediction of human tissue-specific metabolism
DOI: 10.1038/nbt.1487

[10] High-resolution metagenomics targets specific functional types in complex microbial communities
DOI: 10.1038/nbt.1488

[11] Predicting PDZ domain-peptide interactions from primary sequences
DOI: 10.1038/nbt.1489

NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)

[12] Actin and alpha-actinin orchestrate the assembly and maturation of nascent adhesions in a myosin II motor-independent manner
DOI: 10.1038/ncb1763

[13] Talin depletion reveals independence of initial cell spreading from integrin activation and traction
DOI: 10.1038/ncb1765

[14] Epigenetic transcriptional repression of cellular genes by a viral SET protein
DOI: 10.1038/ncb1772

NATURE GENETICS (http://www.nature.com/naturegenetics)

[15] tRNA splicing endonuclease mutations cause pontocerebellar hypoplasia
DOI: 10.1038/ng.204

[16] Detection of sharing by descent, long-range phasing and haplotype imputation
DOI: 10.1038/ng.216

NATURE GEOSCIENCE (http://www.nature.com/ngeo)

[17] Production of bio-refractory fluorescent dissolved organic matter in the ocean interior
DOI: 10.1038/ngeo279

[18] Synchronous basin-wide formation and redox-controlled preservation of a Mediterranean sapropel
DOI: 10.1038/ngeo283

NATURE MATERIALS (http://www.nature.com/naturematerials)

[19] Multi-quantum-well nanowire heterostructures for wavelength-controlled lasers
DOI: 10.1038/nmat2253

[20] Strong magneto-chiral dichroism in enantiopure chiral ferromagnets
DOI: 10.1038/nmat2256

[21] Boosting migration of large particles by solute contrasts
DOI: 10.1038/nmat2254

[22] Spin Rabi flopping in the photocurrent of a polymer light-emitting diode
DOI: 10.1038/nmat2252

Nature MEDICINE (http://www.nature.com/naturemedicine)

[23] RPN2 gene confers docetaxel resistance in breast cancer
DOI: 10.1038/nm.1858

NATURE METHODS (http://www.nature.com/nmeth)

[24] Efficient microRNA capture and bar-coding via enzymatic oligonucleotide adenylation
DOI: 10.1038/nmeth.1244

[25] Genome-wide analysis of transcription factor binding sites based on ChIP-Seq data
DOI: 10.1038/nmeth.1246

[26] mirWIP: microRNA target prediction based on microRNA-containing ribonucleoprotein-enriched transcripts
DOI: 10.1038/nmeth.1247

NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)

[27] Carbon nanotubes as photoacoustic molecular imaging agents in living mice
DOI: 10.1038/nnano.2008.231

[28] Molecular junctions based on aromatic coupling
DOI: 10.1038/nnano.2008.237

Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)

[29] Serotonergic transcriptional programming determines maternal behavior and offspring survival
DOI: 10.1038/nn.2176

[30] Pubertal hormones modulate the addition of new cells to sexually dimorphic brain regions
DOI: 10.1038/nn.2178

[31] The acute light-induction of sleep is mediated by OPN4-based photoreception
DOI: 10.1038/nn.2179

Nature PHYSICS (http://www.nature.com/naturephysics)

[32] Coherent population trapping of an electron spin in a single negatively charged quantum dot
DOI: 10.1038/nphys1054

[33] Electrically driven single-electron spin resonance in a slanting Zeeman field
DOI: 10.1038/nphys1053

Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)

[34] A new tRNA intermediate revealed on the ribosome during EF4-mediated back-translocation
DOI: 10.1038/nsmb.1469

[35] The HP1–p150/CAF-1 interaction is required for pericentric heterochromatin replication and S-phase progression in mouse cells
DOI: 10.1038/nsmb.1470

[36] Structural basis for the activation of PPARgamma by oxidized fatty acids
DOI: 10.1038/nsmb.1474

[37] Structural basis for group A trichothiodystrophy
DOI: 10.1038/nsmb.1478


The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.

Brisbane: 4

Brussels: 7
Roeselare: 15

Santa Catarina: 15

Vancouver: 4

Beijing: 34
Shanghai: 2

Aarhus: 3
Copenhagen: 3
Glostrup: 3

Helsinki: 2

Illkirch: 37
Paris: 6, 15, 20, 21, 35
Poitiers: 7
Toulouse: 20
Villeurbanne: 21

Berlin: 15, 34
Cologne: 15
Frankfurt am Main: 34
Garching: 21
Goettingen: 15, 31
Karlsruhe: 28
Kiel: 18
Munich: 34
Nuremberg: 15
Saarbruecken: 10
Tubingen: 15

Shatin: 2

Debrecen: 36
Szeged: 15

Reykjavik: 16

Dublin: 4, 20

Petach Tikva: 15
Tel-Aviv: 9

Calambrone: 15
Milan: 18
Rome: 5

Akita: 2
Atsugi-shi: 33
Ehime: 2
Fukuoka: 2
Gifu: 2
Kanagawa: 3
Kobe: 2
Kumamoto: 2
Kyoto: 2
Nagoya: 17
Okayama: 3
Osaka: 2, 23
Saitama: 33
Sendai: 2
Shiga: 2, 3
Tokushima: 2
Tokyo: 2, 3, 8, 23, 33, 36
Wakayama: 2
Yokohama: 2, 33

Lumiere: 37

Amsterdam: 15
Arnhem: 15
Nijmegen: 15
Utrecht: 15, 18

Chernogolovka: 20

Singapore: 3

Seoul: 2, 19

Gothenburg: 15
Malmo: 2

Basel: 28
Bern: 15
Zurich: 15

Istanbul: 15

Aberdeen: 4
Birmingham: 4
Cardiff: 4
Edinburgh: 4
Leeds: 15
Leicester: 13, 36
London: 4, 15, 34
Newcastle: 4
Oxford: 31
Southampton: 18


Berkeley: 10
Davis: 12
La Jolla: 1, 9, 32
Palo Alto: 27
San Francisco: 5, 11
Santa Cruz: 19
Stanford: 25
Walnut Creek: 10

Boulder: 26

District of Columbia
Washington: 32

Miami: 17

Atlanta: 19

Maywood: 30

Iowa City: 31

Boston: 4, 24
Cambridge: 4, 11, 19
Worcester: 26

Ann Arbor: 32
East Lansing: 30

New Jersey
Newark: 1

New Mexico
Los Alamos: 10

New York
Albany: 26
New York: 1, 13, 14
Yorktown Heights: 10

North Carolina
Wilmington: 29

Cleveland: 29

Philadelphia: 29
Pittsburgh: 4

Nashville: 1

Dallas: 11

Salt Lake City: 22

Charlottesville: 12

Mukilteo: 10
Seattle: 10


For media inquiries relating to embargo policy for all the Nature Research Journals:

Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]

Katherine Anderson (Nature New York)
Tel: +1 212 726 9231; E-mail: [email protected]

Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]

For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:

Nature Biotechnology (New York)
Peter Hare
Tel: +1 212 726 9284; E-mail: [email protected]

Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]

Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: [email protected]

Nature Materials (London)
Alison Stoddart
Tel: +44 20 7843 4593; E-mail: [email protected]

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]

Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail: [email protected]

Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]

Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]

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Published: 17 Aug 2008

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