Posts Tagged ‘H1N1’

Narcolepsy traced to specific [flu] vaccine batches

4 June, 2012

See on Scoop.itVirology News

“A new Swedish study shows that all Swedes who developed narcolepsy from the swine flu vaccine Pandemrix received the vaccine from 12 of the 35 batches, despite the claim by the responsible agency that no such connection exists.”

There are some slightly disturbing connections between the H1N1 2009 pdm virus and narcolepsy: the virus itself seems to have caused narcolepsy in some of those infected; now a vaccine is implicated – is this an innate property of certain of the virus proteins, possibly?

See on www.thelocal.se

Nano Patents and Innovations: Powerful New Approach To Attack Flu Virus

28 May, 2012

See on Scoop.itVirology and Bioinformatics from Virology.ca

An international research team has manufactured a new protein that can combat deadly flu epidemics.

The paper, featured on the cover of the current issue of Nature Biotechnology, demonstrates ways to use manufactured genes as antivirals, which disable key functions of the flu virus, said Tim Whitehead, assistant professor of chemical engineering and materials science at Michigan State University.

See on nanopatentsandinnovations.blogspot.fr

Pandemic 2009 H1N1 vaccination produces antibodies against multiple flu strains

27 May, 2012

See on Scoop.itVirology News

“The pandemic 2009 H1N1 vaccine can generate antibodies in vaccinated individuals not only against the H1N1 virus, but also against other influenza virus strains including H5N1 and H3N2.”

 

And a possible reason for this could be that the H1N1pdm virus’ haemagglutinin is a natural “ancestral” sequence – the kind that HIV vaccine researchers are looking for for gp120/160, which have been shown to elicit a wider spectrum of cross-reacting antibodies than “evolved” proteins, or ones that have been selected for antigenic escape in humans for a good few viral generations.

 

Flu vaccine graphic by Russell Kightley Media

See on www.eurekalert.org

Flu shot offers surprising benefits for pregnant women; Vaccine may fight stillbirth, preterm birth, and very low birth weight

25 May, 2012

See on Scoop.itVirology News

A new study announced Tuesday finds the H1N1 flu vaccine not only can protect you from getting sick but can actually benefit your baby.

Researchers from the University of Ottawa in Canada examined data from more than 55,000 child births in Ontario during an outbreak of H1N1, comparing mothers who were vaccinated to those who weren’t.

While prior research has found that pregnant women can safely get the flu shot at any stage of their pregnancies — something many doctors vehemently support — the new findings associate H1N1 vaccinations with a significantly reduced risk of stillbirth, preterm birth, and very low birth weight.

“These are all significant results, but especially interesting is the finding that the vaccinated mothers were one-third less likely to have a stillborn child,” said study researcher Deshayne Fell, a graduate student at McGill University who works with the birth record database. “This is one of the only studies large enough to evaluate the association between maternal flu vaccination and stillbirth — a very rare event.”

 

So much for the disinformation about dangers to pregnant women: in fact, Spanish Flu and the recent H1N1 pandemic were both especially dangerous for unprotected pregnant women.

See on www.nydailynews.com

Protection against Killer Flu! No, not H5N1…

17 January, 2012

Depiction of virus mixing in a pig http://www.rkm.com.au

In an issue of Virus Research devoted to commemorating the career of Brian Mahy, who retired recently from the CDC and now as Editor-in-Chief of Virus Research, there is a paper by Taubenberger and Kash on the 1918 H1N1 flu – wherein they say the following:

“In a recent set of experiments, it was shown that mice vaccinated with the monovalent 2009 pandemic H1N1 vaccine were completely protected in a lethal challenge model with the 1918 influenza virus…”

Because the modern pandemic “swine flu” H1N1 HA protein descends directly from the 1918 virus, but in pigs rather than in humans. Remember all the hype around THAT work – resurrecting the legendary Spanish Flu, and how it would kill us all? And here we already have a vaccine, that will completely protect us.

We have vaccine candidates against H5 as well. Time for a universal flu vaccination campaign and pre-emptive strike, people!

Killer Flu hype grinds on

16 January, 2012

The Independent today has a story entitled”Killer flu doctors: US censorship is a danger to science” – thanks, AJ Cann! – which details how the folk in the Netherlands who did the work do not think the USA should not be “…be allowed to dominate the debate over who controls sensitive scientific information that could be misused in biowarfare terrorism”.

Influenza A viruses mixing in susceptible hosts

 

Well, yes, join the club, guys!  The article is quite reasonable – apart from a couple of points, noted below – but it ends on a suitably alarmist note “…the chances of a laboratory strain of H5N1 escaping into the wild remain high if it is stored in conventional flu-virus labs”, and “Regulators should not be sitting idly by, while the threat of a man-made pandemic looms”.  Really?  The undoubtedly very small amount of mutated flu that exists, relative to any engineered bioweapon in US or Russian labs, represents a clear and present threat to world health?

What dismayed me most, however, was how horrifyingly uninformed most of the commenters are – about H5N1 in particular, and science and science funding in general….!  As I could not comment there – Disqus broke, apparently – I will do so here.

As for labelling the article “Killer Flu Doctors” – really!  A little sensationalism, anyone??  Concerning the comment “…the details could be misused by rogue states or by biowarfare terrorists with access to rudimentary scientific knowledge and fairly standard laboratory equipment”: as a practicing molecular virologist, I can tell you that you would need a lot more than “rudimentary scientific knowledge” – you’d need skill in molecular biology, and especially in reverse genetics of (-)strand RNA viruses, as well as more than “fairly standard equipment” to even BEGIN to hope to make anything like a “killer” H5N1 from published details.

Additionally, a H5 N1 flu virus that is  aerosol transmitted in ferrets – and how efficient was that, I ask? – may NOT be similarly transmissible or as easily (if it was easy) between humans.  I will point out that people thought the SARS CoV outbreak was the “Big One” flu pandemic – but although it was aerosol transmissible, it wasn’t nearly as efficiently transmitted as the common flu, so did not spread as fast.

Thus, most of what the doomsayers are predicting could be simply hype – meanwhile, in countries far away from the US which seeks to regulate such work, the virus is already endemic, and mutating freely – and it would be VERY useful indeed to know what to look for!

What are you looking for?

18 April, 2011

It is quite educational sometimes, to look and see what it is people are looking for, when they end up on ViroBlogy.  Here are the queries over the course of the last month:

Search Views
ebola 577
ebola virus 64
rolling circle 44
how did viruses evolve 29
mimivirus 21
despair posters 19
flaviviridae 17
lassa fever 14
bacterial dna replication 11
ebola virus patients 11
viroblogy 9
where did viruses evolve from 9
ebola pictures 9
rift valley fever 9
what did viruses evolve from 9
geminivirus 8
west nile virus structure 8
ebola patient 8
where h1n1 came from 7
ebola virus pictures 7

I count 6 mentions of Ebola, 4 of virus evolution generally…and a gratifyingly high number of queries on rolling circle replication, given our lab’s interest in it.  Of course, I have had long had an obsession with Ebola and similar nasties, and have been deeply interested in the evolution of viruses ever since I started studying them, so it is good to see others share my interests!

So in the spirit of giving people what they want, look for blog posts with titles like “The evolution of viruses using rolling circle replication: its complete non-relevance to Ebola and H1N1 influenza viruses”.  But seriously – I will be putting up some more posts around the most popular subject areas, if only to help make sure that The Truth Gets Out There.

Ed Rybicki

And so it’s over – is it??

26 August, 2010

The WHO recently declared the H1N1 “swine flu” pandemic to be over – on August 10th, 2010.   From the AFP article:

“The world is no longer in phase six of the pandemic alert. We are now moving into the post-pandemic period,” WHO Director General Margaret Chan said

….

Swine flu has killed more than 18,449 people and affected some 214 countries and territories since it was uncovered in Mexico and the United States in April 2009, according to WHO data.

The new virus spread swiftly worldwide despite drastic measures including a week long shutdown in Mexico, prompting the UN health agency to scale up its alerts and declare a pandemic on June 11, 2009, banishing kisses and frowning on handshakes.

Fears about the impact of swine flu on unprotected populations and a harmful mutation sparked a rush for hundreds of millions of dollars worth of specially-developed vaccines and a flurry of public health precautions.

However, those concerns dwindled in late 2009 to be replaced by recriminations in Western nations about the cost of unused vaccines and what some European critics regarded as an unjustified scare.

Amazing, that: the world authorities get it right, help mitigate what could have been a nasty pandemic – then get it in the neck for being alarmist, and helping drug companies make a profit.

Further from the article:

After petering out in Europe and the United States before their winter flu season was over, in recent months swine flu has affected parts of South Asia and “limited areas” of tropical South and Central America, as well as Africa for their second season.

But unlike 2009, when A(H1N1) ousted most other types of flu viruses around the world, known seasonal viruses now are prevalent and even dominant in countries such as South Africa.

Yeeessssss…and that’s all very well, because do you know what happened in South Africa?  They’ve only just released H1N1 vaccine stockpiled for health workers for the duration of the Soccer World Cup, is what – late in the flu season, and almost too late to do any good.  Meaning exactly what was predicted at the beginning of the pandemic, came to pass: there was not enough vaccine for developing countries, and even a year after its emergence, it was still not being distributed evenly.

Not a very good practice run for the Big One, if you ask me: still not enough vaccine being made quickly enough; vaccine not being distributed to at-risk countries; too much fussing over the welcome news that it was not as bad as it could have been.

I’m going to put my faith in plants….

So it wasn’t so bad…THIS time.

13 January, 2010

Influenza A viruses mixing in susceptible hosts

 

I have been waiting with great interest to see what would happen in the wrong northern hemisphere 2009-2010 winter season with the Mexican – sorry; politically incorrect, aka pandemic H1N1 – flu – and it has pretty much happened, and it wasn’t nearly as bad as it could have been.

From ProMED:

 

INFLUENZA PANDEMIC (H1N1) (05): VACCINE UPDATE

**********************************************

A ProMED-mail post
Date: Mon 11 Jan 2010
Source: Reuters News [edited]

Countries re-think swine flu vaccine orders

- ——————————————-

The United States said on Monday [11 Jan 2010] it had cut in half its order for influenza pandemic (H1N1) 2009 virus vaccine from Australia’s CSL Ltd, but said it is not certain how far orders from other suppliers will be trimmed. While U.S. officials are still calculating how much swine flu vaccine they will need, it is becoming increasingly clear that the United States will not need all 251 million doses it ordered from 5 companies. …

Several other governments have started to cut orders for [pandemic] H1N1 vaccines because the pandemic has not turned out to be as deadly as originally feared and most people need only one dose, not 2, to be fully protected.

…Germany’s Bild newspaper reported that the German government had agreed to cut its vaccine order with GlaxoSmithKline Plc by one-3rd. The newspaper said the agreement would save states about 133 million euros (USD 193 million). On Friday [8 Jan 2010], Britain said it was in talks with Glaxo about reducing supplies. ….

…While the pandemic is slowing down in North America, the World Health Organization said on Monday [11 Jan 2010] the virus was still active in parts of central, eastern and southeastern Europe, North Africa and South Asia. Governments are torn between trying to encourage companies to make influenza vaccine and wasting money on doses that are never given. But bulk antigen — the vaccine before it is put into a syringe – — can be stored and might be used in next year’s seasonal vaccine.

The U.S. government was still promoting vaccination, reminding people that influenza is unpredictable and that [pandemic] H1N1 could come back in a 3rd wave. One potentially large market for the vaccine is children. Children under 10 need 2 doses of vaccine to be fully protected and some U.S. school districts were planning more vaccination clinics this week to get children a 2nd dose. …
[Byline: Maggie Fox]

- –

Communicated by:
ProMED-mail Rapporteur Mary Marshall

Communicated by:
ProMED-mail

 

Influenza virus A H1N1 2009: gets to parts the other flu doesn’t reach

14 September, 2009

Flu virus life cycle. Copyright Russell Kightley Media

The September 2009 issue of Nature Biotechnology has a letter concerning the receptor specificity of AH1N1 2009 pandemic influenza virus – which accounts pretty well for why it CAN be pretty nasty, and for why it may get nastier yet.

Childs et al., in a letter entitled “Receptor-binding specificity of pandemic influenza A (H1N1) 2009 virus determined by carbohydrate microarray“, describe what amounts to a tour de force analysis of the receptor binding of a number of influenza viruses, which concludes with the statement that:

“The differences in receptor binding between the 2009 pandemic and seasonal H1N1 viruses may therefore account, at least in part, for the higher virus replication and greater pathology reported in the lungs of ferrets, mice and nonhuman primates infected with pandemic viruses, than observed with contemporary seasonal viruses.”

Which would help explain why some otherwise healthy young people are dying of the virus, while others are getting only mildly ill.  But we get ahead of ourselves: in January last year I wrote in MicrobiologyBytes about recpetor specificities of A-type influenza viruses, in the context of how H5N1 was less likely to mutate to easy human-to-human transmissibility than had origianlly been thought.

I wrote at the time:

According to a letter in the January 2008 issue of Nature Biotechnology, it is a characteristic structural topology, and not just the α2,6 linkage, that enables specific binding of HA to α2,6 sialylated glycans. The authors state:

…recognition of this topology may be critical for adaptation of HA to bind glycans in the upper respiratory tract of humans. An integrated biochemical, analytical and data mining approach demonstrates that HAs from the human-adapted H1N1 and H3N2 viruses, but not H5N1 (bird flu) viruses, specifically bind to long α2-6 sialylated glycans with this topology. This could explain why H5N1 viruses have not yet gained a foothold in the human population.

Apparently the critical shape in humans is umbrella-like, whereas the avian receptor is characteristically cone-like. Again from the paper:

The topology of α2-3 and α2-6 is governed by the glycosidic torsion angles of the trisaccharide motifs-Neu5Aca2-3Galb1-3/4GlcNAc and Neu5Aca2-6Galb1-4GlcNAc, respectively (Supplementary Fig. 3 online).

Ram Sasisekharan and colleagues showed that human-adapted viruses with mixed α2,3/α2,6 binding ability that bound the umbrella-type receptor were efficiently transmitted, whereas viruses with the same basic specificity that did not have HA binding specificity to “long” α2,6, were not.

The present paper reports the following investigation:

“We have compared directly, by carbohydrate microarray analysis, the receptor-binding characteristics of two isolates of the novel pandemic H1N1 virus, Cal/09 and A/Hamburg/5/2009 (Ham/09), with those of a seasonal human H1N1 virus, A/Memphis/14/96-M (Mem/96), as representative of a virus well adapted to humans [and a reassortant human H3N2 virus A/Aichi/2/68 x PR8 (X31)]. As the HA of the novel H1N1 pandemic virus originated from a virus similar to triple reassortant swine H1N1 viruses, we compared one such example, A/Iowa/1/2006 (Iowa/06), isolated from a human infection, and an older close relative of classical swine H1N1 viruses, A/New Jersey/76 (NJ/76), the human isolate that initiated the concern of a pandemic threat in 1976.”

This is a really comprehensive analysis – for such a short communication – which throws up a number of interesting points.  First, I was not aware it was possible to do “carbohydrate microarrays”!  Second, the paper shows quite conclusively that the swine-derived AH1N1 viruses have a significantly wider range of receptor specificities than a standard seasonal AH1N1 virus, and – but to a lesser extent – than the reassortant H3N2 virus X31.

Carbohydrate microarray analyses of the six viruses investigated.
From the following article (with permission from NBT):
Receptor-binding specificity of pandemic influenza A (H1N1) 2009 virus determined by carbohydrate microarray.
Robert A Childs, Angelina S Palma, Steve Wharton, Tatyana Matrosovich, Yan Liu, Wengang Chai, Maria A Campanero-Rhodes, Yibing Zhang, Markus Eickmann, Makoto Kiso, Alan Hay, Mikhail Matrosovich & Ten Feizi.
Nature Biotechnology 27, 797 – 799 (2009).
doi:10.1038/nbt0909-797

flu_receptor

Legend:
Numerical scores for the binding signals are shown as means of duplicate spots at 5 fmol per spot (with error bars). The microarrays consisted of eighty sialylated and six neutral lipid-linked oligosaccharide probes, printed on nitrocellulose-coated glass slides. These are listed in Supplementary Table 1 and arranged according to sialic acid linkage, oligosaccharide backbone chain length and sequence. The various types of terminal sialic acid linkage are indicated by the colored panels as defined at the bottom of the figure.

And what does all this mean, exactly?  The authors sum it up well:

These results indicate that no major change in receptor-binding specificity of the HA was required for the emergent pandemic virus to acquire human-like characteristics and become established in the human population. …

The broader specificity, namely, the ability to bind to 2-3- in addition to 2-6-linked receptors is also pertinent to the greater virulence of the pandemic virus than seasonal influenza viruses observed in animal models, and its capacity to cause severe and fatal disease in humans, despite the generally mild nature of most infections. Binding to 2-3-linked receptors is thought to be associated with the ability of influenza viruses to infect the lower respiratory tract where there is a greater proportion of 2-3- relative to 2-6-linked sialyl glycans, although long chain 2-3-linked sialyl (poly-N-acetyllactosamine) sequences are present in ciliated bronchial epithelial cells in humans where they are the receptors for another human pathogen, Mycoplasma pneumoniae.

So there you have it: the viruses can get deeper in to your lungs than the standard flu – which, if it happens, can make you seriously ill.

So what happens if it gets better at binding the 2,3-type receptors in humans?  Well, we’re only in the middle of the pandemic.  We may yet find out the hard way.


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