MIT: Genetic Changes In A 2014 Indian H1N1pdm09 Virus

Flu Virus binding to Receptor Cells – Credit CDC

 

# 9810

 

A little over a week ago, in EID Journal: Emergence of D225G Variant A/H1N1, 2013–14 Flu Season, Florida, we re-visited one of the mutations linked to greater virulence in the (formerly pandemic, now seasonal) A/H1N1pdm09 virus.

 

This relatively rare amino acid substitution at position 225 (222 using H1 Numbering) from aspartic acid (D) to glycine (G) allows the virus to bind to receptors found deeper in the lungs, and is linked to the development of more severe pneumonia.

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A 2013 study in Influenza Other Respir Viruses called A(H1N1)pdm09 hemagglutinin D222G and D222N variants are frequently harbored by patients requiring extracorporeal membrane oxygenation and advanced respiratory assistance for severe A(H1N1)pdm09 infection linked this, and the D225N mutation to more severe respiratory symptoms.

While probably the best known, and most studied, of the virulence enhancing mutations in the pH1N1 virus, D225G/N is certainly not the only one.  And in truth, there are likely other  mutations – or combinations of amino acid substitutions – that would increase the virus’s transmissibility, replication, antiviral resistance, or pathogenicity that we don’t even know about.

 

With the D225G/N mutation, it is believed that while it increases virulence, it reduces transmissibility.   But that may simply mean that the right combination of concurrent changes hasn’t emerged to increase both . . . yet.

 

Last November, in When Influenza Goes Rogue, we looked at the long history of extreme variability between flu seasons, and the emergence of mutated, or `drifted’ viruses.  And by now everyone knows that this year we are experiencing exactly that scenario with an antigenically drifted H3N2 virus.

 

The point being that flu viruses – even seasonal flu viruses that have been around for a long time – can occasionally throw us a curve. 

 

This winter we’ve seen India reporting a large number of pH1N1 cases – which they call `swine flu’ – supposedly with an unusually high mortality rate.    We’ve seen these sorts of reports from India in the past, and so it has been difficult to determine if anything is really different about this year’s flu strain (see India swine flu toll inches towards 1500).

 

Although the numbers seem high (and likely represent only the smallest tip of much larger iceberg), in a nation of over a billion people –  millions would be expected to contract the flu in an average year - and of those, thousands would likely die. 

A couple of weeks ago, in India’s H1N1 Outbreak, we looked at some of these reports along the Indian Government’s denials that anything untoward was occurring . India’s National Institute of Virology (NIV) and their National Centre for Disease Control (NCDC) both reported No mutation of H1N1.

 

Today, however, we’ve a report that suggests (based on very limited data) that perhaps something has changed with the H1N1 virus, and that it may be affecting its transmissibility, and severity, in India.

 

First, this press release, and then a link to the study.

 

Analysis suggests a more virulent swine flu virus in the Indian subcontinent

Cell Press

A flu outbreak in India that has claimed over 1200 lives may not be identical to the 2009 North American strain, as recently reported in India. A comparative analysis conducted by scientists at the Massachusetts Institute of Technology (MIT) shows that the flu virus in India seems to have acquired mutations that could spread more readily and therefore requires deeper studies. As flu season in India winds down, the researchers call on officials to increase surveillance of this and future flu outbreaks and rethink vaccination strategies to account for potential new viruses.

The MIT analysis, which compared viral proteins important for virulence and transmissibility in the 2009 and 2014 flu epidemics, was conducted by professor Ram Sasisekharan, PhD, at the Koch Institute for Integrative Cancer Research, and his research scientist colleague Kannan Tharakaraman, PhD. It appears in the March 11 issue of the journal Cell Host & Microbe.

"It has been extensively reported in India that a virus similar to A/California/07/2009 is responsible for the current outbreak," Sasisekharan says. "Examination of the Indian H1N1 flu viruses that circulated in 2014 shows amino acid mutations that make them distinct (in terms of receptor binding, virulence, and antigenic drift) from the A/California/07/2009 virus."

"It is widely believed that the current H1N1 flu vaccine is still effective for the most part," he adds.  "Effectiveness of the current H1N1 flu vaccine is debatable, and there have been calls for updating the vaccine. The Indian H1N1 viruses that circulated in 2014 are different compared to the 2009 vaccine strain A/California/07/2009."

(Continue . . .. )

 

This commentary (see below), which calls for greater testing and genetic sequencing on the Indian Subcontinent, notes that - despite the vastness of the Indian subcontinent, only two sequences have been deposited during 2014–2015 from India, suggesting poor surveillance and potentially limiting the response to a deadly outbreak.

Based on an analysis of Indian-origin strain A/India/6427/2014, they reported finding:

 

Although there are limited Indian-origin influenza sequences available in the public database to make any causal inference on the perceived increased fatalities in India, examination of the 2014 Indian H1N1 HA sequences shows traits with potential cause for concern. Amino acid changes in specific positions in the receptor binding site (RBS) of 2009pdmH1N1 have been shown to impact glycan RBS specificity and have been linked to increased virulence and disease severity.

Among these changes, the Indian-origin strain A/India/6427/2014 contains amino acid changes T200A and D225N compared to the 2009pdmH1N1 pandemic strain. The T200A amino acid change has been shown to improve human glycan receptor-binding of 2009pdmH1N1 HA (Xu et al., 2012b). The D225N mutation has been linked to increased virulence and disease severity in patients infected by the 2009 pdm virus (Ruggiero et al., 2013).

 

A third mutation,  K166Q, was also detected and has been linked to increased severity of pH1N1 in middle-aged adults during the 2013-14 flu season (see CIDRAP Study: Middle-aged adults susceptible to recent flu virus mutation).

The lack of any recent sequencing of H1N1 viruses from India is particularly frustrating in light of recent news reports. The authors write:  It is unknown if the strain A/India/6427/2014 is still in circulation; however, the apparent severity of the current outbreak seems to suggest that it could be.

 

The entire report/commentary – which emphasizes the need for more robust and timely influenza surveillanece and sequencing data -  may be accessed at:

 

Influenza Surveillance: 2014–2015 H1N1 “Swine”-Derived Influenza Viruses from India

Kannan Tharakaraman , Ram Sasisekharan

DOI: http://dx.doi.org/10.1016/j.chom.2015.02.019

Summary

The 2014-15 H1N1 outbreak in India has reportedly led to 800 fatalities. The reported influenza hemagglutinin sequences from India indicate that these viruses contain amino acid changes linked to enhanced virulence and are potentially antigenically distinct from the current vaccine containing 2009 (Cal0709) H1N1 viral hemagglutinin.

MIT: Two Avian Flu Receptor Cell Binding Studies

 

 

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We’ve a pair of avian flu studies, published today in the online journal Cell, that look at the current ability of both the H7N9 and H5N1 viruses to bind to human receptor cells.

 

While there may be other factors at play, the primary barrier that prevents these viruses from sparking a pandemic appears to be their preferential binding to avian receptor cells.

 

We’ve discussed receptor binding often in the past (see Study: Dual Receptor Binding H5N1 Viruses In China & PLoS: Human-Type H5N1 Receptor Binding In Egypt) but to review:

 

Flu Virus binding to Receptor Cells – Credit CDC

 

Human adapted influenza viruses have an RBS - Receptor Binding Site (the area of its genetic sequence that allows it to attach to, and infect, host cells) that – like a key slipping into a padlock -`fit’ the receptor cells commonly found in the human upper respiratory tract; the alpha 2,6 receptor cell.

 

Avian adapted flu viruses, like the H5N1 virus, bind preferentially to the alpha 2,3 receptor cells found in the gastrointestinal tract of birds.

 

While there are some alpha 2,3 cells deep in the lungs of humans, for an influenza to be successful in a human host, most researchers believe it needs to a able to bind to the a 2,6 receptor cell.

 

The $64 question that the research team lead by Ram Sasisekharan, the Alfred H. Caspary Professor of Biological Engineering at MIT, have endeavored to answer is: what type - and how many - changes would these viruses need in order to become more transmissible in humans?

And the authors suggest, it’s probably not a lot.

 

Particularly with the H7N9 virus. 

 

Quick links to the abstracts to these two studies (both studies are, alas, behind pay walls), and then a look at the press release, that describes their findings.

 

Glycan Receptor Binding of the Influenza A Virus H7N9 Hemagglutinin

Cell, 06 June 2013
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.cell.2013.05.034

Authors

Kannan Tharakaraman, Akila Jayaraman, Rahul Raman, Karthik Viswanathan, Nathan W. Stebbins, David Johnson, Zachary Shriver, V. Sasisekharan, Ram Sasisekharan

Highlights

• The hemagglutinin of H7N9 virus does not efficiently bind human receptors
• A single residue change in receptor binding site increases binding to human receptors
• Mutations on hemagglutinin may reduce the effectiveness of current H7 vaccines

(Continue . . . )

 

 

 

Structural Determinants for Naturally Evolving H5N1 Hemagglutinin to Switch Its Receptor Specificity

 

Cell, 06 June 2013
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.cell.2013.05.035 

Authors

Kannan Tharakaraman, Rahul Raman, Karthik Viswanathan, Nathan W. Stebbins, Akila Jayaraman, Arvind Krishnan, V. Sasisekharan, Ram Sasisekharan

Highlights

• Hallmark mutations do not switch receptor preference of recent H5 strains
• Structural comparison of H5 and H2 hemagglutinin receptor complexes
• Determination of key H5Nl receptor-binding features needed for quantitative switch
• Recent strains may require a single base pair change to switch receptor preference

(Continue . . . )

 

While the full text of the articles are behind a pay wall, we do have a press release from MIT that tells us, in general terms, what these studies found. A few excerpts below, but follow the link to read it in its entirety.

 

 

Keeping an eye on bird flu

June 6, 2013

MIT studies of two influenza viruses reveal genetic mutations that could result in pandemic flu.

Anne Trafton, MIT News Office

 

(EXCERPTS)

New research from MIT shows that two recently emerged bird flu strains, which do not spread easily now, could become much more infectious with just one or a few genetic mutations.

 

The studies, which focused on the H5N1 and H7N9 flu strains, should help public health officials monitor evolving flu viruses for potential human-to-human transmission. They could also guide the development of new vaccines, says Ram Sasisekharan, the Alfred H. Caspary Professor of Biological Engineering and senior author of two papers appearing in the June 6 online edition of the journal Cell.

 

<SNIP>

 

H5N1

In the new Cell paper, the MIT team studied the structure of HA proteins from hundreds of H5N1 strains and identified three HA regions where one or two mutations would enable the HA to bind efficiently to human receptors. Most of these regions affect the base of the receptor-binding site.

 

The researchers also found that H5N1 has been evolving rapidly since 2005, but none of the current strains have all of the mutations needed to spread from human to human. However, the researchers found one strain that needs only a single amino-acid switch to become highly infectious, and several others that need only two. “There are multiple different ways that this can happen,” says Sasisekharan, who is also a member of MIT’s Koch Institute for Integrative Cancer Research.

 

Furthermore, because of all of the viral evolution that has occurred since 2005, the H5N1 vaccines that governments have stockpiled would probably no longer be effective, Sasisekharan says. “There is cause for concern,” he says. “Yet these findings open opportunities to make sure that some of these newer strains do become part of the stockpiling, because they are closer to human adaptation.”

 

H7N9

 

H7N9 has infected at least 132 people this year, mostly in China, and there have been 37 deaths, according to the World Health Organization — a lower fatality rate than that of the H5N1 virus.

The MIT researchers found that although the current circulating forms of H7N9 bind weakly to human receptors, a change in just one amino acid would dramatically increase the HA protein’s binding strength. “It was not a marginal increase; we saw a pretty significant increase in receptor binding,” Sasisekharan says.

 

“Our research provides insights to help keep track of potentially important mutations so that proactive steps can be taken to be better prepared against dangerous viruses.”

(Continue . . . )

 

 

Whether any avian influenza strain can make the right changes, and become a human pandemic strain, remains a mystery.

 

Yesterday, in a NEJM Perspective, David M. Morens, M.D., Jeffery K. Taubenberger, M.D., Ph.D., and Anthony S. Fauci, M.D. wrestled with this problem in:

 

Pandemic Influenza Viruses — Hoping for the Road Not Taken

This  remains one of the great debates in influenza science - and the question will likely only be settled after one finally does.

MIT: The Risks Of An Emerging H3N2 Pandemic Virus

 

Credit Wikipedia

 

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At the risk of piling on this morning, even as we track H7N9 and nCoV, it is worth recalling that last summer our attention was heavily focused on outbreaks of several variant swine flus, which infected hundreds of people who attended state and county fairs across the Midwest.

 

Asymptomatic Pigs: Revisited

MMWR: H3N2v Related Hospitalizations In Ohio – Summer 2012

The Return Of H1N1v

 

While we talk about the H3N2 virus as if it were a single entity – or at worst, a handful of strains - in truth there are more than a thousand variations of that virus, and most are currently only found in pigs and swine.

 

Descendents of the 1968 pandemic H3N2 virus continue to circulate outside of the human population, which has led researchers at MIT to consider its pandemic potential in a new study that appears today in Nature’s Scientific Reports.

 

Antigenically intact hemagglutinin in circulating avian and swine influenza viruses and potential for H3N2 pandemic

Kannan Tharakaraman, Rahul Raman, Nathan W. Stebbins, Karthik Viswanathan, Viswanathan  Sasisekharan & Ram Sasisekharan

Article number: 1822  doi:10.1038/srep01822

Received  21 December 2012 

Accepted 23 April 2013

Published 10 May 2013

The 2009 swine-origin H1N1 influenza, though antigenically novel to the population at the time, was antigenically similar to the 1918 H1N1 pandemic influenza, and consequently was considered to be “archived” in the swine species before reemerging in humans.

Given that the H3N2 is another subtype that currently circulates in the human population and is high on WHO pandemic preparedness list, we assessed the likelihood of reemergence of H3N2 from a non-human host.

(Continue . . . )

 

Follow the link to read the entire (and highly technical) study.

 

But briefly, what these researchers found was a wealth of H3N2 strains circulating in pigs and birds that are antigenically different enough from the strains that have circulated in humans to have pandemic potential.

 

For more on this, in a less technical vein, we go to this MIT press release.

 

Potential flu pandemic lurks

MIT study identifies influenza viruses circulating in pigs and birds that could pose a risk to humans.

Anne Trafton, MIT News Office

May 10, 2013

In the summer of 1968, a new strain of influenza appeared in Hong Kong. This strain, known as H3N2, spread around the globe and eventually killed an estimated 1 million people.

 

A new study from MIT reveals that there are many strains of H3N2 circulating in birds and pigs that are genetically similar to the 1968 strain and have the potential to generate a pandemic if they leap to humans. The researchers, led by Ram Sasisekharan, the Alfred H. Caspary Professor of Biological Engineering at MIT, also found that current flu vaccines might not offer protection against these strains.

 

“There are indeed examples of H3N2 that we need to be concerned about,” says Sasisekharan, who is also a member of MIT’s Koch Institute for Integrative Cancer Research. “From a pandemic-preparedness point of view, we should potentially start including some of these H3 strains as part of influenza vaccines.”

 

The study, which appears in the May 10 issue of the journal Scientific Reports, also offers the World Health Organization and public-health agencies’ insight into viral strains that should raise red flags if detected.

 

<SNIP>

Genetic similarities

 

In the new study, the researchers compared the 1968 H3N2 strain and about 1,100 H3 strains now circulating in pigs and birds, focusing on the gene that codes for the viral hemagglutinin (HA) protein.

 

<SNIP>

 

Seeking viruses with an antigenic index of at least 49 percent and glycan-attachment patterns identical to those of the 1968 virus, the research team identified 581 H3 viruses isolated since 2000 that could potentially cause a pandemic. Of these, 549 came from birds and 32 from pigs.

(Continue . . . )

 

 

 

 

Until a few years ago it was widely believed that a variant of a currently circulating flu strain – like H1N1 or H2N2 – would have a tough time sparking a pandemic as levels of community immunity would be too high. 

 

The events of 2009 have shown that to be a false assumption.

 

At the time we were intently focused on the H5N1 avian flu, only to have an upstart H1N1 virus unexpectedly jump from swine to humans in North America, and spark the first pandemic in more than 40 years. 

 

All of which should serve as a sober reminder that as we focus on the events in China and the Middle East, that nature can throw us a curveball from practically any direction. 

MIT: Researchers Testing A Broad Spectrum Antiviral

 

 

 

# 5748

 

Overnight Crof over at Crofsblog carried an excerpt (see Broad-spectrum antiviral therapeutics) from a PLoS One article on research being done at MIT on developing a unique antiviral drug approach, dubbed Double-stranded RNA (dsRNA) Activated Caspase Oligomerizer (DRACO).

 

While the popular media has already jumped on this story, all but proclaiming that a `cure for the common cold’ is at hand, extensive testing and research lies ahead before that can become a reality.

 

Nonetheless, this is a fascinating story.

 

If future testing shows this drug to be both safe and effective on humans, this could one day end up being a major advance in medical science. 

 

From the MIT Newsroom, we’ve a press release that explains this new discovery.

 

Photo Credit – MIT

The microscope images above show that DRACO successfully treats viral infections. In this set of four photos, dengue hemorrhagic fever virus kills untreated monkey cells (lower left), whereas DRACO has no toxicity in uninfected cells (upper right) and cures an infected cell population (lower right).

 

New drug could cure nearly any viral infection

 

Researchers at MIT’s Lincoln Lab have developed technology that may someday cure the common cold, influenza and other ailments.

Anne Trafton, MIT News Office

August 10, 2011

 

Most bacterial infections can be treated with antibiotics such as penicillin, discovered decades ago. However, such drugs are useless against viral infections, including influenza, the common cold, and deadly hemorrhagic fevers such as Ebola.

 

Now, in a development that could transform how viral infections are treated, a team of researchers at MIT’s Lincoln Laboratory has designed a drug that can identify cells that have been infected by any type of virus, then kill those cells to terminate the infection.

 

In a paper published July 27 in the journal PLoS One, the researchers tested their drug against 15 viruses, and found it was effective against all of them — including rhinoviruses that cause the common cold, H1N1 influenza, a stomach virus, a polio virus, dengue fever and several other types of hemorrhagic fever.

 

The drug works by targeting a type of RNA produced only in cells that have been infected by viruses. “In theory, it should work against all viruses,” says Todd Rider, a senior staff scientist in Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group who invented the new technology.

 

(Continue . . . )

PLoS One: A Single Mutation That Enhances H1N1 Transmission

 

 

 

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By just about any standard, we dodged a bullet with the pandemic of 2009. Despite hundreds of thousands of hospitalizations and tens of thousands of deaths (far more than were officially counted), it could have been far worse.

 

But we may not be out of the woods just yet.

 

It isn’t lost on scientists that in 1957, the Asian Flu pandemic seemed to disappear completely for more than a year, only to return in 1959 and again after a two year lull during the 1962-63 flu season.  

 

NEJM 2009

 

Influenza viruses are – as we’ve said before – unpredictable.

 

 

Two things we look for in an emerging virus are its pathogenicity – its ability to cause disease, and its transmissibility in humans – often measured by its R0 (pronounced `R nought’)  or basic reproductive number.

 

This R0 number describes the average number of new cases caused by one infectious person entering a totally susceptible population If less than 1.0,  outbreaks are likely to sputter and die out. 

 

With an R0 greater than 1.0, an outbreak has `legs’, and can spread through a community.

 

Determining the R0 of a virus can only be done in retrospect, and that number may vary considerably from one community to another.  The best researchers can usually come up with is an estimated range.

 

For the 2009 H1N1 virus, that number has usually been pegged at between 1.4 and 1.6.   Fairly low for a pandemic virus, but sufficient to ensure its survival and spread. 

 

The 1918 pandemic virus, in comparison, has been estimated to have an R0 between 2.0 and 3.0.  There are some estimates that run even higher.

 

 

In order to spread efficiently, a virus must be able to bind to human receptor cells – preferably those found in the upper airway.  While H1N1 does bind to human α2,6 receptor cells, it appears to do so more weakly than do many other flu viruses.

 

Additionally, in 2009 researchers at MIT and the CDC found that a portion of the PB2 gene – which is normally found in efficiently transmitted influenza viruses – was missing.

 

From MIT News,  July 3rd 2009.

 

MIT, CDC find H1N1 flu virus ill-suited for rapid transmission

But researchers say new strain bears watching, could mutate

(EXCERPT)

Recent studies have shown that a viral RNA polymerase known as PB2 is critical for efficient influenza transmissibility. (RNA polymerase controls the viruses' replication once they infect a host.) The new H1N1 strain does not have the version of the PB2 gene necessary for efficient transmission.

 

 

While we’ve been relatively fortunate so far, the question becomes, what would it take to make the 2009 pandemic virus more dangerous?

 

While there is probably more than one answer to that question, once again researchers from MIT and the CDC have been investigating, and have recently presented the results of a laboratory generated single point mutation that confers enhanced transmissibility to the H1N1 virus (at least in ferrets).

Ferrets are often used in influenza studies because their respiratory physiology, and susceptibility to influenza viruses, is close to that of humans.

 

The study, which appears in the March 2nd edition of Plos One, is called:

A Single Base-Pair Change in 2009 H1N1 Hemagglutinin Increases Human Receptor Affinity and Leads to Efficient Airborne Viral Transmission in Ferrets

Akila Jayaraman, Claudia Pappas, Rahul Raman, Jessica A. Belser, Karthik Viswanathan, Zachary Shriver, Terrence M. Tumpey, Ram Sasisekharan

 

The 2009 H1N1 influenza A virus continues to circulate among the human population as the predominant H1N1 subtype. Epidemiological studies and airborne transmission studies using the ferret model have shown that the transmission efficiency of 2009 H1N1 viruses is lower than that of previous seasonal strains and the 1918 pandemic H1N1 strain.

 

We recently correlated this reduced transmission efficiency to the lower binding affinity of the 2009 H1N1 hemagglutinin (HA) to α2→6 sialylated glycan receptors (human receptors). Here we report that a single point mutation (Ile219→Lys; a base pair change) in the glycan receptor-binding site (RBS) of a representative 2009 H1N1 influenza A virus, A/California/04/09 or CA04/09, quantitatively increases its human receptor-binding affinity.

 

The increased human receptor-affinity is in the same range as that of the HA from highly transmissible seasonal and 1918 pandemic H1N1 viruses. Moreover, a 2009 H1N1 virus carrying this mutation in the RBS (generated using reverse genetics) transmits efficiently in ferrets by respiratory droplets thereby reestablishing our previously observed correlation between human receptor-binding affinity and transmission efficiency. These findings are significant in the context of monitoring the evolution of the currently circulating 2009 H1N1 viruses.

 

 

For a less technical take on all of this, MIT News has an article describing the ramifications of this discovery. 

 

 

Keeping an eye on H1N1

MIT scientists identify a mutation that could allow the flu virus to spread much more easily.

 

 

Despite all of our technology, and an unprecedented two-year focus on the 2009 H1N1 virus, scientists are just beginning to unravel the secrets of the internal workings of flu viruses.

We can readily observe changes to the virus’s structure, but only rarely can we predict what those changes may mean in terms of virulence or transmissibility.

 

We know, for instance, that the H275Y mutation confers oseltamivir resistance, and although we’ve been watching the D225G `Norway’ mutations around the globe for more than a year, the jury is still out on its clinical significance (see Eurosurveillance: Debating The D222G/N Mutation In H1N1).

 

It isn’t enough to simply observe mutations occurring in the influenza virus.  

 

We need to know that they mean.

 

To that end, this research has identified a potentially dangerous single point mutation that – should it begin appearing in the wild – could signal the start of a new wave of illness. 

 

While that may not happen with the 2009 H1N1 virus, knowing what to look for gives us a decided advantage when tracking the evolution of this – and any other – influenza virus.

MIT: Forecasting Flu Pandemics

 

 

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The old adage (attributed to George E. P. Box, Professor Emeritus of Statistics at the University of Wisconsin) is that:

 

“All models are wrong, but some models are useful.”

 

We use models to try to mathematically simulate real-life events.  Mathematical and computer models are used to analyze everything from city traffic flow, to your supermarket’s inventory control, to weather forecasting.

 

Models that attempt to simulate scenarios which are based on rare events – those without much historical data – are naturally more difficult to develop.

 

Epidemics and pandemics are fairly rare life-threatening events that require a massive, sometimes global response.

 

Knowing when and where to put resources, and what steps need to be taken in advance to prepare for an outbreak, are things that better models could conceivably tell us.

 

Today, an interesting article from MIT’s Technology Review, which looks at the future of pandemic modeling and prediction.

 

Included are quotes from a number of researchers, including Klaus Stohr, director of influenza vaccine franchises at Novartis - Martin Meltzer, a health economist with the CDC – and Cecile Viboud, an epidemiologist at the National Institutes of Health.

 

Although we are still a long way off from being able to predict when the next pandemic will arrive, or even which virus will be the cause, this is fascinating article and well worth reading in its entirety.

 

 

Forecasting Flu Pandemics Hinges on Insights into the Virus

Scientists have made strides in predicting how influenza outbreaks will spread, but now the pressure is on for a breakthrough way to model how deadly new strains form.

• Monday, December 6, 2010
• By Lauren Gravitz