mBio: Not All LPAI Flu Subtypes Are Created Equally

Credit NIAID

 

 

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Until avian H7N9 showed up a couple of years ago, LPAI (Low Pathogenic Avian Influenza) in birds was considered to constitute a minor human health threat, and our concerns were mostly they would evolve into HPAI (highly pathogenic) strains – with most of that concern focused on H5 and H7 subtypes.

 

H7N9 showed us that an avian influenza could be LPAI in birds and yet extremely pathogenic in humans.

Furthermore, in the summer of 2013 Taiwan reported the first known human infection with an avian H6N1 virus, and a few months later mainland China reported the first three cases of H10N8 (two fatal), further widening the range of avian subtypes capable of causing serious illness in humans.

 

Suddenly, there seemed to be more to keep an eye on than just HPAI H5 and H7.

 

All of which brings us to a fascinating study, published yesterday in the open-access journal mBio, that attempts to compare the pathogenicity of different HA Subtype LPAI flu strains in mammals, and finds some subtypes are far more virulent than others.

Researchers constructed identical LPAI avian flu viruses – differing each only by their hemagglutinin protein (H1-H16) - and tested them in mice and against human cell cultures.

They found the H1, H6, H7, H10, and H15 HA genes demonstrated enhanced virulence in mice and were destructive to human bronchial epithelial cells (in vitro), while chimeric H2, H3, H5, H9, H11, H13, H14 and H16 subtypes caused no significant disease.

 

Leading the study is noted NIAID virologist Jeffrey Taubenberger, who was the first to sequence the the genome of the 1918 Spanish Flu virus.  First some excerpts from the mBio article (follow the link to read in its entirety), followed by a link and excerpt from the press release.

 

Contemporary Avian Influenza A Virus Subtype H1, H6, H7, H10, and H15 Hemagglutinin Genes Encode a Mammalian Virulence Factor Similar to the 1918 Pandemic Virus H1 Hemagglutinin

Li Qi^a, Lindsey M. Pujanauski^a, A. Sally Davis^a, Louis M. Schwartzman^a, Daniel S. Chertow^a,b,  David Baxter^c, Kelsey Scherler^c, Kevan L. Hartshorn^d,  Richard D. Slemons^e,  Kathie-Anne Walters^c,  John C. Kash^a,  Jeffery K. Taubenberger^a

ABSTRACT

Zoonotic avian influenza virus infections may lead to epidemics or pandemics. The 1918 pandemic influenza virus has an avian influenza virus-like genome, and its H1 hemagglutinin was identified as a key mammalian virulence factor. A chimeric 1918 virus expressing a contemporary avian H1 hemagglutinin, however, displayed murine pathogenicity indistinguishable from that of the 1918 virus. Here, isogenic chimeric avian influenza viruses were constructed on an avian influenza virus backbone, differing only by hemagglutinin subtype expressed. Viruses expressing the avian H1, H6, H7, H10, and H15 subtypes were pathogenic in mice and cytopathic in normal human bronchial epithelial cells, in contrast to H2-, H3-, H5-, H9-, H11-, H13-, H14-, and H16-expressing viruses. Mouse pathogenicity was associated with pulmonary macrophage and neutrophil recruitment. These data suggest that avian influenza virus hemagglutinins H1, H6, H7, H10, and H15 contain inherent mammalian virulence factors and likely share a key virulence property of the 1918 virus. Consequently, zoonotic infections with avian influenza viruses bearing one of these hemagglutinins may cause enhanced disease in mammals.

IMPORTANCE Influenza viruses from birds can cause outbreaks in humans and may contribute to the development of pandemics. The 1918 pandemic influenza virus has an avian influenza virus-like genome, and its main surface protein, an H1 subtype hemagglutinin, was identified as a key mammalian virulence factor. In a previous study, a 1918 virus expressing an avian H1 gene was as virulent in mice as the reconstructed 1918 virus. Here, a set of avian influenza viruses was constructed, differing only by hemagglutinin subtype. Viruses with the avian H1, H6, H7, H10, and H15 subtypes caused severe disease in mice and damaged human lung cells. Consequently, infections with avian influenza viruses bearing one of these hemagglutinins may cause enhanced disease in mammals, and therefore surveillance for human infections with these subtypes may be important in controlling future outbreaks.

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From the  American Society for Microbiology we get the following press release:

 

Some flu viruses potentially more dangerous than others

WASHINGTON, DC - November 18, 2014 - Certain subtypes of avian influenza viruses have the potential to cause more severe disease in humans than other avian influenza subtypes and should be monitored carefully to prevent spread of disease, according to a study published this week in mBio®, the online open-access journal of the American Society for Microbiology.

The work, directed by researchers at the National Institute of Allergy and Infectious Diseases in Bethesda, Md., found that flu viruses expressing the low pathogenicity avian H1, H6, H7, H10 or H15 hemagglutinins (genes that encode the major surface protein for the virus) led to fatal infections in mice and caused more cell damage in normal human lung cells grown in culture as compared to avian influenza viruses with other subtypes. The 1918 H1 subtype hemagglutinin has been already identified as a key virulence factor in the pandemic influenza virus of 1918. That virus, which caused the so-called "Spanish flu," spread rapidly around the world, resulting in approximately 50 million deaths.

"Viruses with these avian hemagglutinins have some type of inherent virulence motif to them, in that they induce a marked inflammatory response in mammals including human cells in culture," said senior study author Jeffery K. Taubenberger, MD, PhD, chief of the Viral Pathogenesis and Evolution Section of NIAID's Laboratory of Infectious Diseases. In 2013-2014 there have been close to 400 cases of avian influenza H7N9 infections in people in China, many severe, along with small numbers of severe human infections with H10N8 and H6N1 subtypes. "From a public health and epidemiology standpoint, it's useful to know that avian viruses of these subtypes (for example, H6, H7, or H10) might lead to more severe infections in humans and is something to look out for."

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Morens & Taubenberger - Influenza Viruses: Breaking All the Rules

BSL-4 Lab Worker - Photo Credit –USAMRIID

 

 

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Perhaps the most memorable line from the movie Contagion came when Laurence Fishburne, as the director of the CDC said, “Someone doesn't have to weaponize the bird flu. The birds are doing that.”

 

Nevertheless, there has been much debate in recent years over the wisdom of creating new, potentially dangerous, life forms in the laboratory.  Projects that, at least in view of some biosecurity experts, could pose a significant danger to the public.

 

Last year, the United States' Office of Science Policy at the NIH released a 4 page set of guidelines for DURC (Duel Use Research of Concern) projects, and ordered a review of all current life sciences projects.

 

For those unfamiliar with the lexicon of biomedical research, DURC in this new policy is defined as:

 

. . . life sciences research that, based on current understanding, can be reasonably anticipated to provide knowledge, information, products, or technologies that could be directly misapplied to pose a significant threat with broad potential consequences to public health and safety, agricultural crops and other plants, animals, the environment,

 

While this new policy does not automatically halt or defund research found to meet the DURC definition, it does require greater agency oversight and an assessment of the risks and benefits of any research, along with the development of appropriate risk and safety measures.

 

The debate continues, however over the safety, and advisability, of some of these lab experiments.

 

Today in mBio we’ve a perspective from noted virologist Jeffery K. Taubenberger & epidemiologist and medical historian David M. Morens on how nature continually conducts these types of experiments 24/7, without regard for the rules of mankind.

 

Regardless of how you feel about this type of research, you’ll want to read:

 

 

Influenza Viruses: Breaking All the Rules

Jeffery K. Taubenberger^a, David M. Morens^b

Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases^a

Office of the Director,^b National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA

ABSTRACT

Influenza A viruses (IAV) are significant pathogens able to repeatedly switch hosts to infect multiple avian and mammalian species, including humans. The unpredictability of IAV evolution and interspecies movement creates continual public health challenges, such as the emergence of the 2009 pandemic H1N1 virus from swine, as well as pandemic threats from the ongoing H5N1 and the recent H7N9 epizootics. In the last decade there has been increased concern about the “dual use” nature of microbiology, and a set of guidelines covering “dual use research of concern” includes seven categories of potentially problematic scientific experiments. In this Perspective, we consider how in nature IAV continually undergo “dual use experiments” as a matter of evolution and selection, and we conclude that studying these properties of IAV is critical for mitigating and preventing future epidemics and pandemics.

 

The views expressed in this article do not necessarily reflect the views of the journal or of ASM.

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mBio: An H7N9 Perspective by Morens, Fauci & Taubenberger

Credit CDC

 

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In an article that appears later today  in the open access journal mBio, well known NIH scientists and researchers David M. Morens, Jeffery K. Taubenberger, and Anthony S. Fauci describe the history of H7 influenza viruses both in animals and in humans, and discuss why China’s emerging H7N9 virus is viewed with concern.

 

I’ll update this blog with a link to the article when it goes live, but for now we have a press release from the American Society for Microbiology, which provides us with some details.

 

UPDATED:

 

H7N9 Avian Influenza A Virus and the Perpetual Challenge of Potential Human Pandemicity

David M. Morens, Jeffery K. Taubenberger and Anthony S. Fauci doi:10.1128/mBio.00445-13

 

 

 

 

H7N9 influenza: History of similar viruses gives cause for concern

The H7N9 avian flu strain that emerged in China earlier this year has subsided for now, but it would be a mistake to be reassured by this apparent lull in infections. The virus has several highly unusual traits that paint a disquieting picture of a pathogen that may yet lead to a pandemic, according to lead scientists from the National Institute of Allergy and Infectious Diseases. David Morens, Jeffery Taubenberger, and Anthony Fauci, in a paper published in mBio®, the online open-access journal of the American Society for Microbiology, describe the history of H7 viruses in animal and human disease and point out that H7 influenza has a tendency to become established in bird, horse, and swine populations and may spillover repeatedly into humans.

 

“The evidence as a whole is complex and the implications of past outbreaks for predicting the future course of the current H7N9 epizootic [an epidemic among animals] are uncertain," write the authors.

 

The outbreak of H7N9 earlier this year led China to temporarily close scores of live poultry markets in an effort to limit the spread of the virus. Although this previously unrecognized strain of avian influenza A has now been associated with 132 confirmed human infections and 39 related deaths (as of June 14), the rate at which new cases are recognized has dwindled in recent weeks.

 

In their minireview, Morens, Taubenberger and Fauci point out that despite this apparent hiatus, viruses like H7N9, which have subtype 7 hemagglutinin, are a cause for heightened concern because of several highly unusual characteristics. First, H7 viruses have repeatedly been involved in numerous explosive poultry outbreaks including incidents in New York, Canada, Mexico, the Netherlands, and Italy, and in almost all of these cases the virus eventually spilled over into humans. Also, H7 viruses have the ability to mutate from a low pathogenicity form to a high pathogenicity form in birds, a scenario that can lead to large-scale culling and ultimately to human exposure to the virus among poultry workers.

 

H7N9 also shares many characteristics with another influenza strain that continues to spillover into humans: highly pathogenic avian influenza H5N1. Among other commonalities, both viruses have a clinical picture that includes bilateral pneumonia, acute respiratory distress syndrome, and multi-organ failure, and it appears they are both currently unable to easily infect most humans but cause severe disease in individuals with uncharacterized genetic susceptibilities.

 

The fact that many H7 viruses tend to infect conjunctival cells is also cause for concern. Some, but not all, cases of human H7 infection feature prominent signs and symptoms in the eyes, including itching, swelling, and tearing, that could enhance person-to-person spread in an H7N9 outbreak.

 

The authors point out that many H7 viruses have adapted to infect mammals, including horses and pigs, which raises the possibility that H7N9 could adapt in a similar fashion. The possibility that H7N9 might infect pigs is particularly troubling, as swine are considered a "mixing vessel" for viruses - a breeding ground for novel viral reassortants like the 2009 H1N1 pandemic influenza strain commonly known as "swine flu".

 

The sum of these observations is this: we do not know what H7N9 will do next. Although avian influenza viruses have not caused widespread human transmission in 94 years of surveillance, there have been numerous instances of avian influenza spillover and H7N9 "might arguably be more likely than other avian viruses to become human-adapted," write the authors.

 

Regardless of its future, H7N9 certainly holds lessons for preventing human and animal pandemics. All the unknowns surrounding the virus make a strong case for enhancing basic and applied research into the evolution of influenza viruses and for better integration of influenza virology within human and veterinary public health efforts.

 

"We have a unique opportunity to learn more of influenza's many secrets, and thereby enhance our ability to prevent and control an important disease that seems destined to appear again and again, in multiple guises, far into the foreseeable future," write the authors.

 

 

While certainly not in the same league, a little over 3 months ago (on the day we first learned of the emergence of the H7N9 virus) I penned my own Brief History Of H7 Avian Flu Infections, which you may wish to revisit.

mBio: Taubenberger et al. On the 1918 Spanish Flu

Credit CDC PHIL

 

 

# 6549

 

mBio, the American Society for Microbiology’s online, open access journal, has published a long and fascinating review this morning on what we’ve learned over the past 15 years about the 1918 H1N1 `Spanish Flu’ pandemic virus, written by some of the biggest experts in the field.

 

At this point, I’ll just step aside and invite you to read:

 

 

Reconstruction of the 1918 Influenza Virus: Unexpected Rewards from the Past

 

Jeffery K. Taubenberger, David Baltimore, Peter C. Doherty, Howard Markel, David M. Morens, Robert G. Webster and Ian A. Wilson

 

doi:10.1128/mBio.00201-12

 

Highly recommended.

mBio: Lethal Synergism of H1N1 Pandemic Influenza & Bacterial Pneumonia

 

 

 

CDC PHIL - Photomicrograph of Streptococcus (Diplococcus) pneumoniae bacteria

 

# 5856

 

 

While the vast majority of people who contracted the H1N1 pandemic flu of 2009 recovered without incident, a very small minority saw severe – sometimes fatal – illness. 

 

Often during 2009 we saw reports of severe lung damage. Damage that in some cases was compared to what has been seen in H5N1 bird flu and during the great pandemic of pandemic of 1918.

 

A few of the stories from back then include:

 

In early September of 2009, in Pathology Of Fatal H1N1 Lung Infections, we looked at a report by Helen Branswell that looked early autopsy results.

 

 

Lung damage in fatal swine flu cases more bird flu than seasonal flu: expert

By Helen Branswell Medical Reporter (CP) 

TORONTO — The lungs of people who have died from swine flu look more like those of the victims of H5N1 avian influenza than those of people who succumb to regular flu, the chief of infectious diseases pathology at the U.S. Centers for Disease Control says.

 

Study of about 70 fatal H1N1 cases so far also reveals there may be more incidences of co-infections with bacteria than was earlier thought, Dr. Sherif Zaki told The Canadian Press in an interview.

 

A couple of weeks later in More On The Pathology Of Novel H1N1, we saw a report by Maggie Fox, then Health and Science Editor for Reuters, who brought us more details of this  story, including comments by Dr. Sherif Zaki of the U.S. CDC who  stated that "This is almost exactly what we see with avian flu. This looks like avian flu on steroids."

 

That same month, I wrote about the use of ECMO (Extracorporeal Membrane Oxygenation) in the treatment of severe lung injury in H1N1 victims in The ECMO Option.

 

In early December (see NIH: Post Mortem Studies Of H1N1) the NIH announced the results of a series of autopsies conducted on H1N1 victims in New York City over the summer, which are chronicled in the Archives of Pathology & Laboratory Medicine.

 

The NIH put together a press release, which provided highlights of the study.

 

FOR IMMEDIATE RELEASE
Monday, Dec. 7, 2009

Media Contact: Anne A. Oplinger
(301) 402-1663
niaidnews@niaid.nih.gov

New York Autopsies Show 2009 H1N1 Influenza Virus Damages Entire Airway

In fatal cases of 2009 H1N1 influenza, the virus can damage cells throughout the respiratory airway, much like the viruses that caused the 1918 and 1957 influenza pandemics, report researchers from the National Institutes of Health (NIH) and the New York City Office of Chief Medical Examiner. The scientists reviewed autopsy reports, hospital records and other clinical data from 34 people who died of 2009 H1N1 influenza infection between May 15 and July 9, 2009. All but two of the deaths occurred in New York City. A microscopic examination of tissues throughout the airways revealed that the virus caused damage primarily to the upper airway—the trachea and bronchial tubes—but tissue damage in the lower airway, including deep in the lungs, was present as well. Evidence of secondary bacterial infection was seen in more than half of the victims.

 

The team was led by James R. Gill, M.D., of the New York City Office of Chief Medical Examiner and New York University School of Medicine, and Jeffery K. Taubenberger, M.D., Ph.D., of the National Institute of Allergy and Infectious Diseases (NIAID) at NIH. The findings are reported in the Archives of Pathology & Laboratory Medicine, now available online and scheduled to appear in the February 2010 print issue.

<SNIP>

“This pattern of pathology in the airway tissues is similar to that reported in autopsy findings of victims of both the 1918 and 1957 influenza pandemics,” notes Dr. Taubenberger.

 

While many people continued to insist that swine flu was no worse than seasonal flu, obviously something was different in the way it produced severe lung damage.  

 

A year into the pandemic, I summarized many of the ways that the 2009 H1N1 virus differed from seasonal flu in There’s No Flu Like A New Flu.

 

While the overall incidence of these complications was relatively low, those who suffered from them often experienced extremely severe illness.

 

 

All of which serves as prelude to an open access study, published today in mBio, called:

 

Lethal Synergism of 2009 Pandemic H1N1 Influenza Virus and Streptococcus pneumoniae Coinfection Is Associated with Loss of Murine Lung Repair Responses

John C. Kash^a, Kathie-Anne Walters^b, A. Sally Davis^a, Aline Sandouk^a, Louis M. Schwartzman^a, Brett W. Jagger^a, Daniel S. Chertow^a, Qi Li^a, Rolf E. Kuestner^b, Adrian Ozinsky^b, and Jeffery K. Taubenberger^a

 

 

The entire study is available, and is well worth reading, but briefly:

 

Scientists at NIAID and the Institute for Systems Biology (ISB) infected experimental mice with both seasonal flu and the 2009 H1N1 pandemic flu, and after 48 hours exposed some of them to Streptococcus pneumoniae, one of the main causes of pneumonia.

 

Mice that were exposed only to the two flu strains showed expected flu symptoms, but all survived.

Mice that were exposed to seasonal flu and S. pneumoniae experienced minor lung damage, but once again, all survived.

 

But all of the mice infected with the pandemic H1N1 virus, and S. pneumoniae showed severe weight loss, lung damage, and 100% mortality

 

Excerpts from the press release below explain what else they found:

 

American Society for Microbiology

 

2009 H1N1 pandemic flu more damaging to lungs, opens opportunities for bacterial infection

(EXCERPT)

The lung tissues of the dead mice revealed that the alveoli were severely inflamed and the surfaces of the bronchioles were wiped clean of the protective layer of cells called the epithelium. There was also increased bacterial replication in the lungs of the co-infected mice, a sign that the bacteria were thriving there.

 

Looking at the mouse genes that were expressed during infection revealed more details about how the pandemic influenza virus sets the stage for lethal bacterial infections. Mice infected with the pandemic flu virus and S. pneumoniae had a similar inflammatory response as the other mice, but they lack responses that would repair and regenerate their damaged epithelial cells, those protective tissues that would otherwise keep bacteria from penetrating to deeper layers of tissue.

 

All these factors add up to big problems in the lung: as compared with seasonal flu, infection with the pandemic strain of flu was associated with more extensive damage to the epithelium that requires more extensive tissue repair. This opens the body up to attack from bacterial invaders, including Streptococcus pneumoniae.

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So not only did this duel infection lead to greater lung damage, and increased bacterial replication, it also disabled the lung’s ability to repair itself.

 

Since it can take 6 months or longer to develop a vaccine for a novel influenza virus, these results may suggest a bigger role for the 23-valent Pneumonia vaccine (PPVSV) during a future pandemic. 

 

More than a year after the end of the 2009 pandemic, scientists are still uncovering basic information about how pandemic flu differs from seasonal flu. 

 

With luck, work like this will provide better ways for us to deal with an outbreak, when the next one arrives.

Morens and Taubenberger: A New Look At The Panzootic Of 1872

 

 

 

# 4995

 

 

One of the most fascinating events in relatively modern infectious disease history occurred in the fall of 1872, when a massive wave of (presumably) equine influenza swept across North American, infecting much of the horse population from Canada to Mexico – and killing up to 10%.

 

You’ll find an excellent history of this outbreak from Horsetalk.co.nz.

 

How equine flu brought the US to a standstill

A Boston fire wagon without its horses.

September 26, 2007

 

Australia's equine flu outbreak may have crippled the racing industry, but an 1872 outbreak in North America brought the entire US economy to a virtual standstill.

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This was at a time in history when horses were the primary means of transportation, and the economic effects of this months long epizootic were substantial, and some have suggested it contributed to the economic Panic of 1873 the following year.

 

Ian York author of the Mystery Rays blog wrote about this incident back in December of 2009 in a blog called Influenza before 1918, part II: 1872.  A brief excerpt:

 

Without horses, business slammed to a halt; the mail didn’t run, groceries didn’t reach the cities, crops weren’t harvested or transported.  After a few weeks, most of the horses recovered and business followed, but the epizootic swept across the country (intensely tracked by the newspapers of the day, warning each city in turn that it was going to be attacked), finally fizzling out the following summer in British Columbia.

 

Little remembered today, this was a huge story in 1972.  The assumption has been that this was sparked by some drift or shift in an already existing equine influenza.

 

But David Morens and Jeffrey K. Taubenberger of the NIH bring us tantalizing details of a concurrent outbreak of poultry deaths across the country, and that raises some interesting questions.

 

Without the ability to analyze and identify pathogens from that era, researchers are understandably hampered in their understanding of what exactly what transpired 140 years ago.  

 

But Taubenberger and Morens discuss a plausible scenario where a highly pathogenic avian virus may have jumped species and infected horses, pigs, deer, and in some cases, even humans.

 

My thanks to mixin on FluTrackers for posting this link.

 

Morens and Taubenberger (2010) An avian outbreak associated with panzootic equine influenza in 1872: an early example of highly pathogenic avian influenza? Influenza and Other Respiratory Viruses 4(6), 373–377.

Abstract

Background An explosive fatal epizootic in poultry, prairie chickens, turkeys, ducks and geese, occurred over much of the populated United States between 15 November and 15 December 1872. To our knowledge the scientific literature contains no mention of the nationwide 1872 poultry outbreak.

Objective To understand avian influenza in a historical context.

Results The epizootic progressed in temporal-geographic association with a well-reported panzootic of equine influenza that had begun in Canada during the last few days of September 1872. The 1872 avian epizootic was universally attributed at the time to equine influenza, a disease then of unknown etiology but widely believed to be caused by the same transmissible respiratory agent that caused human influenza.

Conclusions Another microbial agent could have caused the avian outbreak; however, its strong temporal and geographic association with the equine panzootic, and its clinical and epidemiologic features, are most consistent with highly pathogenic avian influenza. The avian epizootic could thus have been an early instance of highly pathogenic avian influenza.

 

 

Jeffrey  K. Taubenberger and David Morens are, of course,  familiar names to followers of influenza and virology.

 

Both are researchers at NIAID. Taubenberger, quite famously, was the first to sequence the the genome of the 1918 Spanish Flu virus while David Morens is a prominent medical historian and professor.

 

Both are extensively published, and have collaborated often in the past.

 

As this report is too good to try to summarize, I’ll simply suggest you follow this link and read it in its entirety.

Morens, Taubenberger & Fauci: What’s Next For H1N1

 

 

 

# 4946

 

 

In an open access perspective article appearing in the journal mBio, well known NIH scientists and researchers David M. Morens, Jeffery K. Taubenberger, and Anthony S. Fauci give their take on the future of the novel 2009 H1N1 virus.

 

 

The 2009 H1N1 Pandemic Influenza Virus: What Next?

1. David M. Morens, Jeffery K. Taubenberger, and Anthony S. Fauci

ABSTRACT

History suggests that the 2009 pandemic H1N1 influenza virus faces extinction unless it mutates to avoid already high global population immunity. The immune escape mechanisms potentially at its disposal include antigenic drift, antigenic shift via genetic reassortment, and intrasubtypic reassortment.

 

Going back to the late 19th century, the evolutionary histories of past pandemic viruses are examined in an effort to better understand the nature and extent of the immune pressures faced by the 2009 pandemic virus in the immediate future.

 

While human influenza viruses have often surprised us, available evidence leads to the hope that the current pandemic virus will continue to cause low or moderate mortality rates if it does not become extinct.

 

The FULL TEXT is available here.

 

For those who prefer the Press Release condensed version, we have that as well:

 

NIH scientists consider fate of pandemic H1N1 flu virus

Whither pandemic H1N1 virus? In a new commentary, scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, review the fates of previous pandemic influenza viruses in the years following a pandemic and speculate on possible future courses for the 2009 pandemic H1N1 (pH1N1) virus during the upcoming flu season and beyond.

 

The authors estimate that at least 183 million Americans (about 59 percent of the total U.S. population) have some immunity to pH1N1 because they were exposed to related viruses or vaccines prior to 2009, were immunized against pH1N1 or developed immunity following infection with the pandemic virus.

 

To stay in circulation in the face of such high levels of population immunity, the pH1N1 virus must adapt either through abrupt or gradual changes. The authors briefly examine a number of earlier pandemics and trace paths taken by the causative viruses. Some—for reasons not well understood—died out, while others, like those of 1889 and 1918, returned in an explosive fashion. Such an explosive return of pH1N1 virus is unlikely, note the authors, because global levels of immunity are already high and will increase further through immunization with 2010-2011 seasonal influenza vaccines, which contain the pH1N1 strain.

 

In light of what is known about pH1N1, the NIAID authors express a cautious optimism that unless it disappears entirely the virus will follow a route like that of 1968 pandemic virus, that is, it will persist in a form that causes relatively few deaths.

 

Nevertheless, the authors caution against complacency. As they acknowledge, many gaps remain in understanding how a given pandemic influenza virus adapts to increased immunity in humans. For that reason, influenza vaccination for everyone older than six months is a wise public health measure to maintain high levels of population-wide immunity. Immunization with 2010-2011 seasonal flu vaccine is particularly urged for babies older than six months, children, teens and young adults as the best way to protect individuals in those potentially more susceptible age groups from illness.