Showing posts with label NIH. Show all posts
Showing posts with label NIH. Show all posts

CIDRAP News Coverage Of The H5N1 NIH Workshop

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BSL-4 Lab Worker - Photo Credit –USAMRIID

 

 

# 6794

 

For the past couple of days researchers and policy makers have been meeting at the National Institutes of Health (NIH) to discuss the future of HHS funded H5N1 avian influenza gain-of-function studies – research that seeks to enhance the host range, transmissibility, or pathogenicity of the H5N1 virus.


Research of this type has been voluntarily suspended since very early this year when – due to a prolonged debate over the publication of a pair of controversial research papers (see The Furor Over H5N1 Research Continues) - a group of the world’s leading researchers announced a moratorium on specific types of bird flu research (see Scientists Announce 60 Day Moratorium On Some H5N1 Research).

 

Although not being webcast, Lisa Schnirring at CIDRAP NEWS has been providing excellent daily coverage of this NIH workshop. 

 

Follow the links below to get the details.

 

H5N1 researchers question proposed HHS funding framework

Lisa Schnirring * Staff Writer

Dec 17, 2012 (CIDRAP News) – Federal health officials are in the midst of crafting a framework for funding H5N1 avian influenza gain-of-function studies, and today at a workshop they heard varied feedback from researchers, biosecurity experts, and others.

 

The 2-day workshop, held at the National Institutes of Health (NIH), is the latest chapter in an intense scientific controversy that was triggered by the publication of two recent studies involving lab-engineered H5N1 strains that showed signs of being transmissible in mammals.

(Continue . . .)

 

 

Experts at NIH meeting say H5N1 research moratorium may end soon

Lisa Schnirring * Staff Writer

Dec 18, 2012 (CIDRAP News) – As a meeting to discuss issues related to federally funded H5N1 avian influenza research wrapped up today, experts anticipated that a voluntary moratorium on work with lab-modified strains that have increased transmissibility might end soon and said they sensed agreement about lab biosecurity levels.

 

The National Institutes of Health (NIH) held the 2-day meeting to gather feedback from flu researchers, others in the science community, and the public on its draft framework for funding H5N1 gain-of-function studies and to continue an international dialogue on issues related to benefits and risks of the research.

(Continue . . .)

»» Read More

NIAID Video: How Influenza Pandemics Occur

 

 

 

# 6581

 

NIAID, the National Institute of Allergy and Infectious Diseases, has recently released a 3 1/2 minute video that explains, very nicely, the emergence and potential spread of new influenza viruses.

 

The NIAID Youtube Channel is a terrific resource, with more than 2 dozen informative videos, covering a variety of medical and research topics.


This video is somewhat similar to the NIAID video I highlighted last April (see NIAID Video: Antigenic Drift).

 

Well worth a look.

 

»» Read More

NEJM: Adult-Onset Immunodeficiency in Thailand and Taiwan

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M. fortuitum a “rapidly-growing” Mycobacterium Credit CDC PHIL

 

# 6511

 

 

Investigators at the NIH have identified an antibody suspected to be the cause of a noninfectious AIDS-like syndrome observed in Asia in recent years, one that can make people susceptible to opportunistic infections like those from nontuberculous mycobacteria (NTM).

 

Mycobacteria are slender, rod-shaped bacteria commonly found in the environment throughout the world.

 

Generally divided into three groups, the most famous are the bacilli that cause cause Tuberculosis and Leprosy (Hansen’s Disease) – while the third group - responsible for NTMs - are less well known.

 

Nontuberculous mycobacterial (NTMs) infections are rarely seen among non-HIV positive (or otherwise pulmonary or immune compromised) patients, but has been observed with increasing frequency over the past decade, particularly in Asia.

 

A couple of cites from the last decade include:

J Infect. 2006;53:77–84

Emergence of disseminated infections due to nontuberculous mycobacteria in non-HIV-infected patients, including immunocompetent and immunocompromised patients in a university hospital in Taiwan.

Lai CC, Lee LN, Ding LW, Yu CJ, Hsueh PR, Yang PC.

 

Clin Infect Dis. 2007 Aug 15;45(4):421-7. Epub 2007 Jul 5.

Disseminated nontuberculous mycobacterial infection in patients who are not infected with HIV in Thailand

Chetchotisakd P, Kiertiburanakul S, Mootsikapun P, Assanasen S, Chaiwarith R, Anunnatsiri S

 

 


While some sort of immune compromising condition has been associated with these opportunistic infections, until now the mechanism behind them has been a mystery. 

 

Today, an NIH study appearing in the NEJM finds that high-titers of anti–interferon-γ autoantibodies (i.e. an antibody directed against the body’s own immune system) are associated with opportunistic infections -like NTM - in non-HIV positive patients.

 

Interferon-y (IFN-γ) – or type II interferon - is a cytokine that is a critical component of our body’s innate and adaptive immune system. Antibodies that inhibit or neutralize their function would be expected to greatly assist opportunistic infections in spreading.

 

First a link to the study, then more details from the NIH press release.

 

 

Adult-Onset Immunodeficiency in Thailand and Taiwan

 

Sarah K. Browne, M.D., Peter D. Burbelo, Ph.D., Ploenchan Chetchotisakd, M.D., Yupin Suputtamongkol, M.D., Sasisopin Kiertiburanakul, M.D., Pamela A. Shaw, Ph.D., Jennifer L. Kirk, B.A., Kamonwan Jutivorakool, M.D., Rifat Zaman, B.S., Li Ding, M.D., Amy P. Hsu, B.A., Smita Y. Patel, M.D., Kenneth N. Olivier, M.D., Viraphong Lulitanond, Ph.D., Piroon Mootsikapun, M.D., Siriluck Anunnatsiri, M.D., Nasikarn Angkasekwinai, M.D., Boonmee Sathapatayavongs, M.D., Po-Ren Hsueh, M.D., Chi-Chang Shieh, M.D., Ph.D., Margaret R. Brown, B.S., Wanna Thongnoppakhun, Ph.D., Reginald Claypool, R.N., Elizabeth P. Sampaio, M.D., Ph.D., Charin Thepthai, M.Sc., Duangdao Waywa, M.Sc., Camilla Dacombe, R.N., Yona Reizes, R.N., Adrian M. Zelazny, Ph.D., Paul Saleeb, M.D., Lindsey B. Rosen, B.S., Allen Mo, B.S., Michael Iadarola, Ph.D., and Steven M. Holland, M.D.

N Engl J Med 2012; 367:725-734 August 23, 2012

Conclusions

Neutralizing anti–interferon-γ autoantibodies were detected in 88% of Asian adults with multiple opportunistic infections and were associated with an adult-onset immunodeficiency akin to that of advanced HIV infection.

 

And more details from NIH/NIAID.

 

NIH Researchers Find Possible Cause Of Immune Deficiency Cases In Asia

Autoantibody May Cause Susceptibility to Opportunistic Infections

WHAT:


A clinical study led by National Institutes of Health investigators has identified an antibody that compromises the immune systems of HIV-negative people, making them susceptible to infections with opportunistic microbes such as nontuberculous mycobacteria (NTM). In this study conducted at hospitals in Thailand and Taiwan, the researchers found that the majority of study participants with opportunistic infections made an antibody against interferon-gamma (IFN-gamma), a cell-signaling molecule thought to play a major role in clearing harmful infections. The study findings will appear online in the August 23rd issue of the New England Journal of Medicine.

 

NTM are close relatives of the bacterium that causes tuberculosis and can cause severe lung disease. NTM and other opportunistic infections are common in people with immune deficiency diseases, such as AIDS, but they are rare in people with healthy immune systems. However, researchers in Southeast Asia have recently reported several cases of NTM infections in people with no known problems with their immune systems.

 

The study, led by Sarah Browne, M.D., of the National Institute of Allergy and Infectious Diseases, and Peter Burbelo, Ph.D., of the National Institute of Dental and Craniofacial Research, enrolled 203 people, ages 18 to 78 years old. Of these participants, 52 had NTM infections, 45 had other opportunistic infections with or without NTM co-infection, 58 had tuberculosis, and 48 were healthy volunteers. All participants were HIV-negative.
The investigators examined participant blood samples for antibodies to cell-signaling molecules such as IFN-gamma. Eighty-eight percent of the people with NTM or other opportunistic infections had antibodies that blocked their own IFN-gamma (called autoantibodies).

 

The autoantibodies inhibited IFN-gamma function, hindering the immune system’s ability to clear infection, causing a syndrome that made these study participants more vulnerable to opportunistic infections. More work is needed to determine why people in Southeast Asia appear to be predisposed to the development of this autoimmune condition.

Because the average age of the study participants with NTM or other opportunistic infections was 50 years, the investigators speculate that these antibodies develop over time as a result of combined genetic and environmental factors. Having identified the likely cause of this syndrome, the study authors say it may be possible to treat the underlying problem by targeting the cells that make the IFN-gamma autoantibodies.

ARTICLE:
SK Browne et al. Adult onset immunodeficiency in Thailand and Taiwan. New England Journal of Medicine. DOI: 10.1056/NEJMoa1111160 (2012).

»» Read More

NIH: News From The Human Microbiome Project

 

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Photo Credit HMP

 

# 6385

 

Last year in The Other Reason Not To Abuse Antibiotics I touched briefly on beneficial intestinal bacteria (gut flora or microbiota), and how the use of antibiotics can adversely disrupt their balance.

 

The study of these ubiquitous micro-organisms that reside not only in our intestines, but on our skin, in our nasal passages, oral cavities, gastrointestinal tract, and urogenital tract has gained momentum over the past several years.

 

One of the big reasons is the NIH sponsored Human Microbiome Project, which defines their goal as:

 

 

The Common Fund's Human Microbiome Project (HMP) aims to characterize the microbial communities found at several different sites on the human body, including nasal passages, oral cavities, skin, gastrointestinal tract, and urogenital tract, and to analyze the role of these microbes in human health and disease. HMP includes the following initiatives.

 

 

Today, in advance of the publication today and tomorrow of a number of research articles in PLoS and in the journal Nature, we’ve a couple of lengthy press releases describing this international project’s recent accomplishments, along with an announcement on the PLoS Blog of the availability of this collection.

 

 

First, from the NIH – news that researchers have defined the normal bacterial makeup of the human body.

 

 

NIH Human Microbiome Project defines normal bacterial makeup of the body

Genome sequencing creates first reference data for microbes living with healthy adults

Microbes inhabit just about every part of the human body, living on the skin, in the gut, and up the nose. Sometimes they cause sickness, but most of the time, microorganisms live in harmony with their human hosts, providing vital functions essential for human survival. For the first time, a consortium of researchers organized by the National Institutes of Health has mapped the normal microbial makeup of healthy humans, producing numerous insights and even a few surprises.

 

Researchers found, for example, that nearly everyone routinely carries pathogens, microorganisms known to cause illnesses. In healthy individuals, however, pathogens cause no disease; they simply coexist with their host and the rest of the human microbiome, the collection of all microorganisms living in the human body. Researchers must now figure out why some pathogens turn deadly and under what conditions, likely revising current concepts of how microorganisms cause disease.

 

In a series of coordinated scientific reports published on June 14, 2012, in Nature and several journals in the Public Library of Science (PLoS), some 200 members of the Human Microbiome Project (HMP) Consortium from nearly 80 universities and scientific institutions report on five years of research. HMP has received $153 million since its launch in fiscal year 2007 from the NIH Common Fund, which invests in high-impact, innovative, trans-NIH research. Individual NIH institutes and centers have provided an additional $20 million in co-funding for HMP consortium research.

 

“Like 15th century explorers describing the outline of a new continent, HMP researchers employed a new technological strategy to define, for the first time, the normal microbial makeup of the human body,” said NIH Director Francis S. Collins, M.D., Ph.D. “HMP created a remarkable reference database by using genome sequencing techniques to detect microbes in healthy volunteers. This lays the foundation for accelerating infectious disease research previously impossible without this community resource.”

(Continue . . . )

 

 

In another press release from the University of North Carolina at Charlotte, we get details on how this research was conducted, and the surprising individuality and diversity among health human biomes.

 

 

Human Microbiome Project finds vast individuality in healthy human bacterial populations

(EXCERPT)

To define the normal human microbiome, HMP researchers sampled 242 healthy U.S. volunteers (129 male, 113 female), collecting tissues from 15 body sites in men and 18 body sites in women (including three vaginal sites). Researchers collected up to three samples from each volunteer at sites such as the mouth, nose, skin (two behind each ear and each inner elbow),and lower intestine (stool).

Where doctors had previously isolated only a few hundred bacterial species from the body, HMP researchers now calculate that more than 10,000 species occupy the human ecosystem. Moreover, researchers calculate that they have found between 81 and 99 percent of all the genuses of microorganisms in healthy adults.

Defining "a" human biome, however, can be difficult, as HMP researchers found immense variation in bacterial communities, both in bacterial diversity and in bacterial group abundances -- variation that includes population differences both between areas in each body and between similar areas in different bodies.

Each body site can be inhabited by organisms as different as those in the Amazon Rainforest and the Sahara Desert. Further, these sites on different individuals are populated with different assemblages of bacteria, or with some of the same bacteria, but in markedly different proportions.

(Continue . . . )


From the Public Library of Science Blog we get details on this expanding collection of research.

 

Announcing the Human Microbiome Project Collection

For the first time, a consortium of researchers has mapped the full community of microbes that inhabit various parts of the healthy human body. Many of these findings will be published today in a new PLoS collection. The PLoS Human Microbiome Project Collection consists of articles from the project’s consortium members, who generate, leverage, and explore microbiome analytical techniques. The articles have been culled from PLoS ONE, PLoS Genetics, and PLoS Computational Biology with more being added to the collection as they are published.

(Continue . . .)

 

The PLoS Microbiome collection features 13 new research papers published today. To access these papers, please visit:

 

PLoS Collections: The Human Microbiome Project Collection (2012) www.ploscollections.org/hmp

»» Read More

NIAID Video: Antigenic Drift

 

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# 6288

 

 

NIAID, part of the NIH, has just released a short (3 minute) video that nicely illustrates how flu viruses change antigenically over time, and eventually mutate so that the current flu vaccine no long is effective.

 

 

 

As the seasonal H3N2 virus that has been covered in the flu vaccine over the past 3 years has begun to accumulate changes like the ones discussed in this video, in the fall a new H3N2 strain will be incorporated in the flu shot.

 

There are currently 18 videos on the NIAID Youtube site, and links to others on other channels.



Well worth taking a look.

»» Read More

NIH Video: Dual Use Research Of Concern (DURC)

 

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NIH Brochure on Dual Use Research

 

# 6264

 

 

Over the past few months an obscure acronym has made it’s way into numerous blogs, news headlines, and even popular usage; DURCDual Use Research of Concern.

 

While it is the current debate over controversial H5N1 transmissibility studies that has prompted its emergence (see The Biosecurity Debate On H5N1 Research), DURC has been a matter of national concern for a number of years.

 

The NIH produced a 7 minute video in 2010 highlighting the concerns of DURC, called Dual Use Research: A dialogue.  Click the link, or the image below to watch.

 

image

 

 

Last week the  Office of Science Policy at the NIH released a 4 page set of guidelines for DURC (Duel Use Research of Concern) projects designed to beef up oversight and biosecurity of U.S. funded projects.

 

The scope of this new policy is to cover research on the most dangerous of biological organisms, listing;

 

a)  Avian influenza virus (highly pathogenic) 
b)  Bacillus anthracis
c)  Botulinum neurotoxin
d)  Burkholderia mallei
e)  Burkholderia pseudomallei
f)  Ebola virus
g)  Foot-and-mouth disease virus
h)  Francisella tularensis
i)  Marburg virus

j)  Reconstructed 1918 Influenza virus

k)  Rinderpest virus
l)  Toxin-producing strains of Clostridium botulinum
m) Variola major virus
n)  Variola minor virus
o)  Yersinia pestis

 

Specifically any research that seeks to:

 

a)  Enhances the harmful consequences of the agent or toxin; 

b)  Disrupts immunity or the effectiveness of an immunization against the agent or toxin without
clinical or agricultural justification;

c)  Confers to the  agent or toxin resistance to clinically or agriculturally useful prophylactic or
therapeutic interventions against that agent or toxin or facilitates their ability to evade detection methodologies;

d)  Increases the stability, transmissibility, or the ability to disseminate the agent or toxin; 

e)  Alters the host range or tropism of the agent or toxin;  

f)  Enhances the susceptibility of a host population to the agent or toxin; or

g)  Generates or reconstitutes an eradicated or extinct agent or toxin listed in Section (III.1) above.

 

 

For more on DURC, the NSABB, and the Office of Biotechnology Activities, you may wish to visit the following links.

Brochure on Dual Use Research

Video on Dual Use Research

International Meetings

NSABB FAQs

Summary of NSABB Reports and Activities

Responsible Communication of Life Sciences Research with Dual Use Potential

Global Status of Strategies for Addressing the Intersection of Science and Security

Roundtable at the ASM Biodefense and Emerging Diseases Research meeting

»» Read More

U.S. Issues New DURC Oversight Rules

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BSL-4 Lab Worker - Photo Credit –USAMRIID

 


# 6252

 

 

While the current H5N1 research row has centered around the publication of two specific research projects (see NSABB To Re-examine H5N1 Research Risks), the bigger issues at play involve how we oversee (and fund) future life sciences research in order to avoid future controversies.

 

To that end, today the 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, materiel, or national security

 

The scope of this new policy is to cover research on the most dangerous of biological organisms, listing;

 

a)  Avian influenza virus (highly pathogenic) 
b)  Bacillus anthracis
c)  Botulinum neurotoxin
d)  Burkholderia mallei
e)  Burkholderia pseudomallei
f)  Ebola virus
g)  Foot-and-mouth disease virus
h)  Francisella tularensis
i)  Marburg virus

j)  Reconstructed 1918 Influenza virus

k)  Rinderpest virus
l)  Toxin-producing strains of Clostridium botulinum
m) Variola major virus
n)  Variola minor virus
o)  Yersinia pestis

Specifically any research that seeks to:

 

a)  Enhances the harmful consequences of the agent or toxin; 

b)  Disrupts immunity or the effectiveness of an immunization against the agent or toxin without
clinical or agricultural justification;

c)  Confers to the  agent or toxin resistance to clinically or agriculturally useful prophylactic or
therapeutic interventions against that agent or toxin or facilitates their ability to evade detection methodologies;


d)  Increases the stability, transmissibility, or the ability to disseminate the agent or toxin; 


e)  Alters the host range or tropism of the agent or toxin;  


f)  Enhances the susceptibility of a host population to the agent or toxin; or


g)  Generates or reconstitutes an eradicated or extinct agent or toxin listed in Section (III.1) above.

 

 

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.

 

As far as `teeth’ in this new policy, if perceived risks cannot be satisfactorily mitigated Federal Agencies may request voluntary redaction of scientific papers, may move to `classify’ the research, or may withhold or terminate financial support.

 

Agencies that conduct or fund life sciences research are instructed to perform a review to identify any projects that meet the DURC definition, and if found, to:

 

 

c)  Assess the risks and benefits of such projects, including how research methodologies may
generate risks and/or whether open access to the knowledge, information, products, or technologies  generates risk.


d)  Based on the risk assessment, in collaboration with the institution or researcher, develop a risk
mitigation plan
to apply any necessary and appropriate risk mitigation measures.  In addition:

  • i)  For DURC that is proposed and not yet funded, departments and agencies will assess
    whether to incorporate risk mitigation measures in the grant, contract, or agreement.

  • ii)  For currently funded DURC, funding departments and agencies will consider modifying the grant, contract, or agreement to incorporate risk mitigation measures. If such modifications are not possible or desirable, departments and agencies will seek voluntary implementation of mitigation measures by the institution. 

 

 

You can access the full policy on the Office of Biotechnology Activity’s News Page:

 

Now Available:

US Government Issues Policy on Oversight of Life Science Dual Use Resarch of Concern:

The purpose of this Policy is to establish regular review of United States Government funded or conducted research with certain high-consequence pathogens and toxins for its potential to be dual use research of concern (DURC) in order to: (a) mitigate risks where appropriate; and (b) collect information needed to inform the development of an updated policy, as needed, for the oversight of DURC. The fundamental aim of this oversight is to preserve the benefits of life sciences research while minimizing the risk of misuse of the knowledge, information, products, or technologies provided by such research.

(March 29, 2012)

 

 

And just as I was finishing this post up, I saw that Lisa Schnirring at CIDRAP NEWS has an excellent overview of this new policy.   Read it at:

 

US debuts life sciences dual-use research policy

Lisa Schnirring * Staff Writer

 

It will be interesting to see how this new policy is received by scientists working in the life sciences field.

»» Read More

How Parrot Fever Changed Public Health In America

 

 

 

Dr. Charles Armstrong - credit National Library of Medicine

 

# 6222

 

We’ve a report today out of the UK of a suspected outbreak of Chlamydophila psittaci, or `Parrot Fever’, in Tayside, Scotland. While somewhat rare, this form of pneumonia usually responds well to antibiotics if it is diagnosed and treated in time.

 

It’s an interesting enough report (h/t Shiloh on FluTrackers), but unlikely to turn into a big story. It does, however, allow me to revisit a fascinating piece of American history.

 

The STV story is linked below, but when you return, I have the tale of how the 1929 Parrot Fever epidemic in the United States helped to change public health in America.

 

 

Suspected outbreak of potentially fatal 'parrot fever' cases

A number of patients thought to have contracted the bug from inhaling dust from dry bird droppings.

13 March 2012 16:04 GMT

 

 


Just 10 years after the end to the horrific Spanish flu pandemic, which claimed more than 600,000 American lives (and tens of millions worldwide), a new and mysterious pneumonia began to spread in the northeast.

 

It began when Simon Martin, a worker at the Chamber of Commerce in Annapolis, Maryland bought a parrot for his wife Lillian 10 days before Christmas.

 


Hoping to keep it a surprise, he enlisted his daughter (Edith) and son-in-law (Lee) to keep the bird until Christmas day, but by Christmas Eve, the bird began to show signs of illness.

 

By morning, in a scene reminiscent of a Monty Python sketch, they had a late parrot on their hands.

 

Unfortunately, by New Years, Lillian, Edith & Lee were all seriously ill. A local doctor, who had read about a parrot fever outbreak in South America, put the pieces together about a week later.

 

In no time, newspapers had the story, and the country – still reeling from the Stock Market crash of October – and with memories of the 1918 Spanish Flu still relatively fresh – suddenly began to fear a new pandemic was on the way.

 

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 Sarasota Times Newspaper – Jan 8th, 1930

 

It didn’t help that 1929 also saw the biggest surge in influenza and pneumonia cases since the end of the great influenza. Newspapers, looking for something other than bad economic news to print, banged the `pandemic gong’ loudly.

 

By now, several employees at the pet shop were sick, and the mayor of Baltimore telegrammed the U.S. Public Health Service urgently requesting assistance. Within hours, Dr. Charles Armstrong – a pathologist with the USPHS – was put in charge of the investigation.

 

Three days later, more cases were detected hundred of miles away in Toledo, Ohio. By January 11th, there were two deaths and more than a dozen cases reported.

 

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Lawrence Journal-World - Jan 11, 1930

The newspapers had a field day, and `Polly Pandemic Paranoia’ swept the nation.

 

Upon discovering that the pet store in Baltimore had sold 36 parrots before Christmas, Armstrong and his team began tracking them down. Meanwhile, the health department began notifying local health departments around the country to be on the look out for possible cases.

 

Fortunately, it doesn’t take long before it becomes apparent that only those in close contact with parrots were at risk, and that actual the number of cases was very, very small.

 

Curiously, most of the victims were elderly widows.

 

While their age may have predisposed them to pneumonia, it was also suggested that some of them allowed their birds pluck seeds from between their lips or teeth (a trick I can remember my Grandmother performing in the 1950s!).

 

After a week of screaming headlines, the newspapers did an about-face and began to ridicule the story – even going so as to begin printing parrot jokes. Overnight the Polly Pandemic became a national joke.

 

But the investigative work continued.

 

Within a week, the story would take horrific turn, as a number of the investigators began to fall seriously ill. 

 

Several of them died.

 

On February 8th, lead investigator Charles Armstrong was admitted to the hospital with a 104 degree fever. George McCoy, director of the US Public Health Services’ very small and underfunded Hygienic lab, took over and in a daring move created a serum (this was before antibiotics were available) from the blood of a recovered patient, which he gave to Armstrong.

 

Armstrong would recover, and eventually wrote that there had been 169 cases of parrot fever nationwide, along with 33 deaths (including Dr. Daniel S. Hatfield and Dr. William Stokes of the Baltimore Health Department, and Henry (Shorty) Anderson of the Hygienic Lab)

 

 

In March, 9 more employees at the Hygienic Laboratory became sick, and McCoy ordered the lab evacuated, the test animals euthanized and incinerated, and the lab fumigated.

 

The outbreak was finally quashed, but out of it (and concerns over the recent rise in flu) came funding from Congress for a new, better staffed and equipped laboratory to replace the old Hygienic Lab.

 

They also gave it a new name: The National Institute of Health.

 

 

I’ve only covered the highlights of this fascinating story, and I would invite you to read Jill Lepore’s  New Yorker article from June 1st, 2009 for a far more detailed and vivid account:

 

American Chronicles

It’s Spreading

Outbreaks, media scares, and the parrot panic of 1930.

by Jill Lepore June 1, 2009

 

Jill Lapore also was interviewed on NPR’s All things Considered:

In 1929, Parrot Fever Gripped The Country

 

 

Dr. Charles Armstrong (September 25, 1886 – June 23, 1967) would go on to investigate many more disease outbreaks in his career, and would contract St. Louis Sleeping Sickness (St. Louis encephalitis) during the 1934 epidemic (but would recover).

 

The NIH has a full biography of this early disease detective available for free download (PDF) at:

 

"Charles Armstrong, M.D.: A Biography"

 

You can also find other accounts of this famous episode in public health in the 1939 book, Modern Miracle Men by John Drury Ratcliff (available HERE on Google Books) and in 2007’s Government and public health in America by by Ronald Hamowy (also available through Google Books here).

 

 

And you can review some of the early history of the NIH, including the origins of the Hygienic Laboratory after the Civil War, at the following NIH site:

 

Origins of the National Institutes of Health


Navigation map

 

 

As a parting shot, I wrote about another `Parrot Fever’ outbreak in the Netherlands back in 2007, in my blog To You, My Heart Cries Out Chlamydia.

 

(No apologies for the title)

»» Read More

NIH: Investigating A Potential Treatment For Hendra & Nipah Viruses

 

 

# 5911

 

 

The movie `Contagion’ showed the world how a bat virus could mutate, evolve, and move into the human population. While the movie used a fictionalized MEV-1 virus, bats in some parts of the world are known to carry deadly pathogens, such as the Nipah and Hendra viruses.

 

While human infections with these two viruses have been relatively uncommon, when they have occurred they have proven particularly lethal, with fatality rates exceeding 60%.

 

Nipah was first identified in Malaysia in 1998, where it jumped to local swine herds from bats, and along with infecting hundreds of people, it caused the loss over 100 lives. The virus was then exported via live pigs to Singapore, where 11 more people died.

 

Over the past decade, Nipah has caused a number of small outbreaks across Southern Asia, although the most intense activity has been centered around Bangladesh.

 

The Hendra virus was first isolated in 1994 after the deaths of 13 horses and a trainer in Hendra, a suburb of Brisbane, Australia. A stable hand, who also cared for the horses, was hospitalized, but survived.

 

Another outbreak took place in MacKay, 1000 km to the north of Brisbane, the previous month. Two horses died, and the owner was hospitalized several weeks later with meningitis.

 

He recovered, but developed neurological symptoms and died 14 months later.

 

Subsequent studies have showed a high prevalence of the newly identified Hendra virus in Pteropid fruit bats (flying foxes) in the region.

 

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Nipah/Hendra Virus & Fruit Bat Home Range – WHO

 

Although very similar, unlike Hendra, the Nipah virus has been shown to be transmissible from human-to-human. Like all viruses, both have the potential to mutate and evolve - and over time - become better adapted to their hosts.

 

According to the World Health Organization there are currently no effective treatments for either of these diseases (see here and here), but according to a new study just published in the journal Science Translational Medicine, there is hope that may change.

 

The study is called:

 

Sci Transl Med 19 October 2011:
Vol. 3, Issue 105, p. 105ra103
Sci. Transl. Med. DOI:

10.1126/scitranslmed.3002901

A Neutralizing Human Monoclonal Antibody Protects African Green Monkeys from Hendra Virus Challenge

Katharine N. Bossart, Thomas W. Geisbert, Heinz Feldmann, Zhongyu Zhu, Friederike Feldmann, Joan B. Geisbert, Lianying Yan, Yan-Ru Feng, Doug Brining, Dana Scott, Yanping Wang, Antony S. Dimitrov, Julie Callison, Yee-Peng Chan, Andrew C. Hickey, Dimiter S. Dimitrov, Christopher C. Broder,† and Barry Rockx

 

The NIH – which supported this research – issued a press release yesterday afternoon describing this study:

 

Embargoed for Release
Wednesday, October 19, 2011
2 p.m. EDT

Antibody treatment protects monkeys from Hendra virus disease

NIH-supported group exploring whether protection extends to Nipah virus disease

A human antibody given to monkeys infected with the deadly Hendra virus completely protected them from disease, according to a study published by National Institutes of Health (NIH) scientists and their collaborators. Hendra and the closely related Nipah virus, both rare viruses that are part of the NIH biodefense research program, target the lungs and brain and have human case fatality rates of 60 percent and more than 75 percent, respectively. These diseases in monkeys mirror what happens in humans, and the study results are cause for hope that the antibody, named m102.4, ultimately may be developed into a possible treatment for people who become infected with these viruses.

 

In May 2010, shortly after the NIH study in monkeys successfully concluded, Australian health officials requested m102.4 for emergency use in a woman and her 12-year-old daughter. They had been exposed to Hendra virus from an ill horse that ultimately was euthanized. Both the woman and child survived and showed no side effects from the treatment.

(Continue . . . )

 

 

The human monoclonal antibody (hmAb) m102.4 has been the object of Hendra-Nipah research for a number of years. In 2009 research published in PLoS Pathogens  illustrated its protective effect against Nipah in ferrets.

 

A Neutralizing Human Monoclonal Antibody Protects against Lethal Disease in a New Ferret Model of Acute Nipah Virus Infection

 

 

Now that this hmAb has been shown effective against the Hendra virus in primates, researchers hope they may have the basis for what will eventually become a viable treatment for these deadly viruses.

 

For more on human monoclonal antibodies, and their potential to treat influenza, you may wish to revisit a couple of blogs I wrote in 2009 and 2010:

 

Research: Monoclonal Antibodies Against Influenza
Monoclonal Antibodies Revisited
»» Read More

NIH: Any Combo Of Prime-Boost Flu Vaccine Protects Toddlers

 

 

# 5759

 

 

Children 6 months of age or older, who have never received a flu vaccine before, are recommended to receive a priming vaccine and a booster – one month apart – the first time.

 

For children over the age of 6 months, the TIV flu shot may be used, and for healthy children 24 months or older, the LAIV nasal spray may be substituted.

 

Until now, a lack of clinical studies have left some doubts as to whether a combination of the TIV flu shot and LAIV nasal vaccine would perform equally as well.

 

From the NIH today, we’ve a report on clinical trials conducted at Saint Louis University, along with investigators at Vanderbilt University in Nashville, and the Cincinnati Children's Hospital – funded by NIAID -that looks at the immune responses in toddlers who received one of four different flu shot combinations:

 

  • two injections of a TIV vaccine
  • two LAIV nasal spray vaccines
  • A LAIV nasal spray followed by a TIV shot
  • a TIV shot followed by the LAIV nasal spray

 

The good news . . . particularly for children at least 2 years of age with an aversion to needles . . . is that two sprays of the LAIV vaccine appear to produce the same level of antibody response as two flu shots.

 

And when a child receives at least one of their vaccines via the LAIV nasal spray, they produced a wider array of immune T cells, which may help protect against other flu strains.

 

This from NIH News.

 

 

Any Prime-Boost Mix of Injected or Spray Flu Vaccine Shields Toddlers

Broadest Immune Response from Nasal Spray Vaccine, NIH-Funded Study Finds

Children younger than 3 years old receive the same protective antibody response from the recommended two doses of licensed seasonal influenza vaccines regardless of whether the two doses are injected by needle, inhaled through a nasal spray or provided through one dose of each in any order, according to researchers funded by the National Institutes of Health. Doctors usually give young children two matching vaccines, and one goal of the study was to determine whether giving two different types of vaccines works just as well.

Daniel Hoft, M.D., Ph.D., conducted a trial of influenza vaccines in young children.
Credit: Saint Louis University

 

<SNIP>

 

The researchers found that all four dosing patterns were safe and induced similar levels of protective antibodies. However, when the investigators looked at responses from the T-cell arm of the immune system, a striking difference emerged. They could not detect influenza-specific T cells in children who received only TIV, according to Dr. Hoft. But, he added, “The kids who received at least one dose of LAIV nasal spray vaccine produced significant amounts of three important T-cell subtypes that are likely to confer additional protection beyond that afforded by antibodies alone.”

 

Previous studies have demonstrated that children are better protected against influenza infection and disease by LAIV than by TIV, Dr. Hoft noted. However, few studies have examined the T-cell responses elicited by LAIV when given to very young children who have little prior natural exposure to seasonal influenza viruses. Distinguishing T-cell responses due to vaccination from those arising after natural exposure to influenza virus becomes more difficult as a child ages, he explained. Because the children in the trial were all younger than 3 years old, the researchers could be confident that spikes in levels of the three T-cell subtypes they detected were likely due to the vaccinations.

 

Children who received only one dose of LAIV had T-cell responses similar to those who received two, and the order of vaccine types did not make a significant difference in the size of the T-cell response. However, because LAIV has sometimes been associated with increased incidence of wheezing in the youngest recipients, the results of this trial suggest that the best regimen for kids younger than 24 months may be TIV followed by LAIV, Dr. Hoft said. Larger clinical trials are required to confirm the safety and efficacy of such an approach, he added. 

 

(Continue . . . )

 

The results are published today in the Journal of Infectious Diseases, and the abstract may be read at:

 

Live and Inactivated Influenza Vaccines Induce Similar Humoral Responses, but Only Live Vaccines Induce Diverse T-Cell Responses in Young Children

Daniel F. Hoft, Elizabeth Babusis, Shewangizaw Worku, Charles T. Spencer, Kathleen Lottenbach, Steven M. Truscott, Getahun Abate, Isaac G. Sakala, Kathryn M. Edwards, C. Buddy Creech, Michael A. Gerber, David I. Bernstein, Frances Newman, Irene Graham, Edwin L. Anderson and Robert B. Belshe

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NIH: School Closings Effective In 2009 Pandemic

 

 

 

# 5573

 

One of the most contentious issues during the opening days and weeks of the 2009 novel H1N1 outbreak was the wisdom of closing schools to reduce transmission of the virus.

 

Since the virulence of the virus was largely unknown during those opening weeks, school closures were recommended by the CDC, and by other public health entities around the world.  

 

The closing of schools, and other venues where people gather (sporting events, restaurants, shopping malls), has long been argued as being potentially an important mitigation strategy during a pandemic.

 

By early May (2009), however, it was apparent that the severity of this particular influenza virus was less than originally feared, and many public health agencies moderated their recommendations  (see CDC No Longer Recommending School Closures For A/H1N1).

 

Some school districts, in the U.S., and elsewhere around the world, continued to close schools on a case-by-case basis well into the fall of 2009.

 

In a future, more severe pandemic, the extended closing of schools will once again likely be considered to help reduce the spread of the virus.

 

It isn’t an easy decision, however.  School closings are controversial, and the issues are complex  (see The Debate Over School Closures).

 

Critics point out that working parents rely on schools to watch their kids for much of the year during the day, and many low income families benefit from the school lunch program.

 

And of course, when schools are closed during a pandemic, some kids may congregate elsewhere and spread the virus anyway.

 

 

It is important, therefore, to get some idea of the benefits that school closings would generate. To that end we’ve seen several studies over the past two years that have produced varying estimates.

 

Study: Pandemic Mitigation by Early School Closure
Study: Student Behavior During Pandemic School Closings
School Closures Revisited
Study: Effect Of School Closures On Viral Transmission

Today we’ve a new study by the NIH’s Fogarty International Center, Arizona State University and colleagues at the Mexican Institute for Social Security that appears in PLoS Medicine that looks at the epidemiology of the H1N1 outbreak in Mexico, and the effects of school closings and social distancing on its transmission.

 

Our first stop are a few excerpts (slightly reformatted) from NIH press release, which summarizes this research article nicely.

 

 

Embargoed for Release
Tuesday, May 24, 2011
5 p.m. EDT

Mexican flu pandemic study supports social distancing

Fogarty research published in PLoS Medicine

Eighteen-day periods of mandatory school closures and other social distancing measures were associated with a 29 to 37 percent reduction in influenza transmission rates in Mexico during the 2009 pandemic. The research was carried out by scientists at the Fogarty International Center at the National Institutes of Health and published in PLoS Medicine.

 

The social distancing measures implemented by the Mexican health authorities in spring 2009 were effective in reducing disease transmission by more than one-third, the study found.

 

Social distancing interventions can be implemented during unusual infectious diseases outbreaks and include school closing, closure of movie theaters and restaurants, and the cancellation of large public gatherings. Mexico implemented a nationwide mandatory school closure policy during an 18-day period in late April and early May 2011.

 

The United States implemented school closure interventions on a local basis during the 2009 pandemic, but the impact of these interventions has yet to be evaluated.

(Continue . . .)

 

 

During a particularly severe pandemic, it has been suggested that schools could be closed for up to 12 weeks. While drastic, that strategy is based – in part – on some of the experiences from the last great pandemic in 1918.

 

 

The chart above, taken from the PNAS journal article entitled Public Health Interventions and Pandemic Intensity During the 1918 Influenza Pandemic , shows the excess mortality in two American cities.

 

The tall spike represents Philadelphia, while the lower curve represents St. Louis.

 

Many researchers believe the startling difference in attack rates, and mortality, in these two cities can be explained by the way each city dealt with the outbreak.

 

In St. Louis, the Health Department closed public venues such as schools, theatres and churches very early in the outbreak, while Philadelphia did not.

 

While are societal costs to closing schools and other public venues, studies continue to show that during a severe pandemic it might very well be worth doing. 

 

Here are some excerpts from the open access article in Plos Medicine.  Follow the link to read it in its entirety.

 

 

 

Characterizing the Epidemiology of the 2009 Influenza A/H1N1 Pandemic in Mexico

Gerardo Chowell, Santiago Echevarría-Zuno Cécile Viboud, Lone Simonsen, James Tamerius, Mark A. Miller, Víctor H. Borja-Aburto

Abstract  (Excerpts)

Background

Mexico's local and national authorities initiated an intense public health response during the early stages of the 2009 A/H1N1 pandemic. In this study we analyzed the epidemiological patterns of the pandemic during April–December 2009 in Mexico and evaluated the impact of nonmedical interventions, school cycles, and demographic factors on influenza transmission.

 
Methods and Findings
. . .   We estimate that the 18-day period of mandatory school closures and other social distancing measures implemented in the greater Mexico City area was associated with a 29%–37% reduction in influenza transmission in spring 2009. In addition, an increase in R was observed in late May and early June in the southeast states, after mandatory school suspension resumed and before summer vacation started. State-specific fall pandemic waves began 2–5 weeks after school reopened for the fall term, coinciding with an age shift in influenza cases.
Conclusions

We documented three spatially heterogeneous waves of the 2009 A/H1N1 pandemic virus in Mexico, which were characterized by a relatively young age distribution of cases. Our study highlights the importance of school cycles on the transmission dynamics of this pandemic influenza strain and suggests that school closure and other mitigation measures could be useful to mitigate future influenza pandemics.

»» Read More

Home Is Where The (fatal) Heart Attack Is

 

 

# 5262

 

telemetrympc__4_

Yep, that’s me - circa 1976 with my (now museum piece) LifePak 5 (and an almost full head of hair).

 

While I try not to tell paramedic `war stories’, or go out of my way to make this blog about me, every once in awhile I can’t resist throwing in a personal anecdote.

 

In August of 1974 I was among the first 36 D.O.T. paramedic graduates in the state of Florida. With portable defibrillators, IVs, Cardiac meds, and radio telemetry on board - everyone expected us to start saving lives left and right.

 

And while our `saves’ went up, they didn’t go up as dramatically as many hoped.

 

Sure, we had some great saves - particularly among younger patients, drowning victims, and trauma.   

 

But overall, our cardiac arrest success rate was dismal.   Perhaps now, after all these years, we may have a better clue why.

 

First, a quickie lesson in heart attacks and EKGs (the readout of the electrical activity of the heart). 

 

In a cardiac arrest, the patient is pulseless, usually non-breathing, and unable to circulate oxygenated blood to the brain and other organs. Death follows generally in 4 to 10 minutes.

 

But not all pulseless arrests are created equal.


This is bad.

(Ventricular Tachycardia)

 

This is very bad

(Ventricular Fibrillation)

 

And this is worst of all.

(Asystole)

 

 

The first two rhythms strips are considered `shockable’ arrhythmias. The heart may not be beating, but there is still some (albeit, chaotic) electrical activity going on. 

 

Applying an electrical shock promptly enough can often restore NSR (normal sinus rhythm) to a stopped heart. 

 

But despite what you may have seen in the movies, and on television, you can shock an asystolic (flatlined) heart all day long without much hope of success.   

 

There are some cardiac meds that can (rarely) convert asystole to fibrillation, but defibrillation alone is generally futile.

 

 

Yesterday the NIH announced  a study comparing the type of cardiac arrests experienced by people at home verses people who collapsed in public.

 

And the results are fascinating.   At least to an old EMT-II like myself.

 

First, some excerpts from the press release, then a link to the NEJM study, after which I’ll be back with a little more.

 

 

Shockable cardiac arrests are more common in public than home

Comprehensive NIH study helps explain discrepancy in survival rates between cardiac arrests in public and at home

Cardiac arrests that can be treated by electric stimulation, also known as shockable arrests, were found at a higher frequency in public settings than in the home, according to a National Institutes of Health-funded study appearing in the Jan. 27 issue of the New England Journal of Medicine.

 

The study compared home and public cardiac arrests under various scenarios. For example, the study considered whether bystanders or emergency medical services (EMS) personnel witnessed the cardiac arrest, and whether the person experiencing the arrest received treatment with an automatic external defibrillator (AED).

 

In every scenario, a higher percentage of public cardiac arrests were classified as ventricular tachycardia (VT) or ventricular fibrillation (VF), the types of abnormal heart rhythms that can be treated by electric shock.

 

More than one-third of the people who had a cardiac arrest in public and were treated with an AED survived. This is a significant improvement over the roughly 8 percent national average of cardiac arrest survival. In comparison, the overall survival for home-occurring cardiac arrests treated with an AED was 12 percent.

(Continue . . .)

 

Ventricular Tachyarrhythmias after Cardiac Arrest in Public versus at Home

 

Myron L. Weisfeldt, M.D., Siobhan Everson-Stewart, Ph.D., Colleen Sitlani, M.S., Thomas Rea, M.D., Tom P. Aufderheide, M.D., Dianne L. Atkins, M.D., Blair Bigham, M.Sc., Steven C. Brooks, M.D., M.H.Sc., Christopher Foerster, M.Sc., Randal Gray, M.A.Ed., Joseph P. Ornato, M.D., Judy Powell, B.S.N., Peter J. Kudenchuk, M.D., and Laurie J. Morrison, M.D. for the Resuscitation Outcomes Consortium (ROC) Investigators

N Engl J Med 2011; 364:313-321January 27, 2011

(Read Full Report . . . )

 

 

Like all studies, there are limitations to this one.

 

Some assumptions regarding the arrhythmias of successfully cardioverted arrest victims using AEDs (which only shock when they detect VT or VF) had to be made in lieu of actual EKG strips.

 

Likewise, home heart attacks (where AEDs are less likely to be found, or the patient’s collapse witnessed) may have started with VT or VF and progressed to asystole by the time rescuers with their EKGs arrived.

 

But even when you take these items into account, it appears that cardiac arrests that occur in public are far more likely to be a `shockable’ (VT or VF) rhythm than those that occur in the home.

 

This likely has more to do with the age, and physical condition of the patient, than the actual location.  Those who are able to be out and about are probably in somewhat better overall health than those who are house bound.

 

All of which points out the benefits of putting more AEDs in public places, and promoting lay person CPR and AED training. 

 

The authors of this NEJM report conclude:

 

Conclusions

Regardless of whether out-of-hospital cardiac arrests are witnessed by EMS personnel or bystanders and whether AEDs are applied by bystanders, the proportion of arrests with initial ventricular fibrillation or pulseless ventricular tachycardia is much greater in public settings than at home. The incremental value of resuscitation strategies, such as the ready availability of an AED, may be related to the place where the arrest occurs. (Funded by the National Heart, Lung, and Blood Institute and others.)

 

 

For more on the recent changes to bystander CPR, you may wish to visit these recent blogs.

 

image

CPR As A Requirement For High School Graduation

AHA Unveils 2010 CPR Guidelines

JAMA: Compression Only CPR

MMWR: Sudden Cardiac Arrest Awareness Month

»» Read More

NIH: Commentary On Universal Flu Vaccines

 

 

# 5121

 

 

 

 

World War I was brought to a halt, in part, due to the massive wave of pandemic influenza that – by November of 1918 - had crippled the ability of soldiers and sailors to fight on both sides of the conflict.

 

Nearly 25 years later, when WWII broke out, concerns arose that once again putting hundreds of thousands of troops in close quarters might spark another global influenza epidemic (it didn’t). 

 

This time, a decade after the influenza virus had finally been isolated, scientists had a new, experimental vaccine that – starting in 1943 -was widely used on servicemen. 

 

This first vaccine was reportedly effective during the 1943-44 and the 1944-45 flu seasons, but suffered an almost complete failure during the 1946-47 season (see doi: 10.1073/pnas.162366899) when the predominate influenza strain shifted sharply antigenically. 

 

First detected on US military bases in Japan in 1946, this new virus spread quickly around the world, but is little remembered today because it produced few excess deaths.

 

What this did demonstrate was that to be effective, influenza vaccines have to be updated each year to keep up with the rapidly evolving influenza virus.

 

More than sixty years later, scientists are still scrambling to stay one-step ahead of the  multiple strains of influenza in circulation, by trying to guess what strains will be infecting people more than 6 months in advance.

 

Some years, they get it right.  Some years . . .  well, it isn’t easy when nature’s lab is open and experimenting 24/7.

 

The Holy Grail for flu vaccine researchers is a universal vaccine – one that would protect against multiple (even antigenically shifted/drifted) strains and that would remain protective for many years.

 

This would solve two huge problems.  

 

First, it would end (or at least greatly reduce) the constant game of playing catch-up with evolving and mutating viruses.


And second, if a shot could be good for 5 or more years, you could vaccinate a much larger portion of the world’s population over time.

 

We could conceivably stop the next global pandemic in its tracks, by already having `herd immunity’.  

 

We aren’t there, of course.   But the NIH, and many other researcher entities are hard at work on finding the breakthrough that will make this a reality.


A few past blogs on this hunt, include:

 

Towards A Universal Flu Vaccine
NIH: Progress Towards A Universal Flu Vaccine
Uncovering Influenza's Achilles Heel

 

 

This week Anthony S. Fauci, M.D., NIAID director, and Gary J. Nabel, M.D., Ph.D., director of the NIAID Vaccine Research Center, have published a commentary on the prospects for a universal vaccine in Nature Medicine.

GJ Nabel and AS Fauci. Induction of unnatural immunity: Prospects for a broadly protective universal influenza vaccine. Nature Medicine DOI: nm.2272 (2010).

 

While this is (alas) behind a pay wall, we can get a pretty fair idea of the contents from this NIH press release.

 

A Flu Vaccine that Lasts

NIH Scientists Consider Prospects for a Universal Influenza Vaccine

WHAT: 
The costly, time-consuming process of making, distributing and administering millions of seasonal flu vaccines would become obsolete if researchers could design a vaccine that confers decades-long protection from any flu virus strain. Making such a universal influenza vaccine is feasible but licensing it may require innovation on several fronts, including finding new ways to evaluate the efficacy of vaccine candidates in clinical trials, conclude scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.

 

In a Nature Medicine commentary, authors Anthony S. Fauci, M.D., NIAID director, and Gary J. Nabel, M.D., Ph.D., director of the NIAID Vaccine Research Center, contrast the envisioned universal influenza vaccine with today’s seasonal influenza vaccines. Current seasonal flu vaccines prompt immune responses that mimic those made following natural exposure to the flu virus. Both exposure and vaccination elicit antibodies directed at the roundish head portion of a lollypop-shaped flu protein called hemagglutinin (HA). But the composition of HA’s head changes from year to year, gradually becoming unrecognizable to previously made antibodies. Thus, vaccination—which induces antibodies tailored to that year’s HA head region—must be repeated annually to maintain immunity to the virus.

 

A universal flu vaccine would have to elicit a type of immune response that rarely occurs naturally, note Drs. Fauci and Nabel. A detailed understanding of flu virus structure may make such a vaccine possible, they add. For example, scientists have identified a region of HA’s stem that is shared among diverse strains, and a research group at NIAID’s Vaccine Research Center recently created influenza vaccines that elicit antibodies aimed at this shared region, rather than at the quick-changing head. Animals that received the experimental vaccines were protected from a diverse array of flu virus strains.

 

In essence, say the authors, thanks to the growing body of knowledge about flu viruses and their interactions with the cells of humans and animals they infect, it may one day be possible to make a universal flu vaccine that improves on nature. They also outline how such a vaccine might proceed through stages of clinical testing and on toward licensing. For example, they sort the 16 known influenza virus subtypes into three tiers based on their likelihood of causing widespread disease in humans. Drs. Fauci and Nabel suggest that vaccine development might be prioritized to produce first-generation universal influenza vaccine candidates that protect against multiple virus strains within the highest priority group.

 

For more information about NIAID research on influenza, visit the NIAID flu Web portal.

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