ICAAC Video: How Quickly A Virus Can Spread In A Building

 

# 9051

 

The 54rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) runs through September 9th in Washington D.C. , and this morning we’ve an absolutely fascinating video sponsored by the American Society for Microbiology showing just how quickly a single introduction of a virus into an office environment can spread to contaminate an entire building.

 

Of particular interest, this conversation explores how their results relate to this week’s Enterovirus (HEV-D68) outbreak (see Enterovirus D-68 (HEV-D68) Update).

 

First, the press release on the study, then a link to the video on  MicrobeWorld’s Youtube channel.

 

How Quickly Viruses Can Contaminate Buildings and How to Stop Them

EMBARGOED UNTIL: Monday, September 8, 2014, 9:00 a.m. EDT

(Images are courtesy Gerba Lab and are free to use. First image is Gerba and a student working on samples and second is a sampling sponge.)

WASHINGTON, DC – September 8, 2014 – Using tracer viruses, researchers found that contamination of just a single doorknob or table top results in the spread of viruses throughout office buildings, hotels, and health care facilities. Within 2 to 4 hours, the virus could be detected on 40 to 60 percent of workers and visitors in the facilities and commonly touched objects, according to research presented at the 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), an infectious disease meeting of the American Society for Microbiology.

There is a simple solution, though, says Charles Gerba of the University of Arizona, Tucson, who presented the study.

“Using disinfecting wipes containing quaternary ammonium compounds (QUATS) registered by EPA as effective against viruses like norovirus and flu, along with hand hygiene, reduced virus spread by 80 to 99 percent,” he says.

(Continue . . . )

The video is available on the http://www.microbeworld.org/podcasts/asm-live website right now, but should be moved to the MicrobeWorld’s Youtube channel later today.

 

Monday, September 8

9:00 a.m. -- How Quickly Viruses Can Contaminate a Building
Using tracer viruses, researchers found that contamination of just a single doorknob or table top results in the spread of viruses throughout office buildings, hotels, and health care facilities. Within 2 to 4 hours, the virus could be detected on 40 to 60 percent of workers and visitors in the facilities and commonly touched objects. Simple use of common disinfectant wipes reduced virus spread by 80 to 99 percent.

Charles Gerba, University of Arizona, Tucson

 

 

Sigh.  Based on this, and the viral threats lining up, guess I’m gonna need to lay in a bigger supply of hand sanitizer.

ECDC Influenza Virus Characterization – June 2014

Credit NIAID

 

# 8889

 

Although we talk about seasonal flu strains like H1N1, H3N2, and influenza B as if they were single entities, in truth within each sub-type are numerous clades, sub-strains, and variants. 

 

These influenza viruses are constantly mutating (via antigenic drift) as they replicate and spread, and are engaged in a perpetual game of  viral king-of-the-mountain, as they jostle for dominance and superiority in the global community.

 

Success for these strains is always fleeting, though,  as they leave behind varying degrees of immunity in their hosts and must either evolve or eventually die out for lack of susceptible hosts.  All which makes the flu world dynamic and ever-changing, and presents a genuine challenge for vaccine manufacturers to stay ahead of.

 

To keep abreast of the changes to the flu strains in circulation, labs around the world send samples to the WHO Collaborating Centre in London for classification, and the ECDC publishes reports roughly once a month.  These reports can help give us some idea whether the strains contained the latest vaccine match up antigenically with those strains currently circulating.

 

As you might expect, given the diversity of flu strains in circulation, the best that can be hoped for is that the majority of viruses tested are antigenically similar to the components in the vaccine.  That said, we won’t really have a good idea of how well this year’s vaccine will perform until the flu season is over, next spring.

 

The summary is printed below.  The full report is available as a PDF File.

 

Influenza virus characterisation, June 2014

29 Jul 2014

Abstract

​During the 2013–14 season, A(H1N1)pdm09, A(H3N2), B/Victoria- and B/Yamagata-lineage influenza viruses have continued to co-circulate in EU/EEA Member States. The relative prevalence has varied between countries. Viruses with collection dates after 31 December 2013, from 22 countries, have been received by the WHO Collaborating Centre in London.

• Type A and type B viruses have been received at a ratio of nearly 20:1.
• A(H3N2) and A(H1N1)pdm09 viruses have been received in similar numbers.
• Recently circulating A(H1N1)pdm09 viruses belonged to genetic subgroup 6B. Viruses in subgroup 6B are antigenically similar to the vaccine virus, A/California/07/2009.
• Recently circulating A(H3N2) viruses have fallen within genetic group 3C represented by the recommended vaccine virus for the 2013–14 and 2014–15 seasons, A/Texas/50/2012, with viruses of genetic subgroup 3C.3 predominating. Antigenic analysis using antisera raised against cell-propagated H3N2 viruses indicates that the majority of circulating viruses are antigenically similar to those in circulation in the 2012–13 and 2013–14 influenza seasons. Antisera raised against two reference viruses representative of viruses in genetic subgroup 3C.3 – with HA gene sequences encoding several amino acid substitutions compared to other viruses in genetic group 3C.3 – have been prepared. These antisera recognised the majority of test viruses well.
• Two genetic clades of B/Yamagata-lineage viruses continue to circulate: clade 3 represented by B/Wisconsin/1/2010 and clade 2 represented by B/Massachusetts/02/2012 (the recommended vaccine component for the 2013–14 and 2014-15 influenza seasons). Viruses in each clade have been received in similar numbers but with viruses in clade 3 predominating in those samples collected in 2014.
• Antigenic characterisation of two viruses of the B/Victoria lineage was performed in June. Neither virus was recognised well by the antiserum raised against the egg-propagated reference virus, A/Brisbane/60/2008, a virus previously recommended as a component of the trivalent influenza vaccine and recommended as a component of quadrivalent influenza vaccines for 2013–14 and 2014–15 influenza seasons. The test viruses were not recognised well by antisera raised against other reference viruses propagated in eggs. The test viruses were better recognised by some, but not all, antisera raised against reference viruses exclusively propagated in cells. Phylogenetic analysis revealed that all B/Victoria-lineage viruses received in 2014 were in genetic clade 1A, the B/Brisbane/60/2008 genetic clade.

ECDC: Influenza Virus Characterization – July 2013

Photo Credit NIAID

 

 

# 7537

 

 

As summer moves inexorably towards fall, those of us in the northern hemisphere begin to think about the upcoming flu season, and just how good of a match this year’s flu vaccine will turn out to be.

 

It requires 6 months of lead time to develop, manufacture, and distribute the yearly seasonal influenza vaccine. During that time it is possible that the strains in circulation can drift antigenically (or change completely) from the strains selected last February for the vaccine.

 

NIAID has a terrific 3-minute video that shows how influenza viruses drift over time, and why the flu shot must be frequently updated, which you can view at this link.

So we watch surveillance reports - like those coming from the CDC’s FluView and the ECDC’s  monthly Virus characterization reports – for any signs that there’s a `new flu’ in town.

 

Today, the ECDC released their latest Influenza Virus Characterization report (for July 2013).

 

While antigenic changes continue to show up in both influenza A/H1N1 and A/H3N2, the good news is – the majority of the viruses being analyzed still appear to be antigenically similar to those in this year’s vaccine. The influenza B vaccine strain also appears to be a good match for the bulk of the B viruses tested.

 

This year, you can get a little added protection, as  a new quadrivalent (4 strain) vaccine will be available which can help protect you against both (Yamagata & Victoria) influenza B strains.

 

This Abstract from the ECDC, follow the link to read the entire report.

 

 

Influenza Virus Characterisation, July 2013

Surveillance reports - 02 Aug 2013

Available as PDF in the following languages:

This document is free of charge.

ABSTRACT

In the course of the 2012–13 season, A(H1N1)pdm09, A(H3N2) and B/Victoria- and B/Yamagata-lineage influenza viruses have co-circulated in ECDC-affiliated countries over what was an extended influenza season. The relative prevalences of each virus type/subtype has varied between countries.

• Type A and type B viruses have been detected in similar proportions but with type A peaking and declining slightly before type B.

• A(H1N1)pdm09 viruses have been detected at approximately twice the level of A(H3N2) viruses.

• The vast majority of A(H1N1)pdm09 viruses have remained antigenically similar to the vaccine virus, A/California/07/2009, but continued to show genetic drift with an increasing prevalence of genetic group 6 viruses.

• The vast majority of A(H3N2) viruses have been antigenically and genetically similar to cell-propagated A/Victoria/361/2011, a genetic group 3C virus and the prototype vaccine virus for the 2012–13 influenza season; group 3C viruses have circulated exclusively in recent months and the recommended vaccine virus for the 2013–14 season, A/Texas/50/2012, is in this genetic group.

• Viruses of the B/Yamagata-lineage have predominated over those of the B/Victoria-lineage.

• B/Victoria-lineage viruses have remained antigenically similar to cell-propagated reference viruses of the B/Brisbane/60/2008 genetic clade.

• B/Yamagata-lineage viruses formed two antigenically distinguishable genetic clades: clade 3 represented by B/Wisconsin/1/2010 (the recommended vaccine component for the 2012–13 influenza season) and, in increasing numbers, clade 2 represented by B/Massachusetts/2/2012 (the recommended vaccine component for the 2013–14 influenza season).

ECDC: Influenza Virus Characterization Summary

 

# 7426

 

The only real constant with influenza strains is that they are constantly changing. As viruses, they leave behind (varying degrees) of immunity in every host they infect. Were they not to change, they would eventually run out of susceptible hosts.

 

Influenza viruses evolve via two well established routes; Antigenic drift & Antigenic Shift (reassortment).

 

Antigenic drift causes small, incremental changes in the virus over time. Drift is the standard evolutionary process of influenza viruses, and often come about due to replication errors that are common with single-strand RNA viruses.

 

Shift occurs when one virus swap out chunks of their genetic code with gene segments from another virus. This is known as reassortment. While far less common than drift, shift can produce abrupt, dramatic, and sometimes pandemic inducing changes to the virus.

 

And while we talk about the four main strains of influenza that are currently circulating in humans (A/H1N1(pdm), A/H3N2, B Victoria, B Yamagata) as if they were single entities - in reality – within each strain, you will find a good deal of diversity.

 

New `prototypes’ from  these strains are constantly being generated (mostly by antigenic drift) and `field tested’ for biological fitness and transmissibility.

 

Most are evolutionary failures.

 

But occasionally, a new, biologically fit virus will emerge that can compete with its parental strains, and it begins to spread.

 

NIAID has a terrific 3-minute video that shows how influenza viruses drift over time, and why the flu shot must be frequently updated, which you can view at this link.

 

 

As flu vaccine formulations must be decided upon six months in advance of each flu season, public health agencies like the CDC, ECDC, the World Health Organization, Hong Kong’s CHP  (and others) spend considerable resources on influenza surveillance, looking for signs of any up-and-coming viral strains.

 

All of which brings us to the ECDC’s latest influenza virus characterization summary, that looks at the ongoing evolution of these seasonal strains over the past 6 months.

 

Influenza virus characterisation: Summary Europe, December 2012 to May 2013

26 Jun 2013

ECDC

The latest issue of ECDC’s monthly series on 'Influenza virus characterisation’ covers the time period from 1 December 2012 to 31 May 2013, spanning the entire 2012-13 season.

 

It is prepared by the European Reference Laboratory Network for Human Influenza (ERLI-Net). Until June 2013, ERLI-Net was called the Community Network of Reference Laboratories for Human Influenza in Europe (CNRL).

 

During the 2012–13 season, A(H1N1)pdm09, A(H3N2) and B/Victoria- and B/Yamagata-lineage influenza viruses have been detected in ECDC-affiliated countries. The relative prevalences varied between countries.

The report summarises the findings as follows:

• Type A and type B viruses have continued to co-circulate in similar proportions.
• A(H1N1)pdm09 viruses have been detected at comparable levels to A(H3N2) viruses.
• A(H1N1)pdm09 viruses continued to show genetic drift from the vaccine virus, A/California/07/2009, but the vast majority remained antigenically similar to it.
• The vast majority of A(H3N2) viruses have been antigenically and genetically similar to cell-propagated A/Victoria/361/2011, the prototype vaccine virus for the 2012–13 influenza season.
• Viruses of the B/Yamagata lineage predominated over those of the B/Victoria lineage.
• B/Victoria lineage viruses were antigenically similar to cell-propagated reference viruses of the B/Brisbane/60/2008 genetic clade.
• Recent B/Yamagata-lineage viruses fell into two antigenically distinguishable genetic clades: clade 2, represented by B/Estonia/55669/2012, and clade 3, represented by B/Wisconsin/1/2010 (the recommended vaccine component for the 2012–13 influenza season).

For further details, download the complete report 'Influenza virus characterisation - Summary Europe, May 2013'.

 

Last February the World Health Organization met with influenza expert from around the globe to decide on this fall’s flu vaccine composition.  Their decision:

 

Recommended composition of influenza virus vaccines for use in the 2013-14 northern hemisphere influenza season

21 February 2013

It is recommended that trivalent vaccines for use in the 2013-14 influenza season (northern hemisphere winter) contain the following:

• an A/California/7/2009 (H1N1)pdm09-like virus^a;
• an A(H3N2) virus antigenically like the cell-propagated prototype virus A/Victoria/361/2011^b*;
• a B/Massachusetts/2/2012-like virus.

It is recommended that quadrivalent vaccines containing two influenza B viruses contain the above three viruses and a B/Brisbane/60/2008-like virus^c.

 

^a A/Christchurch/16/2010 is an A/California/7/2009-like virus;
^b A/Texas/50/2012 is an A(H3N2) virus antigenically like the cell-propagated prototype virus A/Victoria/361/2011;
^c B/Brisbane/33/2008 is a B/Brisbane/60/2008-like virus.

 

* It is recommended that A/Texas/50/2012 is used as the A(H3N2) vaccine component because of antigenic changes in earlier A/Victoria/361/2011-like vaccine viruses (such as IVR-165) resulting from adaptation to propagation in eggs.

 

It is always difficult – six months in advance – to predict which flu strains are likely to predominate in the upcoming flu season. Some years the vaccine is a good match, other years, not so much.

 

The good news is that despite the inevitable evolution of the flu strains in circulation, so far, the vast majority of those tested by the ECDC are described as being antigenically similar to the components of this year’s flu vaccine.

The Lancet: Virological Analysis Of A MERS-CoV Patient

 

Spread of MERS-CoV Credit Dr Ian MacKay VDU MERS-CoV 

 

 

# 7405

 

With the announcement of 9 new MERS-CoV cases over the past week in Saudi Arabia, and unconfirmed media reports of 7 additional cases in Taif, our need to better understand this emerging virus grows greater with each passing day.

 

Overnight The Lancet published a detailed report on the clinical symptoms and virological analysis of the 17th known MERS case – a 73 year old man from the UAE who was first treated at a hospital in Abu Dhabi and was then transferred by air ambulance to Germany on March 19th.

 

The patient, who developed renal failure and sepsis, died 7 days later (see WHO: Update On NCoV Fatality In Germany).

 

Unlike the SARS virus of 2003 – which carried roughly a 10% fatality rate – this new virus has killed a little over half of the cases that we know about. That percentage would drop should we find that surveillance has not been picking up milder cases.

 

While most of these cases have developed severe illness - some, particularly younger patients - have only experienced mild symptoms.

 

The clinical course of the illness appears different from what was seen with SARS – which was primarily characterized as a respiratory infection - whereas MERS-CoV appears to cause a more systemic infection, and often results in renal failure.

 

In today’s study we learn that doctors found the highest concentration of MERS coronavirus in samples taken from the patient’s lower respiratory system, but also found lower amounts of the virus in the patient’s urine, and stool. No virus was detected in the patient’s blood, however.

 

The detection of the virus in the patient’s urine helps explain the high rate of renal failure in MERS-CoV patients, and fits with what we learned previously about the virus’s receptor cell affinity.

 

Last March, in  Nature: Receptor For NCoV Found, we learned that this novel coronavirus uses a well known cell surface protein called dipeptidyl peptidase 4 (DPP4) to enter and infect human cells. 

 

This DPP4 cell surface protein (also called CD26) is evolutionarily conserved in other species, including bats (suspected of being potential host species), non-human primates, and other animals – all of which suggests that this virus might be able to infect a wide range of hosts.

 

In humans, DPP4 receptor cells are found in non-ciliated bronchial epithelial cells of the respiratory tract, and epithelial cells in the in kidney, small intestine, liver and prostate.

 

Locations consistent with the clinical picture of infection we’ve seen over the past year, that has often included both pneumonia and renal failure.

 

These researchers also compared this patient’s virus genome to four others already sequenced, looking at the number of genetic differences between them.

 

Viruses circulating in the wild pick up mutations at a roughly determinable rate.

 

Once you determine that rate (it varies among viruses), you can compare two or more similar viruses, and count the number differences between them.

 

With that information scientists can estimate how long it has been since they all shared a common ancestor.

 

These researchers calculate that these 5 isolates likely shared a common ancestor sometime in mid-2011.  Nearly a full year before the first known cluster of human cases was reported in Jordan, in April of 2012.

 

For a more detailed explanation of how all this works, and previous work on the evolution of the MERS coronavirus, you may wish to revisit EID Journal: Deep Sequencing and Phylogenetic Analysis of NCoV.

 

While the full Lancet study is behind a pay wall, a fairly lengthy abstract is available (free registration req.). Follow the link to read:

 

 

Clinical features and virological analysis of a case of Middle East respiratory syndrome coronavirus infection

Prof Christian Drosten MD, Michael Seilmaier MD, Victor M Corman MD, Wulf Hartmann MD, Gregor Scheible MD , Prof Stefan Sack MD, Wolfgang Guggemos MD, Rene Kallies PhD, Doreen Muth PhD, Sandra Junglen PhD, Marcel A Müller PhD, Walter Haas MD, Hana Guberina MD , Tim Röhnisch MD, Prof Monika Schmid-Wendtner MD, Souhaib Aldabbagh DVM, Prof Ulf Dittmer PhD, Hermann Gold MD, Petra Graf MD, Frank Bonin MD, Andrew Rambaut DPhil, Prof Clemens-Martin Wendtner MD

Summary

Background

The Middle East respiratory syndrome coronavirus (MERS-CoV) is an emerging virus involved in cases and case clusters of severe acute respiratory infection in the Arabian Peninsula, Tunisia, Morocco, France, Italy, Germany, and the UK. We provide a full description of a fatal case of MERS-CoV infection and associated phylogenetic analyses.

<SNIP>

Interpretation

We have provided the first complete viral load profile in a case of MERS-CoV infection. MERS-CoV might have shedding patterns that are different from those of severe acute respiratory syndrome and so might need alternative diagnostic approaches.

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H7N9 Vaccine Realities

 

# 7073

 

While we are far from knowing how serious this H7N9 bird flu virus outbreak in China will ultimately become, there are people in the world who’s job it is to plan for a variety of `worst case’ pandemic scenarios.  

 

So it should come as little surprise that discussions over the possibility of developing an emergency pandemic vaccine for this virus are already underway around the globe.

 

The CDC has acknowledged their intention to pursue the development of a seed vaccine, as part of a series of `routine preparedness measures’ that are taken whenever a new virus threatens.

 

We’ve seen these sorts of precautionary steps before, with the H5N1, H3N2v and H7N9 viruses (see H3N2v Vaccine Trials & Bangladesh To Share H9N2 Bird Flu Virus).

 

This report from Reuters.

 

CDC to prepare bird flu vaccine just in case

By Reuters staff

The U.S. Centers for Disease Control and Prevention (CDC) said on Thursday it was monitoring a new strain of bird flu and has started work on a vaccine just in case it is needed.

 

So far, the strain known as avian influenza A (H7N9) is only in China and has not yet been found to be capable of being transmitted from person to person.

 

The strain has killed five people, and global health officials are debating whether to start mass-producing a vaccine.

 

(Continue . . . )

 

Via Japan’s NHK network, we get a report on an analysis released today by Japan’s National Institute of Infectious Diseases of the  H7N9 virus.

 

While we’ve yet to see direct evidence of human-to-human transmission  - this reassortant H7 virus is said likely able to replicate in the nose and upper airway - a trait that has long been suspected as needed to make avian flu viruses transmit more efficiently in humans.

 

The research team leader, Takato Odagiri, is calling for the development of a vaccine. Follow the link to read:

 

H7N9 flu virus differs from other viruses

 

Japanese researchers say the new strain of influenza virus spreading in China has different characteristics than other avian viruses. They are calling for the development of a new vaccine.

 

Experts at the National Institute of Infectious Diseases released their findings on Thursday. Their findings are based on gene sequences obtained from China of 2 Shanghai men who died from the infection and an Anhui Province woman in serious condition.

 

(Continue . . .)

 

 

And my thanks to Helen Branswell for tweeting this Reuters story earlier today on the complexities involved in switching from a seasonal flu vaccine run (already in progress) to a pandemic vaccine production schedule.

  

 

World experts debate case for new bird flu vaccine

Thu Apr 4, 2013 12:12pm EDT

• Experts in daily talks on risks posed by new China virus
• Researchers analysing samples to find vaccine candidate
• Decision to make vaccine depends on whether H7N9 spreads

By Ben Hirschler and Kate Kelland

LONDON, April 4 (Reuters) - Experts from around the world are in daily talks about the threat posed by a deadly new strain of bird flu in China, including discussions on if and when to start making a vaccine.

 

Any decision to mass-produce vaccines against H7N9 flu will not be taken lightly, since it will mean sacrificing production of seasonal shots. And scientists warn it will take months to get any finished bird flu vaccine to the market.

 

But the groundwork is being laid.

(Continue . . .)

 

We do have some recent experience with rolling out an emergency pandemic vaccine. 

 

Even though the first H1N1 vaccines came off the production line in the fall of 2009, it proved too little & too late to have much of an impact on the second pandemic wave. 

Estimates made In May of 2009 by Dr. Marie-Paule Kieny, director of the WHO's Initiative for Vaccine Research, (see CIDRAP Experts to discuss swine flu vaccine decision May 14) gave our global vaccine production capacity as:

 

. . . .  somewhere between 1 billion and 2 billion doses in a year, based on an estimated seasonal vaccine capacity of about 900 million doses. Current world population is more than 6 billion.

 

"Being conservative, we think there'll be at least between 1 and 2 billion doses," she said.

 

But at the end of the day, things did not go nearly as well as originally planned and the global production of vaccine fell far short of these estimates.

 

In fairness, the yield from the seed virus proved less than anticipated and the use of adjuvants – to reduce the amount of antigen needed per shot – was met with public resistance.

 

 

On the plus side (and this isn’t well appreciated), the vaccine produced came off the assembly line sooner than expected (albeit in small quantities), and has proven to be both safe and effective.

 

Which has to be seen as a considerable victory, even if the ultimate number of doses produced was disappointing.

 

In a world of 7 billion, the reality is that our ability to manufacture and (just as importantly) distribute a pandemic vaccine in  a short amount of time remains severely limited.

 

It is really a matter of unforgiving numbers.

 

Numbers that start with billions of people at risk from any novel pandemic virus, and end with the number of doses of vaccine that can be delivered in six to twelve months.

 

While improvements have been made in global vaccine manufacturing capacity since 2009, rolling out a pandemic vaccine is a huge undertaking.

 

It is likely that relatively few people could expect to see any novel pandemic vaccine in less than six months from the time production started.

 

And most of the world would probably still be waiting after a year.

 

Five  and a half years after she first wrote it, there is probably no better overview of the problems in the creation, production, and distribution of a pandemic vaccine than Maryn McKenna’s  award winning 7-part series the Pandemic Vaccine Puzzle which she penned in 2007 for CIDRAP.

 

Part 1: Flu research: a legacy of neglect
Part 2: Vaccine production capacity falls far short
Part 3: H5N1 poses major immunologic challenges
Part 4: The promise and problems of adjuvants
Part 5: What role for prepandemic vaccination?
Part 6: Looking to novel vaccine technologies
Part 7: Time for a vaccine 'Manhattan Project'?
Bibliography

Well worth revisiting.

ECDC Influenza Virus Characterization

# 6784

 

The only constant with influenza viruses is their ability to change over time. Since immune systems can learn to recognize and defeat previously seen viral infections, they would soon run out of susceptible hosts if they could not continually evolve.

 

Most of the time, these changes are incremental, and are due to a process called Antigenic drift. Drift comes about due to replication errors that are common with single-strand RNA viruses.

 

Over time these minor changes can accumulate to the point that previously infected immune systems will fail to recognize it, giving the virus a fresh supply of hosts. 

 

NIAID has a nice 3-minute video illustrating the process, which you can view on their Youtube Channel or in the box below.

 

 

 

So, while we talk about seasonal A/H3N2 or A/H1N109 as if they are single entities, in truth, there are a good many minor variations on each theme circulating around the world.

 

Within each strain, we can see numerous `clades’, or genetically distinct groups.  We watch the formation, and progress of these clades carefully, since they may eventually require a change in the flu vaccine’s formulation.

 

Roughly once a month the ECDC releases an influenza virus characterization report, providing laboratory analysis of recently collected flu virus samples across Europe. Collection dates only extend through week 39, but this latest ECDC report indicates continued diversity among the viruses in circulation.

 

The vast majority of flu viruses identified (68%) were of the type A/H3N2. Relatively few A/H1N1 viruses were collected.

 

Among the influenza B viruses received, samples were pretty evenly divided between the Victoria lineage (included in last year’s vaccine) and the Yamagata lineage (part of this year’s vaccine).

 

 

Here’s the link to their report, and the abstract.

 

Influenza virus characterisation - Summary Europe, November 2012

Surveillance reports - 14 Dec 2012

Available as PDF in the following languages:

 

ABSTRACT

During the 2011/2012 season, A(H1N1)pdm09, A(H3N2) and B/Victoria and B/Yamagata lineage influenza viruses, with collection dates between 1 January and 30 September 2012 (weeks 1–39), have been detected in ECDC-affiliated countries.

• Type A viruses predominated over type B.
• A(H3N2) viruses predominated over A(H1N1)pdm09 viruses.
• A(H1N1)pdm09 viruses continued to show genetic drift from the vaccine virus, A/California/07/2009, but the vast majority remained antigenically similar to it.
• Antigenic drift of A(H3N2) viruses compared to the A/Perth/16/2209 vaccine virus resulted in a recommendation to change to an A/Victoria/361/2011-like component for the 2012/2013 influenza season.
• B/Victoria lineage viruses fell within the B/Brisbane/60/2008 genetic clade and were antigenically similar to reference cell-propagated viruses of the B/Brisbane/60/2008 genetic clade.
• Recent B/Yamagata-lineage viruses fell into two genetic clades in approximately equal proportions: clade 3 represented by the recommended vaccine component for the 2012/2013 influenza season, B/Wisconsin/1/2010, and clade 2 represented by B/Estonia/55669/2012. Viruses in each clade are antigenically distinguishable.

 

 

The split between clade 2 and clade 3 of the Yamagata B virus lineage bears watching, and A/H3N2 shows the most variety with samples falling into 5 distinct genetic groups.

 

The good news, despite this growing diversity among flu viruses, is that the majority of those collected in Europe through week 39 still appear antigenically similar to this year’s vaccine strains.

Barnstorming Avian Flu Viruses?

Photo Credit – FAO

 

# 6782

 

 

My thanks to Helen Branswell this morning for tweeting the link to a new study that suggests that avian influenza viruses can be spread over considerable distance by the wind.  

Long time readers will recall we’ve visited this question a couple of times before. We’ll review those, but first, the new study which looked at the extensive outbreak of H7N7 in the Netherlands in 2003.

 

From the Journal of Infectious Diseases (the full study is behind a pay wall), we get a fair idea of their findings via the Abstract.

 

Genetic data provide evidence for wind-mediated transmission of highly pathogenic avian influenza

Rolf J.F. Ypma1, Marcel Jonges, Arnaud Bataille, Arjan Stegeman3, Guus Koch4, Michiel van Boven1, Marion Koopmans1,W. Marijn van Ballegooijen1 and Jacco Wallinga

Outbreaks of highly pathogenic avian influenza in poultry can cause severe economic damage, and represent a public health threat. Development of efficient containment measures requires an understanding of how these influenza viruses are transmitted from one farm to the next. However, the actual mechanisms of inter-farm transmission are largely unknown.

 

Dispersal of infectious material by wind has been suggested, but never demonstrated, as a possible cause of transmission between farms. Here we provide statistical evidence that the direction of spread of avian influenza A(H7N7) is correlated with the direction of wind at date of infection.

 

We find the direction of spread by reconstructing the transmission tree for a large outbreak in the Netherlands in 2003, using detailed genetic and epidemiological data. We conservatively estimate the contribution of a possible wind-mediated mechanism to the total amount of spread during this outbreak to be around 18%.

 

Although it occurred nearly 10 years ago, this outbreak of H7N7 continues to interest scientists, as it represents the largest cluster of human infection by H7 flu virus we’ve seen. 

 

This report from the December 2005 issue of the Eurosurveillance Journal.

 

Human-to-human transmission of avian influenza A/H7N7, The Netherlands, 2003

M Du Ry van Beest Holle, A Meijer, M Koopmans³ CM de Jager, EEHM van de Kamp, B Wilbrink, MAE. Conyn-van Spaendonck, A Bosman

An outbreak of highly pathogenic avian influenza A virus subtype H7N7 began in poultry farms in the Netherlands in 2003. Virus infection was detected by RT-PCR in 86 poultry workers and three household contacts of PCR-positive poultry workers, mainly associated with conjunctivitis.

 

More than 30 million birds residing on more than 1,000 farms were culled to control the outbreak.

 

One person - a veterinarian who visited an infected farm – died a week later of respiratory failure. The rest of the symptomatic cases were relatively mild.

 

Normally, when avian flu manages to spread among local farms, we think of transport mechanisms like the farm-to-farm movement of infected birds or eggs, or of contaminated or infected personnel or equipment, or even a bird or small mammal vector.

 

The idea that the virus might be blown (likely carried on dust, or some other particulate) – while unproven -  has come up before.

 

Back in January of 2008 I wrote a blog called The Virus My Friend, Is Blowin' In The Wind where I cast a dubious eye upon claims by the Indian Government that the bird flu virus (H5N1) was being blown by the wind across the border from neighboring Bangladesh, and was infecting hapless Indian Poultry.

 

It wasn’t impossible, of course.  And I went into some of the other types of pathogens (mostly fungi and bacteria) that are known to travel in the wind.

 

Then in May of 2010 (see Viruses Blowin’ In The Wind?) we saw a report in the journal Environmental Health Perspectives, that suggested that it was possible for H5N1 (or any Influenza A virus) to be transported across long distances in the air.

 

Although researchers demonstrated influenza RNA could be detected in ambient air samplings, they didn’t establish that the virus remained viable over long distances.

 

But we have seen studies indicating that the H5N1 virus can – under the right environmental conditions – remain viable for hours or even days in the environment (see EID Journal: Persistence Of H5N1 In Soil and H5N1: Hiding In Plain Sight)

 

Lending at least a little credence to the idea that they might survive on the wind long enough to infect downwind farms.

 

It has also been suggested that dried chicken droppings (`poultry dust’) may also serve to spread the virus, and Indonesian authorities have mentioned this as a possible vector (see Indonesian Updates And Vector Concerns).

 

Hong Kong authorities also mentioned the possibility (of at least short-range windborne transmission) in a highly detailed epidemiological report issued by the University of Hong Kong, on the outbreak of H5N1 on a solitary chicken farm in the New Territories in 2008.

 

Epidemiology Report of the Highly Pathogenic Avian Influenza H5N1 Outbreak in December 2008 in a Chicken Farm in Ha Tsuen, New Territories

 

Excerpt

(ii) The strong winds and gust from the north and north-east from 4 to 6 December 2008 could have deposited potentially contaminated dust and leaves from the trees into the nearby shed no. 17 via its north opening. These contaminated materials could then have gathered at the corner of the shed where the initial high mortality in poultry occurred.

 

 

So . . . while none of this is a slam dunk proving wind-borne transmission of viable avian (or any other flu) viruses, we have at least some credible evidence that suggests it may have happened.

 

How big of a factor this plays in the spread of viruses remains to be seen.

 

But it does provide investigators another avenue of epidemiological query when multiple farms in close proximity are infected with avian influenza.

 

 

Note: `Barnstorming’ is an Americanism that some of my readers may not be familiar with.  It refers to the early days of aviation when pilots would fly to rural areas, land in farmer’s fields, and sell rides, or put on an air show for the locals.

Uganda MOH: Update On Marburg Outbreak

  Credit Wikipedia

 

 

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The Ugandan Minister of Health, Dr. Christine Ondoa, has issued the following update on the Marburg virus outbreak which has been ongoing in that nation since October 19th.

 

The major points are that there are now 8 deaths confirmed, and that cases have now been confirmed in three districts; Kabale , Ibanda, and Mbarara.

 

This from the Ugandan Media Centre.

 

 

PRESS STATEMENT ON THE UPDATE OF MARBURG OUTBREAK

October 29th 2012

Today on behalf of the Ministry of Health, I take this opportunity to welcome you all to this press briefing organized to update you on the outbreak of Marburg in the country. You will recall that we declared an outbreak of this highly infectious disease on October 19th and since then the Ministry of Health and its partners have undertaken a number of interventions to control the spread of the disease.

 
I wish to inform you that cases are now reported in the neighbouring districts of Ibanda and Mbarara. However, I want to assure you that the Ministry of Health and its partners are on the ground in the mentioned districts to contain the spread and manage the identified cases.

 

To date, the death toll of both the probable and confirmed cases stands at eight, with the latest being a case that died at the isolation facility at Rushoroza Health Centre III on October 27th (Saturday). The case that was referred from Ibanda Hospital – Ibanda to Mbarara Regional Referral Hospital died on October 24th.

 

I wish to clarify that since the onset of the outbreak, we have collected a total of 45 samples of which nine were confirmed positive; five in Kabale, two in Kampala and two from Ibanda.

 

Working closely with the US Center for Disease Control and Prevention (CDC), we have set up a field diagnostic laboratory at Kabale Regional Referral Hospital. All samples from the affected neighbouring districts will hence be taken to this laboratory for quick diagnostics. This will shorten the time when we get results to three hours from the original 24 hours due to distance. Further serological testing will be undertaken at the Uganda Virus Research Institute (UVRI).

 

Due to the presence of cases in other districts, we have established temporary isolation facilities to accommodate the suspected and confirmed cases. In Ibanda, a temporary isolation ward has been created at Ibanda Hospital, while plans are underway to set up a proper isolation facility by tomorrow.

 

At Mbarara Regional Referral Hospital, a separate temporary has been designated for the suspect Marburg cases. A triage has also been set up at the causality ward.

 

We have assembled a team of experts to work in the newly established isolation facilities and they are expected in these districts today.  We also plan to undertake infection control procedures in these facilities as safety measures for the workers and the admitted patients.

 

Today, the total number of cases admitted is 12. Eight are currently admitted at Rushoroza Health Center III in Kabale. Two confirmed cases, a couple (husband and wife) still remain admitted at Mulago National Referral Hospital. Another two suspect cases are currently admitted at Mayanja Memorial Hospital in Mbarara.

 

There are seven suspect cases (student nurses) quarantined at Ibanda. These cases attended to the confirmed case that later died at Mbarara Regional Referral Hospital on October 24th. Other health workers who attended to the patient are closely being monitored.

 

We have line-listed a total of 436 contacts for close observation in four districts of  Kabale, Kam-pala, Ibanda, Mbarara, Fort Portal and Rukungiri. Those being monitored got into contact with either the dead or confirmed cases. The team continues to monitor them on a daily basis for possible signs and symptoms of this highly infectious disease until they have completed 21 days without showing any signs and symptoms.

 

We have completed an orientation of the Kabale district taskforce on Marburg case presentation and prevention, barrier nursing and infection control. Plans are underway to conduct the orien-tation at Ibanda and at Mbarara Regional Referral Hospital.
We have trained a total of 42 volunteers from the Uganda Red Cross Society and deployed them to conduct house to house community sensitization and active case tracing.

 

We plan to set up burial committees in Ibanda district to manage burials of people suspected to have died of the disease. The committee will be oriented on burial procedures and infection prevention and control. This is one of the control measures to curb the spread of the highly con-tiguous disease.

The Ministry of Health would also wish to clarify on media reports that one of its officers, Dr. Sheila Ndyanabangi, the head of the Mental Health Unit Division, had contracted Marburg and had been isolated. Dr. Ndyanabangi has not been isolated but has been advised to exercise social distancing. She is one of the contacts who are being monitored. She has not developed any signs or symptoms of the disease and therefore cannot be isolated from the community. She is due to complete the 21 days of observation.

 

I once again urge the public to take the following measures to avert the spread of the disease.

• Report immediately any suspected patient to a nearby health unit
• Avoid direct contact with body fluids of a person suspected to be suffering from Marburg by using protective materials like gloves and masks
• Persons who have died of Marburg must be handled with strong protective wear and buried immediately
• Avoid eating dead animals
• Avoid unnecessary public gathering especially in the affected district
• Burial of suspicious community deaths should be done under close supervision of well trained burial teams
• Report all suspicious deaths to a nearby health facility 

Once again the Ministry of Health calls upon the public to stay calm as all possible measures are being undertaken to control the situation. 

 

For a history of the Marburg virus, you may wish to revisit Marburg Virus Reported In Western Uganda.

Pathogens At the Gate

Thermal Scanner – Credit Wikipedia

 

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While there are no indications that the coronavirus detected recently in the Middle East has spread beyond the first two cases, some places around the world are taking this threat very seriously.

 

For example, local media is reporting that thermal scanners have been deployed at the Ninoy Aquino International Airport in the Philippines in an attempt to screen arrivals from the Middle East for possible infection.

 

Whenever a novel virus appears, people’s thoughts understandably turn to a pandemic scenario, even though experience has shown that most emerging viruses don’t have the `legs’ to spark a global epidemic (see Novel Viruses & Chekhov’s Gun).

 

Nevertheless, history tells us that pandemics come along several times each century, and another pandemic is all but inevitable.

 

And so the world’s attention this week has quite naturally focused on the novel coronavirus that killed one man in Saudi Arabia last July and has a Qatari man currently hospitalized in London.

 

Memories of the SARS outbreak in 2002 and 2003 remain vivid, particularly in Asia, where the virus hit hardest.

 

Fortunately, while there is still much we don’t know about this emerging pathogen, there are no immediate signs that this virus poses a pandemic threat.

 

While we may not know when - or which virus - will spark the next global health crisis, we have pretty good idea how it will arrive in most countries.

 

Scheduled airline traffic around the world, circa June 2009 – Credit Wikipedia

 

The world’s airlines carry 2.6 billion passengers each year, on more than 17 million flights.  And as the map above indicates, millions of them are international flights.

 

With most viral diseases having an incubation period of several days or longer, someone who is newly infected with a virus could change planes and continents several times before showing their first signs of illness.

 

Last July, in MIT: Contagion Dynamics Of International Air Travel we looked at a study appearing in PloS One, that simulated the early spread of a pandemic virus via air travel and ranked U.S. airports based on how much they contributed to the spread of the illness.

 

An excerpt from a report that appeared in MIT News.

 

New model of disease contagion ranks U.S. airports in terms of their spreading influence

Airports in New York, Los Angeles and Honolulu are judged likeliest to play a significant role in the growth of a pandemic.

Kennedy Airport is ranked first by the model, followed by airports in Los Angeles, Honolulu, San Francisco, Newark, Chicago (O'Hare) and Washington (Dulles). Atlanta's Hartsfield-Jackson International Airport, which is first in number of flights, ranks eighth in contagion influence. Boston's Logan International Airport ranks 15th.

 

 

All of which begs the question, can we really screen, identify, and isolate infectious airline passengers before they can spread a pandemic virus?

 

 

Sadly, the evidence to date has not been very encouraging.

 

Last April, in EID Journal: Airport Screening For Pandemic Flu In New Zealand, we examined a study that found the screening methods used at New Zealand’s airport were inadequate to slow the entry of the 2009 pandemic flu into their country, detecting less than 6% of those infected.

 

New Zealand did not employ thermal scanners, although countries that did, didn’t fare much better.

  

Proving that `there’s no place like home’ during a global crisis, in Vietnam Discovers Passengers Beating Thermal Scanners, we saw evidence of passengers taking fever-reducers to beat the airport scanners in a desperate attempt to get home.

 

In December of 2009, in Travel-Associated H1N1 Influenza in Singapore, I blogged on a NEJM Journal Watch article on of a new study that has been published, ahead of print, in the CDC’s  EID Journal  entitled:

 

Epidemiology of travel-associated pandemic (H1N1) 2009 infection in 116 patients, Singapore. Emerg Infect Dis 2010 Jan; [e-pub ahead of print]. Mukherjee P et al

Travel-Associated H1N1 Influenza in Singapore

Airport thermal scanners detected only 12% of travel-associated flu cases; many travelers boarded flights despite symptoms.

 

 

In June of 2010  CIDRAP carried this piece on a study of thermal scanners in New Zealand in 2008 (before the pandemic) presented at 2010’s ICEID.

 

Thermal scanners are poor flu predictors

Thermal scanners for screening travelers do moderately well at detecting fever, but do a poor job at flagging influenza, according to researchers from New Zealand who presented their findings today at the International Conference on Emerging Infectious Diseases (ICEID) in Atlanta.

 

And in early 2009, Helen Branswell penned an article for the Canadian Press, that stated:

 

Studies show little merit in airport temperature screening for disease

Monday, 16 February 2009 - 11:58am.

By Helen Branswell

TORONTO — Using temperature scanners in airports to try to identify and block entry of sick travellers during a disease outbreak is unlikely to achieve the desired goal, a report by French public health officials suggests.

(Continue. . .)

 

 

The evidence is pretty clear.

 

With the technology of today, coupled with likelihood of having many pre-symptomatic and asymptomatic carriers, there isn’t much hope to identify more than a fraction of infected travelers.

 

As far as the risk of catching a pandemic flu virus while a passenger on an airliner, in May of 2010 we saw a study that appeared in the BMJ that looked at that very topic (see BMJ: Flu Transmission Risks On Airplanes)

 

BMJ 2010;340:c2424

Research

Transmission of pandemic A/H1N1 2009 influenza on passenger aircraft: retrospective cohort study

Conclusions

A low but measurable risk of transmission of pandemic A/H1N1 exists during modern commercial air travel. This risk is concentrated close to infected passengers with symptoms. Follow-up and screening of exposed passengers is slow and difficult once they have left the airport.

 

Another study, conducted by researchers at UCLA and published in BMC Medicine in late 2009:

 

Calculating the potential for within-flight transmission of influenza A (H1N1)

Bradley G Wagner, Brian J Coburn and Sally Blower^*

Results

The risk of catching H1N1 will essentially be confined to passengers travelling in the same cabin as the source case. Not surprisingly, we find that the longer the flight the greater the number of infections that can be expected. We calculate that H1N1, even during long flights, poses a low to moderate within-flight transmission risk if the source case travels First Class.

(Continue . . .)

 

 

While there will likely be intense public clamor to try to block the entry of a pandemic virus into this, or any other country, the truth is – it is highly unlikely that it will work.

Areas that receive a very small number of arrivals might be able to institute a quarantine system (see Can Island Nations Effectively Quarantine Against Pandemic Flu? ), but even then the ability to identify and isolate infected travelers won’t be 100%.

 

Still, even if the success rate is likely to be low, there may be some value in trying to limit the number of infected persons arriving into a country, particularly during the opening days and weeks of an outbreak.

 

The more introductions of a virus into a population, the more points it will have from which to spread.

 

Since it takes months to produce and deploy a vaccine, and time to prepare a society to deal with a pandemic, any delaying action that can reduce the speed and spread of the virus has value.

 

The takeaway from all of this is that we ignore global healthcare and infectious disease outbreaks – even in the remotest areas of the world – at our own peril.

 

Vast oceans and extended travel times no longer offer us protection, and there is no technological shield that we can erect that would keep an emerging pandemic virus out.

 

The place to try to stop the next pandemic is not at the gate, but in the places around the world where they are likely to emerge.

 

Which makes the funding and support of international public health initiatives, animal health initiatives, and disease surveillance ever so important, no matter where on this globe you happen to live.

SciAm: Excerpts From Nathan Wolfe’s `Viral Storm’

 

 

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Nathan Wolfe is a field virologist . . . a virus hunter . . . who hopes his work, and those of his colleagues, will reveal the identity of the next deadly virus to jump species from animals to humans.

 

Dr. Wolfe founded and directs the  Global Viral Forecasting Initiative (GVFI), a collaboration of more than 100 scientists worldwide who work to serve as a pandemic early warning system.

 

I’ve called Wolfe the `Indiana Jones of Virology’ because he spends about half of each year tramping around the jungles of Africa looking for next doomsday virus (see Nathan Wolfe And The Doomsday Strain).

 

In 2008 the New York Times ran a major story (see Deep In The Rain Forest, Stalking the Next Pandemic) on Dr. Wolfe’s work, and you can learn more from his inspiring 2009 TED TALK  Video Link.

 

 

 

Today Scientific American has excerpts from Dr. Wolfe’s new book, The Viral Storm: The Dawn of a New Pandemic Age, published on October 11th.  Follow the link to read:

 

How an Interconnected Planet Is Fueling the Brewing Viral Storm

In his new book, award-winning biologist and author Nathan Wolfe​ examines the origins and spread of viruses around the globe

For more on the book, and an audio interview with Dr. Wolfe, visit:

 

The Viral Storm

The Dawn of a New Pandemic Age

Referral: CIDRAP On Virus-sharing, Pandemic Vaccine Access

 

# 5489

 

 

While it seems hard to believe, the impasse over the sharing of H5N1 influenza samples out of Indonesia has been ongoing since late 2006.  

 

Since avian influenza viruses evolve over time, it is essential that the world have access to fresh samples, particularly from a region where the virus is endemic and the CFR (case fatality ratio) of known cases is above 80%.

 

Many times between 2007 and 2007 there were signs that an arrangement might be brokered between the Indonesian Ministry of Health and the World Health Organization, but every time the deal fell through.

 

Among the many mentions of these negotiations in this blog, in 2008 I wrote  Despite Progress Indonesia Still Unwilling to Share Virus Samples and in 2009, Geneva: No Deal On Virus Sharing.

 

Over the past two years, very little has been said publicly regarding this stalemate, but work has been going on quietly in the background. 

 

While the impasse with Indonesia has been the focus of the discussion, other developing nations have a stake in the outcome of these negotiations as well. 

 

Which brings us to a report by Lisa Schnirring of CIDRAP News, that outlines renewed efforts to strike a deal on virus sharing.

 

WHO group renews push for pact on virus-sharing, pandemic vaccine access

Lisa Schnirring Staff Writer

Apr 12, 2011 (CIDRAP News) – Leaders from a World Health Organization (WHO) working group on virus sharing and vaccine issues related to pandemic preparedness today said they hope to reach an agreement by Friday (Apr 15) so that it could go to the World Health Assembly (WHA) for a vote in May.

(Continue . . . )