Influenza Virus Mashup

(Sun, 23 Oct 2011 02:33:04 GMT)

Reminder: Please do not post whole articles, just snippets and links, and do not post articles from the Las Vegas Review-Journal. Thanks!

Indonesia

?  Bird flu spreads in 49 villages of Bali (Link)

Cuba

?  Cuba on alert for deadly flu virus development (translated) (Link)

Nicaragua

?  Nicaragua reported 40 new cases of swine flu, but says virus is controlled (translated) (Link)

General

?  Influenza (61): WHO Update (Link)

Commentary

?  Recombinomics: Fuzzy CDC Summary of SOIV / trH3N2 In Humans Needs Update (Link)

?  H (Link)

News for October 22, 2011 is here.

Thanks to all of the newshounds! Special thanks to the newshound volunteers who translate international stories - thanks for keeping us all informed!

Other useful links:

WHO A(H1N1) Site

WHO H5N1 human case totals, last updated October 10, 2011
Charts and Graphs on H5N1 from WHO
Google Flu Trends
CDC Weekly Influenza Summary
Map of seasonal influenza in the U.S.
CIDPC (Canada) Weekly FluWatch
UK RCGP Weekly Data on Communicable and Respiratory Diseases
Flu Wiki Main Page

(Sat, 22 Oct 2011 12:08:00 +0000)

# 5917

On Thursday of this week I wrote about A 5th trH3N2 SOIV Report, where the latest human infection from a recently identified swine flu virus was reported in the state of Maine. Over the past three months four other similar cases have been detected, 1 in Indiana and 3 in Pennsylvania.

While not spreading like the A(H1N1)pdm09 virus did in the spring of 2009, this new SOIV (swine origin Influenza virus) is nonetheless of some concern, since over time it might better adapt to human physiology and become easier to transmit.

How often viruses like this one make the jump from pigs, birds, or other hosts to humans is  unknown, but it probably happens more often than we know. Many viruses may prove only marginally adapted to humans and die out quickly.

With limited testing and surveillance, such one-off, dead-end infections would likely go unnoticed.

However, since 2005 improved testing and surveillance in the United States has picked up 26 novel swine flu infections (excluding the thousands of novel H1N1 infections that sparked the 2009 pandemic).

Most (but not all) had some exposure to pigs. As the CDC has previously indicated:

Likely transmission of swine-origin influenza virus from close contact with an infected person has been observed in investigations of human infections with swine-origin influenza A virus, but has not resulted in sustained human-to-human transmission.

In these five most recent cases, the virus has been a swine H3N2 virus with the M segment gene borrowed from the 2009 H1N1 virus. Essentially a hybrid – a new reassortant virus - that until this summer had not been seen before.

Reassorted viruses can result when two different flu strains inhabit the same host (human or otherwise) at the same time. Under the right conditions, they can swap one or more gene segments and produce a hybrid virus.

 

Five cases in three states over a few months does not a pandemic make, but this pattern does suggest that this new reassortant virus may be circulating (likely in pigs, but possibly in people) at low levels. 

Which leaves us essentially in a mode of watchful waiting.

This novel virus may sputter and die out, finding too few susceptible hosts to keep going, or it could – over time – better adapt to humans and begin to spread.

The good news here is that so far, this new virus does not appear to be exceptionally virulent.  The bad news is that this year’s vaccine is not expected to offer protection against it.

The CDC, along with many local health departments, continue to monitor the situation, and epidemiological investigations on how it is transmitted are ongoing. 

While the current threat to public health appears low, the Sept. 2nd MMWR report on this virus reminds us:

What are the implications for public health practice?

Non-human influenza virus infections rarely result in human-to-human transmission, but the implications of sustained ongoing transmission between humans is potentially severe; therefore, prompt and thorough identification and investigation of these sporadic human infections with non-human influenza viruses are needed to reduce the risk for sustained transmission.

Yesterday, the CDC’s HAVE YOU HEARD website updated the situation with the latest case information from Maine. Follow the link to read it in its entirety, and I’ll return with a postscript.

CDC Confirms 5th Case of New Swine-Origin H3N2 Reassortant in Maine

October 21, 2011 – – CDC has confirmed the fifth case of human infection with a swine–origin influenza A (H3N2) virus that carries the M gene from the 2009 H1N1 virus. This virus was first detected in a child in Indiana in July. Subsequently three additional cases of human infection with swine–origin influenza A (H3N2) viruses carrying the same genetic change were detected in Pennsylvania. Though rare, human infections with swine–origin influenza viruses can occur, usually after close contact with infected swine. The patient in Maine was reported to have attended an agricultural fair where animals, including pigs, were present. The child was not hospitalized. He received antiviral treatment and is recovering from his illness. Though an investigation is ongoing and surveillance for influenza–like–illness is being enhanced, no human–to–human transmission of this virus has been identified in Maine.

 

The patient had not received a seasonal influenza vaccination. However it should be noted that seasonal influenza vaccine would NOT be expected to protect against this swine–origin influenza virus because it is so different from the human viruses in the seasonal vaccine. Seasonal influenza vaccination is important to decrease the risk of getting infected with human seasonal influenza viruses, which are beginning to circulate in the United States for the 2011–2012 season.

 

While there is not a vaccine to protect humans against these swine–origin influenza viruses, there are two FDA–cleared drugs that can be used to treat illness with these viruses. The antiviral drugs oseltamivir and zanamivir – which are used to treat infection with human seasonal viruses – also have shown activity against swine–origin viruses. 

(Continue . . . )

Anytime a novel influenza virus jumps species and demonstrates the ability to infect humans, it is a matter of both scientific curiosity and concern.

We’ve seen a number of novel flu viruses emerge over the past few years (H9N2, H7N7, H10N7, H5N1, etc.), and with the notable exception of the 2009 H1N1 pandemic virus, all have turned out to transmit poorly in humans.

But of course, influenza viruses are notoriously unstable, constantly changing and evolving.  What is true today may not hold true tomorrow.

While it is always possible that the next pandemic will spring directly from the wild, the odds favor that it will come from a farm – where large numbers of animals intermingle, swap viruses, and come in daily contact with humans.

For more on the reassortment potential of avian, swine, and human flu viruses, you can’t do better than  Helen Branswell’s excellent Scientific American article from last December called Flu Factories, or her SciAm Podcast interview.

For earlier posts on this newly discovered trH3N2 swine flu virus, you may wish to revisit:

A 5th trH3N2 SOIV Report

CDC Update On Recent Novel Swine Flu Cases

MMWR: Swine-Origin Influenza A (H3N2) Virus Infection in Two Children

MMWR: Two Novel trH3N2 Flu Infections

Mike Coston at Avian Flu Diary has the links and the commentary: WHO: Call It A(H1N1)pdm09. That's the official terminology for what we used to call H1N1 or swine flu. It's not exactly like changing Stalingrad to Volgograd, but the new term doesn't exactly light up the imagination or enhance public understanding. I'm still classifying this post under plain old H1N1.

(Fri, 21 Oct 2011 16:15:00 +0000)

Photo Credit – CDC PHIL 

# 5916

Two-and-a-half years after its emergence, the virus responsible for the 2009 influenza pandemic continues to go by many names.

The most common nom de flu - embraced by the media and most of the public - has been `swine flu’. 

But that not only raised the hackles of hog farmers, it isn’t terribly specific. After all, there are many different swine influenzas out there, and there is always the possibility of another novel swine virus emerging.

Calling it simply H1N1 makes no distinction between it, and the many iterations of seasonal H1N1 which came before it.

While I’ve used `novel H1N1’ often in this blog, and sometimes  A/H1N1/09 or even pdmH1N1 – there hasn’t been any clear consensus over what to call the 2009 pandemic virus.

Today, in the World Health Organization’s  Weekly Epidemiological Record we learn that a decision was reached late last month at the WHO to call the virus:

A(H1N1)pdm09

While it doesn’t exactly roll off the tongue like `swine flu’ does, it has the decided advantage of being more precise. The scientific community may well embrace this recommended nomenclature, but we’ll have to see if it ever catches on with the media.

Standardization of terminology of the pandemic A(H1N1) 2009 virus

The pandemic A(H1N1)2009 virus has become a seasonal influenza virus, continuing to circulate with other seasonal viruses since August 2010 when WHO declared the end of the influenza A(H1N1) 2009 pandemic. However, the nomenclature of this virus has never been standardized resulting in the use of diverse names for the same virus.

In order to minimize confusion and to differentiate the virus from the former seasonal A(H1N1) viruses circulating in humans before the influenza A(H1N1) 2009 pandemic, the advisers to the WHO technical consultation on the composition of influenza vaccines for the southern hemisphere 2012 season, after discussion on 26 September 2011, advise WHO to use the nomenclature below:

 
A(H1N1)pdm09

This standardization will help to minimize confusion
among scientific community and the general public. 

Via Antara News: No human infected with bird flu in Lombok : minister. Excerpt:

Health Minister Endang Rahayu Sedyaningsih has confirmed that bird flu has infected poultry in Lombok but there was no report of human bird flu cases in the region so far. 

"The virus has indeed spread among poultry. Lombok is among the bird flu endemic regions for poultry, but no human has been reported infected until now," the health minister said here on Monday. 

The minister said 30 provinces were still bird flu endemic in poultry, and only three provinces were free of the disease, namely West Kalimantan, Gorontalo and North Maluku. 

The health ministry was closely collaborating with the agriculture ministry to curb the bird flu or avian influenza problem and to prevent human fatalities as the death rate was still high, at around 70-80 percent. 

Minister Endang urged poultry farmers to improve hygiene. 

"We must wash our hands after touching poultry. This simple thing is the most effective way to prevent influenza, including bird flu," she said.

Meanwhile, Ida at Bird Flu Information Corner reports that B2B H5N1 has spread to West Lombok.

(Fri, 21 Oct 2011 12:30:00 +0000)

Inoculated MacConkey agar culture plate cultivated colonial growth of Gram-negative, small rod-shaped and facultatively anaerobic Klebsiella pneumoniae bacteria. – CDC PHIL.

# 5915

Over the past week a story emerged from South Africa regarding (initially 9, now 10) patients in a private hospital who were diagnosed with an NDM-1 bacterial infection.

Crof, at Crofsblog covered these reports here, here, and here.

Three of these patients have reportedly died, but local authorities have pointed out that all three had `co-morbidities’ that probably played a major role in their deaths.

NDM-1 gained prominence a little over a year ago with the publication of a Lancet article (see NDM-1: A New Acronym To Memorize) that tied India and Pakistan to the emergence and spread of an enzyme that confers resistance in common gram negative bacteria like E.coli and Klebsiella against most antibiotics.

Today the South African Department of Health has posted a statement regarding these recent cases. While calling NDM-1 a `national concern’, it provides little in the way of specifics on this outbreak, and instead seeks to reassure that everything is under control.  

Emergence of NDM-1 in South Africa a national issue

Joint media statement issued by the National Department of Health and Life Healthcare

20 October 2011

 

The emergence of the Klebsiella pneumoniae producing NDM-1 enzyme in South Africa is a matter of national concern. It should be noted that the institution-based outbreak is contained through the effective measures implemented thus far. The possibility of further spread is limited.

 

NDM-1 was identified at Life The Glynnwood Hospital in Benoni, where 10 patients treated were confirmed to have NDM-1. An outpatient at Charlotte Maxeke Hospital in Johannesburg was earlier also confirmed with this multidrug resistant strain of bacteria. There are presently still three patients in Glynnwood Hospital with the NDM-1 bacterium who are in a stable condition.

 

Representatives of the national, provincial and district departments of health met with Life The Glynnwood management and with representatives of Life Healthcare (of which the hospital forms part) as well as with other key roleplayers on Wednesday (19 October) to assess the situation and determine the way forward.

 

Life The Glynnwood was commended for identifying the NDM-1 strain promptly and implementing effective interventions to respond to the outbreak and prevent its spread. These measures include effective treatment and isolation of affected patients, strengthening infection control measures, screening of around 400 patients and staff as well as commissioning an independent clinical audit.

 

A co-ordinating outbreak response team was formed that will meet regularly to monitoring and redirect response to the outbreak when needed. A monitoring system within public and private sector will also be set up.

 

A formal report is being compiled and will be submitted to the Minister of Health. The parties will furthermore work together in formalising a NDM-1 treatment protocol for clinicians. They will also document lessons learned from the experience at Life The Glynnwood to share with other roleplayers. These actions will be of immense value to other hospitals which may be faced with a similar situation in future.

 

Prof Adriano Duse, an appointee of the Department of Health and the Head of Clinical Microbiology and Infection Control at Wits University as well as the National Health Laboratory Services (NHLS) will continue to be the spokesperson on the NDM-1 outbreak.

(Fri, 21 Oct 2011 11:27:00 +0000)

# 5914

Yesterday, the British Medical Journal published the results of a follow up to large Danish cohort study that found no link between cell phone usage and an increase in brain tumors.

Although evidence for it has been scant, for a number of years some scientists have expressed concerns that prolonged exposure to cell phone RF (radio frequency) electromagnetic fields might cause certain types of head and neck cancers.

In 2010, the International Agency for Research on Cancer (IARC) released their long-delayed INTERPHONE report, which was unable to establish a link between cell phone use and brain tumors  (see The IARC Cell Phone Report).

Despite that initial finding, a year later (May 2011) the IARC released a statement (IARC Press Release N° 208) that listed mobile phone use in same `possibly’ carcinogenic hazard category as exposure to gasoline, engine exhaust and lead.

 

For details on this statement, you may wish to revisit IARC: Cell Phones `Possibly Carcinogenic’.

A couple of months later we saw a study that appeared in the Journal of the National Cancer Institute (see Reassuring Study On Cell Phones & Brain Cancer Risks) that found no link between cell phone use and brain tumors in children and adolescents.

While it is unlikely to be the final word on the subject, the study published yesterday in the BMJ follows up on the largest cohort study on mobile phone users to date.

And once again, the news is reassuring; long-term subscribers to cellular phone services showed no increase in brain or central nervous system tumors over non-subscribers. 

Use of mobile phones and risk of brain tumours: update of Danish cohort study

OPEN ACCESS

BMJ 2011; 343:d6387

Patrizia Frei, Aslak H Poulsen, Christoffer Johansen,  Jørgen H Olsen, Marianne Steding-Jessen,  Joachim Schüz

ABSTRACT

Participants All Danes aged ≥30 and born in Denmark after 1925, subdivided into subscribers and non-subscribers of mobile phones before 1995.

 

Main outcome measures Risk of tumours of the central nervous system, identified from the complete Danish Cancer Register. Sex specific incidence rate ratios estimated with log linear Poisson regression models adjusted for age, calendar period, education, and disposable income.

 

Results 358 403 subscription holders accrued 3.8 million person years. In the follow-up period 1990-2007, there were 10 729 cases of tumours of the central nervous system. The risk of such tumours was close to unity for both men and women. When restricted to individuals with the longest mobile phone use—that is, ≥13 years of subscription—the incidence rate ratio was 1.03 (95% confidence interval 0.83 to 1.27) in men and 0.91 (0.41 to 2.04) in women. Among those with subscriptions of ≥10 years, ratios were 1.04 (0.85 to 1.26) in men and 1.04 (0.56 to 1.95) in women for glioma and 0.90 (0.57 to 1.42) in men and 0.93 (0.46 to 1.87) in women for meningioma. There was no indication of dose-response relation either by years since first subscription for a mobile phone or by anatomical location of the tumour—that is, in regions of the brain closest to where the handset is usually held to the head.

 

Conclusions In this update of a large nationwide cohort study of mobile phone use, there were no increased risks of tumours of the central nervous system, providing little evidence for a causal association.

While this study was subject (as are all studies) to some limitations, In an accompanying BMJ editorial (Mobile telephones and brain tumours) professors Anders Ahlbom and Maria Feychting called the evidence in this report `reassuring’.

They cautioned, however, that `continued monitoring of health registers and prospective cohorts is still warranted.’

(Thu, 20 Oct 2011 17:13:00 +0000)

Reassortant H3N2 virus detected in Pennsylvania & Indiana – Source CDC

# 5913

My thanks to  Giuseppe Michieli and Missouri Watcher  on FluTrackers for the links to the State of Maine HAN Advisory (2011PHADV018), and weekly influenza surveillance report describing  the recent detection of a novel Swine Origin Influenza Virus (SOIV) in that state.

This is the fifth such virus detection from across the country over the past 3 months, with 3 previous cases reported in Pennsylvania and 1 in Indiana (see CDC Update On Recent Novel Swine Flu Cases).

In all 5 of these cases, the virus has been a swine H3N2 virus with the M segment gene borrowed from the 2009 H1N1 virus.

From the Weekly Flu Surveillance report:

*Novel Influenza A Virus

•  HETL detected a case of influenza A virus that was inconclusive during subtyping.  On October 17
Federal CDC confirmed this isolate to be the 5th recognized case of human infection with S-OtrH3N2
with the M segment gene from the pH1N1virus (also identified in one case in Indiana and three cases in
Pennsylvania).  Investigation is ongoing. 

More information can be found in a Health Alert, released 10/19/2011 accessible through:  http://www.maine.gov/tools/whatsnew/attach.php?id=313425&an=1. 

The MAINE HAN Message provides the following details:

(EXCERPT)

This child became ill in early October 2011 with symptoms similar to seasonal influenza including fever,
cough, headache, sore throat and myalgia.  Prior to illness, the child had exposure to swine including time
spent in a closed setting at an agricultural fair.  Maine CDC and the Department of Agriculture are currently investigating exposures. Presently this is an isolated event and Maine CDC has not confirmed any person to person transmission.  

Recommendations:  Maine CDC recommends the following for healthcare providers:

 
•  Maintain a heightened awareness for influenza-like illness (ILI) defined as fever greater than 100° with cough or sore throat, in the absence of another known cause.

• Consider influenza testing by PCR for: 
  patients with ILI with recent exposure to pigs.
• patients with ILI who are hospitalized, 
• patients with ILI who have died, 
• patients where a diagnosis of influenza would affect clinical care, infection control, or
  management of contacts. 

•  Consider use of antivirals to quickly limit potential human transmission
•  Vaccinate patients and healthcare workers as a primary strategy to prevent influenza

As I wrote last month in What Lies Beneath, it appears that very limited human-to-human transmission of this virus may have occurred, but the virus does not yet appear capable of sustained and efficient human transmission.

The concern, of course, is that could eventually change. Hence the ongoing epidemiological investigation.

Below you’ll find excerpts from the CDC’s  SOIV page regarding these cases (reformatted for readability).

Reported Human Infections with Swine-Origin Influenza Viruses (SOIV) in the United States since 2005

As of September 9, 2011, 25 cases of human infection with swine origin influenza viruses have been reported in the United States. These are viruses that normally infect pigs. Like human influenza viruses, there are different subtypes and strains of swine-origin influenza viruses.

 

The main swine influenza viruses circulating in U.S. pigs in recent years are swine triple reassortant (tr) H1N1 influenza virus, trH3N2 virus and trH1N2 virus. Of the 25 human cases reported since 2005, 12 have been trH1N1 viruses, 12 have been trH3N2 viruses and one has been a trH1N2 virus.

 

All 25 persons infected with swine viruses recovered from their illness. Eighteen cases occurred in children (persons 18 or younger) and 7 cases occurred in adults. In 21 cases, direct or indirect exposure to swine prior to onset of illness has been identified.

 

Likely transmission of swine-origin influenza virus from close contact with an infected person has been observed in investigations of human infections with swine-origin influenza A virus, but has not resulted in sustained human-to-human transmission.

(Thu, 20 Oct 2011 15:29:00 +0000)

Photo Credit – CDC PHIL

# 5912

There is a belief, at least among some researchers, that there exists some – as yet unidentified -  genetic propensity for contracting the H5N1 virus.

This idea is based primarily on the observation that - despite ample opportunities for exposure – relatively few humans have been infected, and that the few clusters of human-to-human transmissions we’ve seen appear to happen primarily among blood relatives.

While this idea has been around for a number of years, it hasn’t exactly been universally embraced. 

In 2007 the CDC’s Emerging Infectious Diseases Journal published a study suggested that mere chance could account for family clustering.

Little Evidence for Genetic Susceptibility to Influenza A (H5N1) from Family Clustering Data

Virginia E. Pitzer , Sonja J. Olsen†, Carl T. Bergstrom‡, Scott F. Dowell†, and Marc Lipsitch

Abstract

The apparent clustering of human cases of influenza A (H5N1) among blood relatives has been considered as evidence of genetic variation in susceptibility. We show that, by chance alone, a high proportion of clusters are expected to be limited to blood relatives when infection is a rare event.

While this article proposed a plausible alternative theory for family clustering, it didn’t disprove that host genetics played a role in transmission.

In 2008, in the Journal of Infectious Diseases, we saw a study that suggested there might be a heritable susceptibility to death from the influenza virus.

Evidence for a heritable predisposition to death due to influenza.

 

Albright FS, Orlando P, Pavia AT, Jackson GG, Cannon Albright LA.

Abstract (extract)

Evidence for a heritable contribution to death due to influenza was examined using a resource consisting of a genealogy of the Utah population linked to death certificates in Utah over a period of 100 years. The relative risks of death due to influenza were estimated for the relatives of 4,855 individuals who died of influenza.

 

Both close and distant relatives of individuals who died of influenza were shown to have a significantly increased risk of dying of influenza, consistent with a combination of shared exposure and genetic effects. These data provide strong support for a heritable contribution to predisposition to death due to influenza.

While interesting, this study doesn’t provide us with a smoking gene. However, the following year a PLoS ONE  research article (doi:10.1371/journal.pone.0004857) came a bit closer.  

Entitled Host Genetic Background Strongly Influences the Response to Influenza A Virus Infections by Srivastava B, Błażejewska P, Heßmann M, Bruder D, Geffers R, et al., it reports on the results of experiments utilizing seven inbred strains of lab mice that were exposed to influenza A viruses.

From the abstract:

The genetic make-up of the host has a major influence on its response to combat pathogens. For influenza A virus, several single gene mutations have been described which contribute to survival, the immune response and clearance of the pathogen by the host organism.

While mouse models are often useful, what happens in mice doesn’t always correspond to what happens with human physiology.

Another (as far as I can tell, unpublished) study, conducted in Thailand, Singapore, and Indonesia by the South East Asia Infectious Disease Clinical Research Network, looks at whether:

“. . .  host genetic factors may shed light on key pathogenic interactions between H5N1 and human cells . . .  ”

The overview of the study is available on clinicaltrials.gov at:

Host Genetic Susceptibility to Avian Influenza A/H5N1

Hopefully this will provide us with more clues as to why some people appear susceptible to the H5N1 virus, while others less so.

All of which serves as prelude for a study that appeared yesterday in the journal Clinical Infectious Diseases, which provides more evidence supporting the notion that host genetics influences acquisition and transmission of the H5N1 virus.

This study looked at 113 sporadic and 26 cluster outbreaks of the H5N1 virus in Indonesia through July 30th, 2009 and found  human transmission of bird flu to be heavily influenced by host genetic susceptibility.

Below you’ll find a link to the abstract, and an excerpt (slightly reformatted for readability) of the results. Go read it, and when you return I’ll have a little more.

 

Risk Factors for Cluster Outbreaks of Avian Influenza A H5N1 Infection, Indonesia

Tjandra Y. Aditama, Gina Samaan, Rita Kusriastuti1, Wilfried H. Purba, Misriyah, Hari Santoso, Arie Bratasena, Anas Maruf, Elvieda Sariwati, Vivi Setiawaty, Alex R. Cook, Mark S. Clements, Kamalini Lokuge, Paul M. Kelly, and I. Nyoman Kandun

(EXCERPT)

Risk factors for cluster outbreaks were the number of first-degree blood-relatives to the index case (adjusted odds ratio [aOR], 1.50; 95% confidence interval [CI]: 1.20–1.86) and index cases having direct exposure to sources of AI H5N1 virus (aOR, 3.20; 95% CI: 1.15–8.90).

 

Risk factors for secondary case infection were being aged between 5 and 17 years (aOR, 8.32; 95% CI: 1.72–40.25), or 18 and 30 years (aOR, 6.04; 95% CI: 1.21–30.08), having direct exposure to sources of AI H5N1 virus (aOR, 3.48; 95% CI: 1.28–9.46), and being a first-degree relative to an index case (aOR, 11.0; 95% CI: 1.43–84.66).

 

Siblings to index cases were 5 times more likely to become secondary cases (OR, 4.72; 95% CI: 1.67–13.35).

In Indonesia, young age (under 30) and being a blood relative to the index case in a cluster, were both found to significantly increase the odds of catching the virus.

While it is more than a little tempting to hope that some unidentified human genetic quirk limits the ability of the H5N1 virus to ever become a pandemic, the whole point of viral evolution is to figure out a host’s defenses.

 

What may have served as a limiting factor in the past, doesn’t provide a guarantee for the future.

Determining what (if any) genetic factors influence transmission could provide vital clues of just how big of a pandemic threat the H5N1 virus really presents, and might even lead to more effective treatments and prevention.

The difficulty, of course, is that studies like this take time to mount and to interpret, and the virus never sleeps.

Via BBC News: Study finds link between swine flu and stillbirth. Excerpt:

Babies born to mothers who contracted the swine flu virus faced a much greater risk of being stillborn, according to a new study. 

Baby deaths among women infected with the 2009 strain of the virus were five times higher than normal. 

There was also a greater risk of premature births when compared to mothers who had not caught the virus. 

Health workers say the findings reinforce the message that all pregnant women should get immunised against flu. 

The study was carried out by the National Perinatal Epidemiology Unit at the Oxford University and it examined the cases of every pregnant woman in the UK who was admitted to hospital while suffering from flu. 

In 256 mothers infected with the H1N1 flu virus between September 2009 and January 2010, seven of the babies were stillborn and three died shortly after birth. 

That is the equivalent of 39 babies in 1,000 dying, before or shortly after birth, compared to 7 in 1,000 in mothers not infected with the virus.