Death of a young adult Qatari MERS patient who presented with flu-like illness...

So that last post is out of date already.

The Qatari Supreme Council of Health, as it does, has issued an announcement through the media (it has yet to update it's technically troubled website) announcing the death of the previously described 29-year old male with asthma who had been confirmed by an international (presumably UK-based) reference laboratory.

Asthma occurs in about 5% of the world's population, but in higher proportions in particular countries and regions.

This moves the deaths up to 54 with data, possibly 56 in total (see earlier post today for what that means) with a PFC of 48.3% for 56 deaths.

The presentation of this case on August 17th, was of "flu-like illness" which can be anything from fever + cough to much more. What this case highlights, and it is only a single case, is that cases can present with standard upper respiratory tract infection (flu most often starts off that way) which will make it devilishly hard to discriminate from that caused by many other non-MERS-CoV respiratory viruses. In a study of pilgrims leaving the 2012 hajj, 41% had flu-like symptoms (cough, sore throat and fever). I mentioned this in an earlier post (see #3 in the Prof Memish lit review) and the paper in Feb this year from Clinical Microbiology and Infection can be found behind a paywall here. A subsequent article published in Clinical Infectious Diseases this July, also paywalled and by the same group showed that a number of respiratory viruses were lab-confirmed as acquired while in the Kingdom of Saudi Arabia (showed symptoms of  illness), fewer were brought into the country and fewer were taken out. Not much can be concluded from that as I would expect this in any group tested in this way under these circumstances (travelling to a gathering of lots of people from around the world and from different climates  experiencing different respiratory virus seasons). It is not surprising that when you throw people together, they transmit respiratory infections and the the number of cases spikes.

This will be a big challenge if observation alone, rather than prospective laboratory testing, is used as a method to diagnose MERS among hajjis (thanks to AtRG for this phrase), in the coming weeks.

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Tunisian father was MERS-CoV positive...

A retrospective diagnosis by the US CDC has confirmed that the father of a MERS-CoV-positive brother and sister in Tunisia (FluTracker's Cases: #42-35-year old female; 34-year old male) was indeed positive for the CoV as well. 

There was also a mention in BMJ of this cluster.

Earlier testing had not been able to confirm that the father, despite him being a probable case, had transmitted the virus to his children.

This raises the MERS-CoV case tally to 116 based on what has been reported by official Ministries and Councils. I assume we add the 2 deaths for which we have no information - they have been floating around for some time now - to this to make a total of 55 deaths (PFC of 47.4%). Not having the specific details makes these 2 very hard to confirm they are not just clerical or media release errors from the past.

The WHO count (based on what they have been officially told I assume) is at 110 cases with 53 deaths. This number of deaths agrees with what I actually have data for; PFC for the 53/110=48.1%).

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More MERS molecular masterfulness: Egyptian camels contain lots of anti-MERS-CoV antibodies [AMENDED]

Perera and colleagues from China, Japan, Egypt and the United States report in Eurosurveillance that they
have found a high prevalence of Egyptian camels with antibodies to a piece of the Middle East respiratory syndrome coronavirus (MERS-CoV) spike protein.

The group looked at 1,343 human sera (815 from Cairo as part of influenza study; 528 archived from Hong Kong) and 625 animal sera (from goats, sheep, water buffalo, cows, camels, pigs and birds) from Egypt and China (no MERS reported there, so this acts as control population; unfortunately no camels tested from there either). A positive control serum was provided by Prof Drosten from an earlier MERS case.

The novel assay does not need to be used in a biosafety level 3 containment environment (BSL2 is fine) because it does not use whole/live MERS-CoV to capture the human/animal antibodies, rather it uses a piece of the virus; the Spike protein, which is known to attract the lion's share of antibody attention. The Spike protein was merged with HIV (non-infectious) proteins to create a pseudoparticle of proteins that could enter cells, and also bind to MERS-CoV antibody which would prevent entry by the virus-like particle. If there was no antibody, the pseudoparticles could enter cells and this entry could be measured using a marker enzyme reaction. This novel assay (pseudoparticle neutralization test; ppNT) was run in parallel with a more standard micro-neutralization test (MNT; the two tests agreed well but the standard NT needed to be carried out in a BSL3 laboratory), The more traditional MNT pre-incubated infectious MERS-CoV with serum and then measured whether the live MERS-CoV could infect and damage cells. If there was antibody in the serum, it blocked infection (as it can in us). Pseudoparticle/virus will be more or less blocked from cell entry if more or less antibody is present in the serum. So one can determine how much antibody was in the serum sample too. These type of tests measure the ability of antibody in a patient/animal to block virus entry; it's neutralizing ability. 

A high proportion (103/110; 93.6%) of dromedary camels from Egypt had antibodies that could block cell culture infection by a lab strain of the MERS-CoV (MERS-CoV/EMC form Erasmus University Medical Center). 

No humans had antibodies. No animal sera from China (Hong Kong) were positive - this included pigs (n=260) and wild birds (n=204). 

Numbers were sometimes very low but no goats (n=13), sheep (n=5), water buffalo (n=8) or cows (n=25) were antibody-positive in Egypt. Only the camels.

The authors specify that this does not exclude cross-reactivity with a closely related, but non-MERS, CoV that has at some time infected the camels. If only there was some sort of plan to do this sort of virus hunting in mammals.

Click to enlarge.

So how does this fit in with the human acquisition model proposed 1-week ago? Pretty well. It supports previous findings from Omani camels too. Camels could be part of the chain of infection. It says nothing about how they may then go on to be a source of human infections that start of as a respiratory illness, presumably requiring, in most cases, inhalation or self-inoculation (I'm looking at you, nose-pickers) to begin with. For hat we'd need to know anything about survival do MERS-CoV in excreta and on surfaces. I'd also like to see some more animal test results. 

Nonetheless, it looks as though we have some very useful antibody detection assays shaping up to do just that.

Here's hoping for a KSA study next.

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MERS-CoV and deaths rise....[UPDATE]

The latest Kingdom of Saudi Arabia (KSA) Ministry of Health (MOH) announcement (Arabic only for now) provides scarce detail on 4 new cases including 2 deaths.

1. 30-year old, Riyadh, health care worker (HCW), in an intensive care unit (ICU)
2. 47-year old, Hafr Al Batin, multiple comorbidities, contact ("Mkhalt") of another case, in an intensive care unit (ICU)
3. 41-year old, Riyadh, HCW, fatal infection
4. 79-year old, [construction worker=Harf al Batin-place name], multiple comorbidities, contact of another case, fatal infection

The last case on that list is particularly interesting* for their role as a contact, who died. Generally, the second "passage" of infection to a new human host has not been as severe as the first. This once again draws attention to the role of underlying disease (comorbidities) in making any infection, even one that has gone through a human host, fatal.

There are no data on the sex of cases, when the fatal cases were admitted to hospital, or any indication at all of a date of disease onset.

After Wednesday's post of the plateau that ceased after umrah, I would be very interested to know how many recent cases has recent travel with a common destination.

The MERS-CoV lab-confirmed case tally now sits at 115 with 54 deaths (proportion fatal 47%)


*It's very sad that there are real people in these numbers who have died from MERS. You may have noticed that I try and stick with the cold number-crunching aspect of these outbreaks. It's not because I'm a heartless b&^$# but because that is not what this blog is about. That and my editorialisation and expositionary writing consume what little time I have spare. But I don't feel that I have enough information to make any other comments about these or any other lives lost to infectious disease. I personally feel that any unexpected and acute loss of life (if I had to scale loss of life) is the worst kind of loss; it's a waste of potential, a source of great sorrow for all involved and it's something we should all strive to prevent, if we can. I know that's not much to convey, but it's all I can offer from my kinda comfy chair in Brisbane. 

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H7N9 in wild birds...a review of the literature

Not by me though., This was a review just published in EID

Bird flyways that may contribute to H7N9 spread.

by Olson and colleagues.

They found 48 published studies that listed findings of influenza A virus haemagglutin type H7, or neuramonase N9 viruses as well as H9N2. The prevalence was calculated as the number of positive samples divided by the by number tested.

H7N9 has been rarely reported from Delaware (USA), Alberta (Canada), Guatemala, Spain, Egypt, Mongolia and Taiwan but has not been reported from Russia, Japan, South Korea or China from birds sampled between 1976-2012.

The outcome? If you were planning wild bird surveillance to track H7N9 spread in these non-poultry animals, you'll need to sample >30,000 wild birds to find 1 positive for H7N9 (its Asian prevalence was 0.00931%). 

That's a rare bird.

This is just a rough gauge of course because it is entirely dependent on when, where and how thoroughly bird populations were sampled, how they were sampled, what they were tested with and how the sequencing methods performed. It also focuses on HA and NA genes, at the expense of other internal influenza gene segments which also have an important role in the assemblage of new viruses. 

But its a gauge nonetheless.

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New coronavirus genomes....not MERS yet

Unfortunately they aren't MERS-CoV genomes.

Nonetheless, a whole lot of new feline, porcine, murine, SARS, 229E and HKU1, genomes have been directly released from the J. Craig Venter Institute.

These now appear on GenBank with non-sequential accession numbers around the KF272920-KF530271. The sequences were produced using next generation sequencing technology.

Looks like the virome is in the sights of the big data guys.

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Measles, vaccination and infectious disease communication in Queensland...

With measles cases prominent in the news of late, there have been a few interesting reports and interviews from Queensland's local Acting Senior Director for Communicable Diseases, Dr Stephen Lambert.

Measles virus, has a basic reproduction number (R₀) - the average number of new cases from each contact - of 12-18. This defines measles as one of the most contagious infectious diseases of humans. and reflect the ease wish which i is spread through a respiratory route.

Measles also has some serious clinical consequences. Dr Lambert noted that up to a third of infected young adults end up hospitalized. Serious complications can occur including blindness, encephalitis, diarrhoea, ear infection and pneumonia. Most people recover within 2-3 weeks though.

Measles virus is shed from an infected person from 4-days before to 4-days after the characteristic rash appears. Spread occurs from sneezes and coughs that produce small droplets that get inhaled or land on a surface and then are transported by fingers to the nose or mouth. The virus can last out in the open for at least 2-hours.

Measles is a preventable disease. Dr Lambert noted the importance of being up-to-date with your measles vaccination. He has recently had published the idea that airlines could play a greater role in rapidly contacting passengers who may have been in contact with a subsequently identified measles case. They could do this through contact details they already hold, and through social media. This would certainly speed contact tracing and the notification of risk.

Dr Lambert is also busy with E.coli and norovirus outbreaks around south-east Queensland. Still, he has made time to ensure infection prevention and control communication is very well targeted to different audiences - including the public - where it can have a real significant impact. Public health communication, and education, of this quality should be applauded. 

He penned a very nice article "Community Immunity", on vaccination for a magazine called Brisbane's Child. In it he notes the importance of vaccinating children to prevent diseases for which there is now little community memory. Diphtheria, tetanus, measles, haemophilus influenza type b, meningococcal C and poliomyelitis are diseases that once caused significant illness, disfigurement and death. 

It's testament to the success of vaccines that we see so little of these diseases and their severe impact today. The more recently rolled out rotavirus vaccine has decreased hospitalizations of children due to that viral infection by 90% in Queensland alone. Gastroenteritis hospitalizations are down by 60% overall (highlighting the impact of rotavirus).

There is a fantastic quote in this article that touches on the wider impact on not vaccinating your children. Basically, if your child had a peanut allergy you wouldn't expose them to peanuts, or be very happy if someone else did. 

Why then make the choice to allow your children to become seriously ill by acquiring a preventable disease if there is a safe and simple way to avoid that? Also, there are some people who cannot be vaccinated and there are some people in whom the vaccine does not "take". 

Herd immunity protects them because the virus cannot spread as effectively when it's got too few unprotected people to infect and pass among. If the herd does not have a good uptake of vaccination though then it cannot protect them. It's also worth noting that vaccines do not offer absolute immunity to infection. The vaccine does create a shield that prevents you from breathing the virus in and having it land on your cells but they do stop the severe disease associated with infection.

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MERS-CoV cases..updated chart highlighting umrah 2013 peak period

Click to enlarge. Data from the date of announcement (Ministry of Heath,
KUNA, WHO or another media source) rather than date of disease onset.

This chart highlights a slight plateau in cases for several weeks starting in early August, and the subsequent rise in cases per week as the region exited the umrah pilgrimage period. 

It does not prove anything of course, but it's of interest that cases picked up again in the week beginning 18th of August (reports started again on the 2oth). There were no cases reported for nearly 3-weeks prior to  that, the last ones being from the 1st of August.

Thanks to David Spalten (@dspalten) for this idea.

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MERS-CoV by the numbers: recent global case numbers by week

Click to enlarge.
Confirmed MERS-CoV cases (green) and 
deaths (red) each week. Case numbers are
listed on the y-axis, days of each week along
the x-axis.

While the week has not ended, it is interesting to sum up where we are in terms of MERS case announcements. During the week beginning August 11th, there were no new MERS-CoV case reports (I'm using reporting data not disease onset because the latter is appalling sparse).

As you can see on the right, in the following 2.5-weeks, things have heated up a lot. 17 cases so far. 

Why is this so? Completely unknown. Could it be clusters due to a few single but distinct spillovers from the natural host or perhaps transmission events from a common/shared source (recent umrah)? We can only guess.

If the local public health officials can identify this sort of info, it could provide a way to put a lid on current and future rounds of MERS cases and outbreaks.

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New MERS-CoV case, a death, in Qatar

The Kuwait News Agency (KUNA) reports that a 56-year old female has died of MERS in Qatar, according to the Qatar's Supreme Council of Health (SCH).

This is the 2nd death from a Qatari-based infection and the 1st female case. She had several comorbidities. In this instance, comorbidities may serve as reminder that the apparent sex bias in MERS cases (more often males) may not be so much about the sex of the cases, but more about the possible bias towards (older) males with more comorbidities. While principally a respiratory disease, the respiratory virus causing MERS deals very harshly with those that already have a disease of some other sort. 

This brings the tally of MERS case to 111 with 51 deaths (PFC of 45.9%. NB. A recent ProMED listed the deaths at 1 more than they were generally accepted to be at that time. There has not been a WHO update since that so I'm sticking with 51.

Local health authorities have probably seen this already, but the impact of MERS may highlight a need to address the risk factors that drive the prevalence of underlying disease in males in this region.

My first source: FluTrackers

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A scientist who knows how to communicate - and isn't bad with the vaccines either

Kim Stephens has written a nice piece in my local 'paper', brisbanetimes.com.au, on Prof Ian Frazer's latest vaccine achievement. 

You may know Prof Frazer from such things as...the anticancer human papillomavirus (HPV) vaccine, a safe, highly effective but underutilized (in some parts at least) vaccine recommended for kids aged 11 or 12.

Anyone who can make immunological concepts sound as simple as Prof Frazer does in this latest interview should get an award....wait..he already has a couple.

Prof Frazer's latest, globally important achievement, is the human trialing of a herpes simplex virus 2 (HSV-2) vaccine. This is to defend against the virus that most notably gives you genital blisters. A virus down under, you might say. Or you might not.

But the vaccine is not just defensive, apart from preventing disease  it also therapeutic - it can treat the infection you already have. 

Skin cancer is next in case you're keeping tabs.

Thanks to Katherine Arden for alerting me to this story.

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Got a spare $6.3-billion? Experts could use it to discover the missing 320,000+ mammalian viruses we don't yet know about

...or just $1.4-billion for 85% of those. And that's not including the non-mammalian ones. This is according to a new paper in mBio today by Andrew and colleagues from a collaborative team including Prof Ian Lipkin, from Columbia University's Mailman School of Public Health. 

The study advocates for a much more structured, systematic approach to discovery and notes that existing studies, such as the U.S. Agency for International Development's (USAID) Emerging Pandemic Threats (EPT) program including the PREDICT project (more detail in Lancet article here), have made headway into the list already. Each adding valuable assets to our virology intelligence archive.

Finding these viruses, and the animals they reside in, is key to limiting zoonoses. Sure, discovery does not equal simultaneous cure, but ignorance does equal surprise outbreak and death. Most emerging human infectious are caused by animal viruses infecting us. This is well defined by the One Health concept which promotes investigation of all aspects of the network of links between humans and their hairier, more leggy or winged co-habitants.

If we ever want to get ahead of the curve, investing in this sort of research is essential to allow us to know our enemy. It let's us be ready to meet them at the door instead of scrambling to action when they kick our door in! And it is a scramble; just look through the literature and media surrounding any virus that has spilt over from animals to humans in recent decades....a degree of controlled panic over the many things we don't yet know in the early stages of an unexpected emergence. For example: 

• We'd have no laboratory testing methods (culture, PCR or serology) nor the procedures to confirm weird results.
• Which country would "own" the virus, what would we call it (mock you may, but a lot of electrons and ink have been wasted on that story for the MERS-CoV for instance) and how long would it take before commercial detection kits were available (for MERS-CoV - its been nearly 15-months since the first cases in Jordan and still nothing well validated and widely available for use by non-reference laboratories)?
• When would we have enough of the virus to make positive controls for those tests or to kick off research into how the virus does what it does?
• We don't yet know what it does! What is the clinical spectrum of disease, how big is the iceberg let alone it's tip; what are the signs and symptoms; what does it do in different patient groups - those with and without comorbidities, different ages and sex?
• What is the proportion of fatal cases?
• Where did the invader came from?
• How best to handle the pathogen in hospital settings
• How fast and to how many does each case transmit (it will be a while until we can calculate the R₀)?
• What drugs do we already have that can moderate disease?
• How long will it take for an antiviral or vaccine, if they can be prepared, to be available and how long thereafter will antiviral resistance become an issue?
• How many that the virus infects will die?
• Does the virus interact with other viruses, bacteria, fungi or parasites?
• Does it have a peak season and is that affected by the environment?

Pretty much ALL of these things can be addressed if we invest in finding the culprits, their host and begin to unravel how they tick sooner rather than (too) later. Sure, they may never spillover, but when just 1 does, the impact is felt around the world, be it from loss of life, financial instability, healthcare burden, travel and tourism decline, animal culling or just a global feeling of insecurity. Any 1 virus outbreak can wield a lot of power in today's highly interconnected world. 

Count VDU in the cheer squad for this sort of proactive research. Money well invested.

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How MERS may be SARS, but we don't really know

On July 26th, Prof Christian Drosten wrote in Lancet Infectious Diseases about some similarities and differences between the diseases Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS), each linked to a zoonotic coronavirus (CoV) infection.

Drosten is senior author of the 2 publications papers describing gold-standard MERS-CoV laboratory diagnostic methods, all PCR-based, which afford excellent diagnostic and genotyping capabilities upon the user. Unfortunately we have not yet seen much use of the genotyping assays. He has also co-authored papers on the MERS-CoV receptor, viral replication, its naming, discovery of antibodies in camels and MERS case reports. He has an even bigger list of diverse publications on the SARS-CoV.

Drosten is well positioned to say that at first glance it is not the same beast but that we have many things to learn before we can be sure of that. 

Reviewing data from Assiri and colleagues from the same issue of Lancet, he noted that MERS and SARS have some similarities. Cases often presented with fever as a classifying symptom at presentation. Upper respiratory tract symptoms were not common (4-40% of cases had something that could identify an upper airway disease) and so most cases could be clinically differentiated from the common cold.

A major difference from SARS has been the high level of comorbidities associated with MERS cases. However, this needs to be interpreted with caution since for example, a third of people in a pre-MERS study of Saudi Arabian outpatient visits had diabetes, including more than half over the age of 50-years. In that context, the proportion of MERS-CoV positives among his group in the Kingdom of Saudi Arabia (KSA) population may not be so over-represented. It may simply flag the opportunistic nature of the virus. 

MERS also differentiates itself from SARS in its rapid progression to a fatal outcome; again this may be related to the population it is affecting the most; older males with comorbidities. Mechanistically, MERS-CoV differs in its cellular receptor (DPP4 vs ACE2 for SARS-CoV) and its greater replicative efficiency and ability to infect a wider range of cell types in the lower airways compared to SARS-CoV. And then there's the spelling, nucleotide and amino acid sequence differences too!

Drosten also poses some questions: 

1. Can we rely on samples from the upper respiratory tract in which viral loads can be low enough to muddy the waters of result interpretation?
2. We need serological assays and we need to define them using characterized cases. Then we need to roll them out at the population level to better define those icebergs that seem to be everywhere these days

Without further data, we're still left to ponder what would SARS have been like if the CoV got into the KSA? In fact, what do other respiratory viruses do to those with comorbidities in the KSA?

There are similarities and differences between MERS and SARS and between their viral causes. More work is needed. 

The best way to answer the question posed in Drosten's article would have been a direct comparison of the impact of the two viruses in the same population. Thankfully for the hosts, there has been no significant overlap between the 2 outbreaks so far.

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New MERS-CoV positives - is there a brevity competition going on...a shortage of electrons perhaps?

2 MERS-CoV POS, 26 and 19 years, released from hospital.

That is the only relevant text from 68 Google translated press release words on these 2 new cases posted on the Arabic language Ministry of Health website, Saudi Arabia. 56 words on the English-language site. I used half as many just explaining where it came from.

2 other cases were announced as positive and already discharged (the children of the 38M from Harf Al Batin, from where 1 of the cases above also tested positive) as well.

So much for being hopeful of a new era of data sharing on Friday. Must have thought better of it after the weekend.

So we're at 110 cases, 50 deaths (1 still unaccounted for) resulting in a fatal case proportion of 46.4%. That's about 16 cases reported since August 20th after a nearly 3-week pause in new cases being described. That's a rate of 1.2 lab confirmations reported per day. 

Not exactly setting the world on fire but it is worth considering what may be happening among other contacts; those perhaps not defined as close enough to test with PCR. If there are any of course. Hospital-based cases can be a great sentinel of an increase in mild respiratory viruses infections out in the broader community. 

My first source: Avian Flu Diary's article

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Ways in which seasonal and pandemic influenza infections differ

In commenting on another article in the American Journal of Pathology but Gao et al, Kevin Hartshorn nicely summarizes some of the possible reasons why a pandemic influenza kills otherwise healthy young adults more often than a seasonal influenza does. 

The answer is as complex as the milieu of interactions between viral proteins and nucleic acids and our innate and adaptive immune systems, our health, genetic factors, environmental factors and our prior exposure to different influenza viruses - and that's pretty complex!

Hartshorn categorizes the differences between seasonal and emerging influenza impact in young adults using 3 sections:

1. Differences in their ability to cause disease (pathogenicity).
• pandemic influenza generally kill more young adults whereas seasonal influenza kills mostly the elderly and the young
• This is also apparent in ferret animal models
• The viral haemagglutin (HA) protein is key to pathogenesis, playing a central role in pathology due to immune responses and inflammation whereas increases in viral replication are due to the viral replication complex (including PB1, PB2 and PA). Glycosylation of HA is a key pathogenicity determinant because a lack of apical glycosylation allows viral escape from a major non-specific defence; the action of surfacant protein D.
2. Differences in the way the infected host responds to them.
• Pregnant mice and humans show increased severity of disease. This may relate to a reduced innate immune response to pandemic influenza. Bypassing innate immunity may also allow the virus to bypass a key regulatory process, leading to a more over-reactive inflammation.
3. Differences in past history of influenza virus exposures
• Possibly, even with a strong immune cell response, the absence of any prior exposure to a related influenza results in the absence of any cross-protective neutralizing antibodies - the type that can moderate disease - in younger adults compared to older adults. The elderly may have such antibodies from exposures to other H1N1 strains between 1918 and 1957. 

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Is there a better smoking bat or camel?

That teensy fragment of Middle East respiratory syndrome coronavirus (MERS-CoV) sequence (yes, I called it a fragment of that virus) from a Taphozous perforatus bat caused a lot of hassle last week,certainly a disproportionate amount to it's representation of only 0.5% of a MERS-CoV genome. Similarly, the report of MERS-CoV protein-reactive antibodies in camels some weeks back.

In a New York Times (NYT) article discussing the discovery of the 180-203 nucleotide (nt) gene fragment in a Saudi Arabian tomb bat, Donald McNeil opened with..

Health officials confirmed Wednesday that bats in Saudi Arabia were the source of the mysterious virus that has sickened 96 people in the Middle East, killing 47 of them.

The size range represents numbers used in various articles and of the fragment from the public sequence database GenBank (203nt) -"~190 nt" noted in the actual scientific publication). By the way, has so much ever before been written about so tiny a sequence?

Because he did not include in this line, or his article, a list of all the various possible scientific shortcomings, he didn't write in more detail about the difficulties with linking a virus in any sample to the cause of a disease  in humans, he forgot to specify that this was not the actual virion that caused MERS in the human index case in Bisha, he left out the PCR-101 section on why detecting a genetic sequence is not the same as isolating an infectious virus or how to interpret a PCR fragment's sequence....he was, in some circles, criticised. 

Okay, so the bat study did not isolate infectious virus, could not obtain any other sequence, found sequence in a bat from the family Emballonuridae rather than the "expected" Vespertilionidae bats and the positive sample was from bat faeces rather than blood or some other sample more convincing. Perhaps insects, food for T.perforatus, carry MERS-like CoVs? No-one has ever found that though. Is there evidence for 2 CoVs to be completely different except for a stretch of ~100% identity? Don't know, but don't think so. As Prof Andrew Rambaut noted in his very detailed analysis of this fragment, it does differ by 1 nucleotide from many MERS-CoV sequences (so its 99.5%-100% identical). Is there a more likely animal carrying a more similar MERS-CoV strain of virus that is spilling over to humans causing MERS cases? None that has been publicised to date. And therein likes my beef with some of the criticisms I have read this week. 

So far, this finding is the best lead we have in finding an animal source. There is no evidence to dispute the link, any more than there is evidence to prove it. Yes, there may be a another smoking bat or camel or something else out there. But it hasn't been found yet. And the public might like to hear how researchers are progressing rather than wait the very long time it will take to dot Is and cross Ts on the final MERS-CoV life-cycle, once they determine it.

And by the way, there is no other CoV sequence on GenBank that has >90% nucleotide identity with the T.perforatus sequence, except for the human MERS-CoV sequences. That doesn't exclude there being some other recombinant or novel CoV out there, but that is pure speculation; more so than saying that this new sequence represents a strain of the MERS-CoV found in humans.

In succinctly summarising some of the criticism, an article in CIDRAP presents a great overview and hints at what this criticism implies; that stories in the media must get every detail spot on or the writer may be portrayed as a poor scientist.

What? Wait. Seriously??

This was a newspaper article in the New York Times people. It was about 870 words long. It won't be setting global health policy nor will it be creating a WHO disease notification stating Taphozous perforatus bats, in particular, are the primary source of all MERS cases. Or of any cases. I don't doubt this is a prestigious newspaper but this story will likely be nest week's fish 'n chip wrappings (does anyone still use newspaper to wrap fish 'n chips? Is there a digital equivalent of - "yesterday's homepage, tomorrow's archive"?). In my opinion, and I don't mean to speak for all, scientists and health policy makers know that a newspaper is not a peer-reviewed scientific journal and that it's intent is to inform it's readers so they'll come back.

Were the many readers of the NYT misinformed? Perhaps the "health officials" could have been better defined by the NYT article. Presumably it's the authors-researchers may have been a better descriptive (as was used in a follow-up piece), probably more in tune with the public's perception of us. Beyond that the article did a good job of presenting the results of a research paper's relevant findings to the wider audience. They also both caution against over-interpreting the data. The NYT article has that well covered; a transmission route is not clear, more testing needed, more work being done, sample degradation due to a break in the cold chain, it was only 1 bat.

I very much agree with comments in Robert Roos CIDRAP article; the critics are getting carried away. There are many different levels of science communication that reach the general community - the popular press are not Lancet, and vice versa.

If you really want to pick holes in a part of the coverage, you might well ask why so many are looking at a 180-190nt fragment when the ends of that PCR-amplified fragment actually reflect the commercially made oligonucleotide "primers", not the (likely) viral template at all.  The actual fragment that should be analysed from the T.perforatus bat droppings is, at best, 156nt (but only 137nt if the internal nested PCR product was sequenced but the product on GenBank, 203nt long, includes both internal and external primer sequences in it-PCR speak here, sorry). Probably won't change the outcome of any analyses to date (156 still encompasses the nucleotide variation and is still differs by 11% from any non-MERS-CoV sequence), but it is a different number. 

I'm sure a newspaper headline "156 nucleotides of a 30,130 nucleotide genome possibly related to the mystery virus that may have directly or indirectly killed 47 people in Saudi Arabia" would be a real page turner.

So, let's keep up the good work of presenting and trying to deconvolute our own studies, let's keep the public interested and informed without overcooking the message, let's allow for imperfection (as readers of this blog will be all too familiar with), but perhaps let's keep the peer reviews to the scientific literature where they are in demand and required...and keep perspective on these new findings when they come to our attention through the popular press.

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New Ross River virus page starts up

And I do mean starts....not much there yet but will fill in as time permits.

It will be over on the main VDU site...http://www.uq.edu.au/vdu/VDURossRiverVirus.htm

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