Life of (a) PI

From the movie Life of Pi – which is quite different from the Life of a PI.

This may come as a surprise for the PhD students and postdocs in the audience, but professors work too. We just do it differently than you. I know, it may seem as we are busy doing nothing, but in reality, we constantly juggle many tasks, some small, some large – some important, some superfluous. And many – to be honest – quite boring. Importantly, we do a lot of stuff so you don’t have to do them. Even if it doesn’t always seem so, we strive to make your life easier.

My main task is to make sure the research and the research group is functioning. This means setting overarching research goals, bringing in money, equipment, provide national and international contacts and all other things that allows students and staff to go about their business. It also entails a lot of hiring decisions, mentoring and scientific guidance – but equally much at the personal level, keeping folks happy and to be a partner in discussions of science and life.

But it doesn’t end there. Most professors teach (usually around 40-50% of their time), and even if lecturing is part of it, most time is plowed into planning courses, oversee curriculums, answering shitload of emails, meetings with colleagues, students, and the high and mighty folks at department and faculty levels. On top of that, there are the administrative duties, participating in various boards, special committees, answering questions, make budgets, report to agencies, sign invoices, hunt down people, etc.

But what about the science? Don’t professors do science? Well, we do, but not to the extent you may think. I rarely am the first author these days, rather I am the last and corresponding author. This means involvement in planning of the study, scientific guidance during the experiment, advice on stats and writing, steering the communication with coauthors, polishing of language, deciding which journal to submit to, and other things that needs to be done. It is also my responsibility to foster the larger context, the cooperation with other groups and apply for grants – and to train my students in the arts of becoming independent scientists.

Science and education thus make up the two main pillars of a professor’s duties. But there is a third, too, namely communicating science to the public. This is the aspect that varies most between professors: some do tons, some do little, and some do none. I kind of like doing it, which includes hosting this blog, but also to give lectures, or write popular pieces for ornithological magazines. It also includes expert advice to different government bodies, and answering media questions.

This mix of things sometimes make you feel you don’t do anything, or at least that you don’t do enough. So, as a part of inner reflection, I took a look at what I did yesterday. A Monday, just an ordinary Monday – one of many in the life of a PI.

A good way is to look at the emails, of which I received 70:

  • 1 was a confirmation of a submitted article (Yay!)
  • 10 dealt with the organization of an upcoming conference we are hosting (Check it out here)
  • 9 were from proMED (an invaluable resource for keeping abreast with disease information)
  • 1 dealt with a course that just started
  • 20 were either spam from fraudulent publishers, press-releases or commercials (delete, delete, delete)
  • 13 were from our traveling agencies regarding tickets for me and two of my incoming postdocs (no PA for professors)
  • 2 were from the HR department, dealing with hiring issues
  • 1 was from a research proposal from a collaborator in Bangladesh
  • 2 were from EFSA asking me whether I could participate in a panel on IAV (Parma is nice!)
  • 3 were from postdocs or postdoc candidates
  • 3 were from colleagues at the department on various small things
  • 5 were from admin staff to organize events to raise students (important, but not so yay)

Apart from dealing with these emails (I sent 22 emails, myself), I gave a short lecture in a course, wrote an advert for a position as lab technician, read two papers, looked over a poster for a conference, had a meeting with the Head of Department, spoke with three colleagues on different work-related issues (including hiring a PhD student), investigated why a grant hadn’t been paid, discussed the progress of postdoc project, tried to contact a funding agency (but didn’t succeed). All in all, quite a few things, but not much actual scienceing this day – more logistical/management stuff. This was just one day, and every day is unique. Most days I do more writing, be it grant writing or actual science – and other days I do more teaching. But at least you get the gist of it: a professor does many things. Even if frustrating at times, it still is the best job I can imagine.

Upcoming workshop – Ecology meets Epidemiology

dsc_04142On 22-23 March we will host a lunch-to-lunch workshop on disease ecology in Kalmar, Sweden. This workshop is arranged by  One Health Sweden, a network that promotes collaboration between researchers with interest in zoonotic infections and antibiotic resistance in Sweden and beyond.

At the Ecology meets Epidemioloy workshop we wish to gather scientists from biological, veterinarian and medical faculties to discuss the latest topics in disease ecology, ranging from animal ecology, disease epidemiology and immunology. We especially encourage young researchers (PhD students and postdocs) to come and present their work, meet senior researchers and exchange ideas with peers.

You can register now at the workshop’s homepage. From the abstracts we will select presenters for oral communications. Among the keynote speakers we have:

  • Nicolas Gaidet, Animal and Integrated Risk Management unit, CIRAD, France – An ecological approach to health: the case of avian-borne viruses
  • Elinor Jax, Max Planck Institute of Ornithology, Germany – Gene expression profiling of whole blood as a means of detecting an immune response in an avian non-model species
  • Gunilla Hallgren, National Veterinary Institute, Sweden – Anthrax in Sweden, from past to present
  • Lars Råberg, Functional Zoology, Department of Biology, Lund University, Sweden

More information and call for abstract can be found on the homepage – which will be updated as we go along.

It would be great to see you in Kalmar!

This duck and not that duck – what determines the susceptibility to infections?

Seasonal flu is just around the corner here in Sweden, with cases starting to rise week by week. And although the infection dynamic is fairly predictable at the population level, driven by both environmental factors and behavioral changes in the human population, it is not always easy to predict who will be infected or not, and whether an infection will result in mild or severe disease. Ultimately, this will depend on the exposure risk, the underlying condition of the individual, variation in specific genes in both the virus and the host and whether he/she has experienced previous infections, and in such case, how similar the current virus is to previous viruses. In short: complex interactions between the microorganism, the host, and the environment. These are things disease ecologists are interested in!

Unfortunately, for wildlife we know essentially nothing for most pathogens and hosts in terms of disease dynamics. And we know particularly little regarding the immune system and how variation in immune genes translates into protection against pathogens. If you read the literature, most studies look at the adaptive branch of the immune system, especially antibody mediated immunity and the diversity in the genes that make up the MHC loci. The MHC – or Major Histocompatability Complex – are among the most variable genes we know of, responsible for binding and presenting antigens to B- and T-cells and triggering immune processes. Although extremely interesting, they are but a part of the vast array of cells, proteins, and genes involved in immune processes.

In a recent paper, we dived straight into another set of genes: the beta-defensins. This is the first of several papers we will prepare on the subject. β-defensins are cool little proteins, actually kind of bad ass. Their main function is to interact with bacterial cell walls, where they create little pores and thereby interfere with cell homeostasis (think of Swiss cheese). β-defensins are part of the innate immune system and are ancient, present throughout the animal kingdom – and although some have evolved into new functions, such as toxins, the vast majority are involved in the fight against pathogens. Apart from directly killing invading bugs, they are involved in immune signaling and can also target some viral infections.

Our main study species is the Mallard, an important game bird species and the ancestor to domestic ducks – and the main reservoir host for influenza A virus in the Northern Hemisphere. Having studied disease dynamics in this host for a long time, we are now very curious about how variation in immune genes among Mallards translates into susceptibility to different diseases. Fortunately, the time is right for pursuing such questions, as the genome of the Mallard is available, making it easier to develop molecular tools to target specific genes. In a studied published a few weeks ago, we amplified and sequenced five β-defensin genes in a large number of individuals. First we studied these genes in a local population from Sweden, then we expanded it to cover specimens from all over the species’ range – from Europe, North America and Asia – and finally we sequenced the same genes in other species across the waterfowl phylogeny. This allowed as to ask how evolution has shaped β-defensin genes over different time scales. The results are summarized in the abstract, below:

All five genes showed remarkably low diversity at the individual-, population-, and species-level. Furthermore, there was widespread sharing of identical alleles across species divides. Thus, specific β-defensin alleles were maintained not only spatially but also over long temporal scales, with many amino acid residues being fixed across all species investigated. Purifying selection to maintain individual, highly efficacious alleles was the primary evolutionary driver of these genes in waterfowl. However, we also found evidence for balancing selection acting on the most recently duplicated β-defensin gene (AvBD3b). For this gene, we found that amino acid replacements were more likely to be radical changes, suggesting that duplication of β-defensin genes allows exploration of wider functional space. Structural conservation to maintain function appears to be crucial for avian β-defensin effector molecules, resulting in low tolerance for new allelic variants. This contrasts with other types of innate immune genes, such as receptor and signalling molecules, where balancing selection to maintain allelic diversity has been shown to be a strong evolutionary force.

Distribution of AvBD10 alleles across species, whereby coloured shading denotes mallard alleles and black shading denotes alleles found only in non-mallard waterfowl. Species with shading in the same vertical column share the allele denoted by that column. For more info see the original paper here.

To break this down into a more layman text, it means that most alleles are very old, dating back from before the different species split – evidenced by the same allele present in different waterfowl species separated by millions of years’ evolution. It also means that there is strong selection for maintaining function, that is, that mutations that change the amino acid composition largely are purged from the population. However, for one of the genes we saw evidence of balancing selection, where gene diversity in the population is favoured.

We hope this paper will be of interest for the evolutionary biology crowd, but we also see it as a first stepping stone into investigating how genetic variation translates into function. We are continuing with several lines of research, both in the lab and in experimental infections to measure how effective different allelic variants are against different pathogens, and where and how these genes are upregulated upon infection. This is very exciting research, but also a bit of a leap from what we have done in our lab before. It is a certain thrill to charter the unknown, and there’s tons of stuff to learn in order to do it well.

This paper was a collaborative effort involving four labs (Linnaeus University, University of Konstanze, University of Lund, and Wildfowl & Wetlands Trust):

Chapman, J.R., Hellgren, O., Helin, A.S., Kraus, R.H.S., Cromie, R.L. & Waldenström, J. 2016. The Evolution of Innate Immune Genes: Purifying and Balancing Selection on β-Defensins in Waterfowl. Molecular Biology and Evolution 33(12): 3075-3087.

 

 

On the air – participating in a podcast

screen-shot-2016-12-07-at-9-48-08-am

Yes.

I generally say yes to things. In fact, I like to say yes to things.

And although it is fun to say yes, it also comes with a cost, as the more you say yes, the more often you will be asked again. It is a dilemma, for sure, when time is a limited currency.

But saying yes is also a great way to do new stuff. Learn new things, meet new people. This autumn, for instance, I have participated in four different PhD defenses, in three different countries. Although a lot of work, it was great fun!

I also tend to say yes to scicomm stuff, ranging from giving talks to schools to participate in radio and newspaper articles. A few weeks ago I did something new: I said yes to participate in the Linnaeus University podcast ‘Snillen stimulerar’.

This pod is one of the university’s ways of disseminating academic knowledge to the public, but in a casual and entertaining way. If you click here, you can listen to a discussion on my favorite pathogens and diseases. Deadly stuff. A disclaimer, though: it is in Swedish.

So how was it? I enjoyed the experience, and I think the end product managed to be both informative and (surprisingly) fun. In this case, the two hosts – Ingeborg and Anders – took turns asking me questions, and making comments. They were brilliant, and had done their homework on my research, which made it all a rather smooth affair. The fun part is that you have to think on your feet and use a language less ladden with field specific scientific prose.

I hope you like it!

A duck is a duck is a duck, or is it? – Some notes on how to age Mallards in autumn.

Female head

2cy+ female, October. Adult females often show distinct blackish spots and a bright yellow-orange colour of the bill. [90A86379]

There are a lot of ducks on this blog – too many for some readers, perhaps – but it is not that surprising given that Mallards are our main model system for exploring disease ecology questions. Given their abundance, importance as game species, relationship with domestic ducks, synanthropic (yes, google that) behaviors, and propensity to carry interesting viruses and bacteria, it is not strange that ducks have rendered considerable research interest here and elsewhere. Ducks are also very beautiful animals, which helps.

You may think that a duck is a duck is a duck. But really this is not true; there is considerable individual variation in all measured traits in Mallards. The size differs, the plumage varies, as do migration patterns and immunocompetence, and so forth. As scientists, the variation is often what we are most interested in. The topic of today’s post is variation in plumage and the uncertainties of correctly ageing Mallards in the hand.

During our long-term studies of Mallards at Ottenby Bird Observatory in Sweden we have built up a large database of captures and recaptures of birds, which has allowed us to identify birds with known ages. For examples, if a bird was ringed in 2012 as juvenile and recaptured in 2016 we can be confident that this bird is adult at the second capture. Recently we published a study investigating different proposed plumage criteria for ageing Mallards by careful assessment of photos gathered over several years.

Generally, in birds, there is a difference between juvenile feathers (i.e. those attained directly after hatching) and feathers of older generations. In some bird species, this may include color differences, or special markings – such as spots or vermiculation; while in others differences are subtler, as in shape or wear. The key to age determination is the knowledge of in which sequence feathers are replaced (generally termed moult), and when in the year it takes place. In many passerines, birds have one complete moult of flight feathers per year and one or two partial moults of body feathers. Thus, knowing when, where and how birds moult you can search for the presence or absence of juvenile feathers. In non-passerines it becomes a bit messier, for instance with raptors where it may take several years to complete the moult of flight feathers. You could also look at other characters, such as the coloration of soft parts (bill, orbital ring, feet) and eye color, but generally those are less well known.

And what about Mallards? Let’s cite the paper (slightly edited):

“At the age of 2–4 months, juvenile mallards perform a partial moult of some feathers on the head, neck, mantle, scapulars, breast, and flanks in late summer (mainly July–September, correlated to hatching date). Both young and adults undergo pre-breeding moult from August–December, but the process may be prolonged during winter. This moult includes most body feathers, scapulars, tertial coverts, tertials, and tail, but very few lesser, middle, and greater coverts, and no primaries and secondaries. The retained feather groups allow determination of juveniles until replaced during the next year. Young females also retain at least some juvenile tertials and tertial coverts, whereas most males have moulted all tertials by late November. Males are thought to perform more extensive tertial moult due to sexual selection, and perhaps is sexual selection also responsible for the “extra” moult of mainly head and neck feathers noted in males in February–March.

In January–May, females perform a moult (of similar extent as the preceeding one) to acquire an even more cryptic plumage during nesting, brood-rearing, and moult of flight feathers, while males moult into a female-like eclipse plumage in May–July. Both sexes are flightless for about one month when all remiges (primaries and secondaries) are lost simultaneously during the summer (mainly late June–August), latest in successfully breeding females.”

For you non-birders, this may sound awfully complicated, but it is actually not that hard once you know your way around the anatomy of a bird and become familiar with the lingo of ornithology. The take-home message is that during autumn, birds will have a plumage comprised of feathers of different ages and knowing what you look for you should theoretically be able to correctly separate juvenile birds from adult birds.

1 cy Male tail

1cy male, November. Easily recognized as a young bird due to remaining juvenile RR being narrower (and shorter), worn, frayed, and with brown and buff colours. The outermost pair of feathers is often the last to be moulted, but sometimes the central pair is still retained when all the others are post-juvenile.

1 cy male tertials

1cy male, November. This bird has moulted T2 to T4, but still has juvenile T1. The four outer TC are worn and dull brownish, but note that even juvenile two outermost TC occasionally show warm brown tips. [90A88713]

However, in practice this is hard – even for experienced duckologists (see for example the figure just above). Using the photographs, we tested the validity of different criteria, either one by one, or combined, by presenting them to a panel of (mostly) volunteers experienced in age and sex determination of birds. Evaluating their scores compared to the known ages of the birds we found that no single criterion was conclusive (range 48-89% correct), but that when given access to photographs of all plumage tracts, 91 and 95% of male and female Mallards were correctly assigned, respectively. The latter setup is more similar to what is experienced in the field, but nevertheless we urge caution with ageing, especially in late autumn where many juvenile birds may have moulted tail and tertials in a pre-breeding moult and hence are very adult-like in appearance.

I am happy to send a pdf of the paper to those interested, just google my name at Linnaeus University. You could also visit the online Ringers’ DigiGuide at Ottenby Bird Observatory where we have provided quality photos and texts to use for the purpose of ageing and sexing of Mallards, as well as for other species.

The reference for the article is:

Andersson, S., Bengtsson, D., Hellström, M. & Waldenström, J. 2016. Age and sex determination of Mallards Anas platyrhynchos in autumn. Ornis Svecica 26: 61-81.

Say hello to summer

Hi folks, just a short note to say that summer vacations have started and that the blog will be a bit slow for a while. To be honest, the blog has been pretty slow already before the vacations – I hope to be more frequent in the autumn. The lack of posts are partly related to intense work periods, but also due to the fact that I written on my other blog. That blog is not a science blog, but a science fiction blog! Check it out if you want to hear more about old space pulp. Otherwise, enjoy your time in the sun!

Come join our lab – we are hiring

A good day in the duck trap. Photo by Vilhelm Fagerström

A good day in the duck trap. Photo by Vilhelm Fagerström

The Zoonotic Ecology and Epidemiology lab is recruiting two new PhD students, and in the larger research center EEMiS there are another three available positions. Please find descriptions and application instructions for all five positions here.

If you are interested in disease ecology, these two projects are based in my lab:

Readdressing Campylobacter jejuni epidemiology and evolution.

Campylobacter jejuni is the most common zoonotic infection in Europe. Despite a well described epidemiology and targeted interventions to reduce carriage in food animals (especially poultry), human campylobacteriosis remains high in Sweden and the EU. In this doctoral student project, we want to turn the question of campylobacteriosis around. Instead of asking how humans become infected, we will investigate what properties that make specific campylobacters so adapted to their food animal niche. Identifying the genes responsible to a ‘life on the farm’ will: (1) enable a more comprehensive understanding of C. jejuni evolution, (2) pinpoint which traits that underlay emergence of new genotypes in food animals and human disease, and (3) provide new entry points for measures to reduce C. jejuni carriage in food animals.

A vital part in this line of research is to combine epidemiology with phylogenomics where genotypes and phenotypes of C. jejuni from food producing animals are contrasted with strains isolated from non-food animal sources. At our disposal, we have the largest collection in the world of C. jejuni strains from wild birds which, together with new strains, will form the basis for gene-by-gene comparisons with C. jejuni genomes from a reference strain repository. Based on the genetic studies the student will set up phenotypic assays, perform experimental binding studies, and carry out experimental infections in bird models to test the predictions arising from the genomic approach.The successful applicant will interact with other students and researchers within EEMiS, a multidisciplinary center of excellence within Linnaeus University that comprises expertise in ecology, evolution, and microbiology. This project is run together with Sheppard Lab in Swansea

Innate immunity of waterfowl – from genes to function.

The extent to which naturally occurring polymorphisms in immune genes result in individual differences in pathogen susceptibility remains an open question. While inbreeding has been linked to increased disease susceptibility in many species, it is not currently known whether low heterozygosity in general, or at specific immune loci, is responsible. β-defensins are key effector molecules of the innate immune repertoire of higher vertebrates, including birds. Their primary mode of action is the disruption of microbial membranes. However, they are increasingly recognised to have multifaceted roles in immune defence. β-defensins represent an ideal system for the study of host ecoimmunology. Firstly, they have a direct role in killing invading pathogens, and secondly, the functional peptide is encoded by a single exon of 36-38 amino acid residues. These genes thus represent a tractable and biologically relevant tool for elucidating the genetic basis for host immunity. The current project aims to build on knowledge of β-defensin allelic variation within and between wild populations and species in order to develop an in vitro model for assessing host-pathogen interactions. Based on allelic profiles the student will compare the bactericidal properties of defensin alleles in their native conformations. This work may involve folding and oxidation of native peptides, liquid chromatography, structure determination based on NMR data, and development of bioassays for testing. The successful applicant will interact with other students and researchers within EEMiS, a multidisciplinary center of excellence within Linnaeus University that comprises expertise in ecology, evolution, and microbiology.

An illustrated guide to Academic life

Have you just started grad school? Does it seem scary? Fear not, young Padawan – below you’ll find guidance on your road to PhDoom.

(Disclaimer – this is yet another list. The internet is full of them. You don’t have to read it. And more importantly, you don’t need to follow the advice. I wrote the list today mainly because I was bored and tired after handed in a giant application yesterday, and after spent the major part of the night awake with a sick child).

 

1. Read the god damn literature

But, hey, read the literature - find out what people have done before.

You’ll be surprised how much knowledge there already is out there. The Great Idea you want to test in your thesis likely has been thought many times before,  and chances are that it has already been tested by others. A professor at my former university used to remind graduating students about the repetitiveness of science by handing over old books (like 19th century books) on the exact subject of the thesis during the dissertation party. Hence, the best advice I can give is to plow the relevant literature in your field. Follow the references to the original sources, and learn first hand. There are no shortcuts.

2. Get some friends

You may feel lonely at first. It is all new and you have no one to ask.

You may feel lonely at first. It is all new and it feels like everyone is smarter than you. Don’t despair, get some friends instead. Academia is a great place to get to know other people, in your laboratory, in the cohort of PhD students and postdocs, and with the faculty folks (although they are generally more dull). Think of them as your hive mind – knowledge to gain, and knowledge to share. Don’t lock yourself inside your room – go have a coffee with the others (see Swedish fika), have a beer (or coke) at after work sessions, go birdwatching, go whatever as long as it makes you connect with your colleagues. And another free advice: everyone thinks that everyone else is smarter, it is the impostor syndrome – a widespread epidemic in academia – just try to get over it.

3. Water that plant

Water that plant, and watch it grow.

Water that plant, and watch it grow.

Science is a gradual process. There are the occasional big leaps, but generally it is a slow and tedious ride. Have patience, water your manuscript plant every day and after a few weeks, months, or a year, from now it will be a flowering plant published in a glossy magazine. You can not cut corners, science has to be done thoroughly, or not at all.

 4. Broaden your perspectives

You will make friends, see places, explore new things.

Try to get out of your box, your comfort zone. Read studies that don’t relate immediately to your own field. Go to seminars about jelly fish, CRISPRs, dinosaur teeth, or sexual selection – it is a great privilege to have the ability to listen to other peoples’ talks. Use that.

Furthermore, you SHOULD visit conferences and/or other research groups during your PhD studies. This is something your supervisor should help arrange, and most importantly pay for. You. Need. To. Travel. And. See. Places.

 5. Broadcast your findings

And soon you'll give the best talks ever.

Tell the world of your findings! In a conference, on social media, to your grandma, to your cat, to the strangers on the bus – spread your gospel. You could even start a blog…

Importantly, if you believe your findings have a relevance for society at large YOU are the one best suited to broadcast that information. I can guarantee you that policymakers will not read your scientific articles, even if they are printed in high impact journals. Thus, if you have a message it needs to be put forward in the right forum. This is a responsibility that comes with being an expert.

6. Have a social life

Have a social life.

In order to function at work we need to have a life that stretches beyond the university offices. Well, this is advice most people don’t need – most students engage in a range of social activities. But over the years I have met people that always work, and never do anything non-sciency. They often break down in the final year.

And social life does not need to be binge drinking.

7. In the end, focus

Remember to breath.

Remember to breath.

The last stretch of a PhD is writing, writing, and writing. For some even #madwriting. You need to produce a thesis, and the last months are a major undertaking for everyone. In order to make it bearable, make a time line and stick to it. Inform your supervisor(s) and co-authors when to expect drafts of chapters and manuscript, and make sure to follow up associated deadlines. Supervisors are humans, too. Giving a full thesis to read over the weekend is not  a precious gift.

8. Have a mock defense

Don't fear the thesis.

Don’t fear the thesis.

One of the best advice I can give you is to have a mock defense before the real one. Let your friends and colleagues pepper you with questions. Ask them to play the role of the panel, and do it as realistic as possible. You’ll be surprised how well this little exercise can help chase the thesis demon away.

9. Choose your thesis panel with care

As regards thesis, beware the committee.

Each country has their own system, but normally there is some sort of appointed committee that will read and evaluate your thesis. In the Swedish system the opponent (external examiner) has a big role, where he/she discusses the merits of the thesis in an open session. The choice of opponent has great bearings on how the thesis defense will play out, so discuss this carefully with your supervisor. If your goal is to continue in science, a good advice is to choose an opponent in which lab you would like to do a postdoc. Just sayin’.

10. Make plans, and keep to them.

Plan for a life after the completion of thesis.

You can do wonders in life, and a PhD is a bridge to the future, not a dead-end street. Too many students think of post-PhD life as a black hole filled with unemployment and broken dreams. In reality it is often not, but one has to be realistic about the prospects of different career paths. To get a tenure faculty position is hard, and requires skill, heaps of luck, and a vagabond lifestyle for some years ahead. But most people will not carry on in science, and you have to see the non-academic path as excellent alternative, not as a failure. Halfway through grad school is probably a good time to start think about the future, and to plan for how those dreams should be fulfilled.

 12. Enjoy the show

I don’t say it is easy, because it isn’t, but try to enjoy the final show. It is the culmination of a lot of hard work and you get the chance to show the world how good you are in your field. And that is pretty amazing, after all.

Here be ducks

Dear reader,

we have reached peak-lolcats. Let there be ducks.

 

A whole lot of ducks:

Crazy numbers of ducks:

Aggressive goose on the loose:

A man in bread suit that feeds the birds. That’s all:

A Mallard video for your cat:

A very demanding Mallard:

And a guy vacuuming his duckling:

 

Where have all the subtypes gone, long time passing?

Illustration from Roche et al (2014) on an individual-based transmission model for influenza A viruses in waterfowl. The drawing was made by John Megahan, and is used under CC-BY 4.0 license.

Illustration from Roche et al (2014) on an individual-based transmission model for influenza A viruses in waterfowl. The drawing was made by John Megahan, and is used under CC-BY 4.0 license.

By Jonas Waldenström

Ducks and men differ in some obvious ways. Whereas a Mallard is a fluffy, winged animal that dabbles, a man is an elongated, mostly fur-free mammal that intoxicates itself with beverages and too much screen time. There are, however, also shared traits and even shared pathogens, such as the influenza A virus.

But where you and I will experience only a single, or a couple of different influenza virus subtypes in our lives – for instance the H1N1 or the H3N2 that are touring the world today – an average Mallard can walk through up to 4 or 5 over the course of a few weeks in autumn. The diversity of influenza viruses in Mallards and other waterfowl is simply astounding.

For example, in our studies we have isolated 74 subtypes from Mallards caught in single little pond at the edge of a lagoon opening to the Baltic Sea. This is more than any other sampling site on the planet, and a large chunk of the global diversity for this virus.

There are some patterns to this mess. Some subtypes are actually fairly common at all times in autumn, such as H1 and H4 viruses, other subtypes are detected each autumn, but show more outbreak-like patterns. However, there are some subtypes that just pop up seemingly randomly in the population, sometimes years apart. So where do all subtypes go? A single animal is rarely excreting viruses for more than a couple of days, so the viruses have to go somewhere.

Of course there are hypotheses, and opinions. Perhaps some subtypes reside in other hosts, spilling over occasionally to Mallards? Perhaps the viruses can be maintained in the environment, in the water or in the sediment, or even in ice? Perhaps Mallards do not have long-term efficient immune memory to influenza? Perhaps the population size and annual recruitment of juveniles are large enough to maintain transmission of even rare subtypes? Perhaps they are seeded in from aliens?

A lot of hypotheses in the air, but not too much synthesis. Until now. A recent paper published by American researchers in PLOS Biology examines the existing evidence and model how well data fit different hypotheses. The method they used is phylodynamics. And the results are pretty cool.

Some possible epidemiological pathways are depicted in the figure at the start of this post (except the alien one, strangely enough). Viruses can be transmitted directly between individuals or move via the environment, including possible time delay. Both the environment and the host populations experience seasonal changes, some of which we can quantify and use as parameters in epidemiological models. The effect of these parameters can then be used to illustrate how the relationships between strains of the virus would do in simulated phylogenetic trees over time. If you change a parameter, say herd immunity, how will the resulting trees and stats look like after simulations? Will it look like the data we observe in natural populations, or will it look different?

In the left hand panels in the figure below you see how a tree based on human influenza typically looks like. There is little diversity, the antigenetic landscape (the part the immune system reacts to) changes with small steps, with accumulating mutations (A), and the phylogenetic tree has few, but long branches that stretches forward (G). A typical avian-based set, as seen in the panels to the right, show a mix of colors of different co-occurring lineages with large antigenic diversity (C), and the tree is more a thorny bush (I). In the middle panel you have an example of avian viruses based on direct transmission only. This model isn’t overly well matched with what is observed in nature, and predicts fewer circulating viruses (B), and a different tree topology (H). By doing this sort of analyses over and over again, one is left with the most plausible models. (I know this description is over simplistic, but this is a blog piece after all)

Figure from Roche et al (2014) used under CC-BY 4.0 license. Original caption: (A–C) Time series of influenza prevalence in humans, avian system with only direct transmission, and avian system with mixed transmission, respectively. Basic reproduction ratio, R0, is set to 1.5 for direct transmission, and environmental durability is set at 20 d when this transmission route is included. Colors represent antigenic distance between the introduced strain and the dominant variant at time t. (D–F) The black line represents antigenic diversity through time (i.e., number of antigenic strains), whereas the grey line demonstrates temporal changes in the antigenic distance of the dominant strain to the introduced strain. Time is expressed in years. (G–I) Associated reconstructed phylogenies. (J–L) Co-infection patterns for the situations depicted previously.

Figure from Roche et al (2014) used under CC-BY 4.0 license. Original caption: (A–C) Time series of influenza prevalence in humans, avian system with only direct transmission, and avian system with mixed transmission, respectively. Basic reproduction ratio, R0, is set to 1.5 for direct transmission, and environmental durability is set at 20 d when this transmission route is included. Colors represent antigenic distance between the introduced strain and the dominant variant at time t. (D–F) The black line represents antigenic diversity through time (i.e., number of antigenic strains), whereas the grey line demonstrates temporal changes in the antigenic distance of the dominant strain to the introduced strain. Time is expressed in years. (G–I) Associated reconstructed phylogenies. (J–L) Co-infection patterns for the situations depicted previously.

By tweaking the models and conducting lots of statistics, the research team could show that the two main factors explaining the diversity of co-existing avian influenza hemagglutinin subtypes were “subtype-specific differences in host immune selective pressure and the ecology of transmission (in particular, the durability of subtypes in aquatic environments).” Host immunity is interesting, and something we have worked with ourselves (see here, for instance). The most notable finding was however that they could show the importance of the environmental “storage effect”. Viruses could reenter the population of ducks from the environment – hidden in water or in sediment, perhaps – and start new chains of infection.

The question now is how to prove this, experimentally. Several studies have shown that virus can retain infectiousness for long time if stored in water in the laboratory, and some epidemiological work has suggested that reinfection from the aquatic environment can happen from one breeding season to the next. On the other hand, in our duck trap we see very little evidence for this being a frequent mode of transmission. During autumn, we have a massive deposition of fecal matter from infected ducks in and outside the trap, but when we put in naïve ducks in the trap again in spring, they rarely become infected until the next autumn.

However, perhaps even rare re-introductions of subtypes may be sufficient to re-establish locally extinct subtypes, cause new events of short-lived infection cycles, and then disappear again? Or maybe these virus transmission events are more prone to take place in certain environments than in others? In our case, the duck trap regularly freezes over, sometimes all the way to the bottom, and that may be too hard for our RNA virus friends/foes?

Anyway, always exiting with new well-written articles. Go read it yourself, and don’t forget the 22 supplementary files and appendices.

On a final note, let’s sing:

Where have all the subtypes gone, long time passing?
Where have all the subtypes gone, long time ago?
Where have all the subtypes gone?
Water and mud swallowed them everyone?
Oh, when will we ever learn?
Oh, when will we ever learn?

 

Link to the article:

Roche, B., Drake, J.M., Brown, J., Stallknecht, D.E., Bedford, T. & Rohani, P. 2014. Adaptive Evolution and Environmental Durability Jointly Structure Phylodynamic Patterns in Avian Influenza Viruses. PLOS Biology, 10.1371/journal.pbio.1001931

*******************************************************************************************************************

If you enjoyed this post, or other posts on this blog, why not follow the blog via email, Feedly or get updates via Twitter by following @DrSnygg?