No more signed reviews

Peer-reviewing manuscripts is an important service to the scientific community. I had a personal policy to sign my reviews, but yesterday I changed my mind. I will no longer sign my reviews.

The reason I had for signing my reviews is that it forced me to be precise, fair and accountable for my statements.
Once, I almost sent out a really shitty review (of the type: “this paper is so stupid I don’t even want to spend time to explain why”).
Then I realized how unfair and un-constructive such a review is, and how angry I would be as an author if I got such a review. Plus, I realized that I would never write the same thing in a non-anonymous situation. So, I decided to always ask myself, during the writing of a review, whether I would also make the statements I was making, if the situation was not anonymous. And the simplest way to make sure that I wouldn’t hide behind anonymity is to actually write my name.

Signing is not necessary and sometimes awkward

Yesterday I was talking about the issue of signing with two colleagues. And they gave me good reasons why signing reviews is not necessary and sometimes awkward.

1. It is not necessary because the editor will know your name. So even if you don’t sign, there is a senior colleague who sees what you write, and you are not anonymous.

2. It can be awkward if you write a very positive review and sign your name, because it may be seen as if you are just doing the authors a favor in the hope that they will return the favor at another stage.

These two reasons resonated with me and I decided to no longer sign my reviews.

Of course there is another reason why people don’t sign their reviews: it is considered too risky for junior scientists to sign critical reviews.

Double blind

On a related note, I wish reviewing was anonymous in the other direction. I don’t want to know who the authors are of the paper I am reviewing, because I know about implicit bias and I don’t want it to affect my review. If I know the reputation (or absence of reputation) of the authors, this is going to affect my review, whether I want it or not. My opinion about a manuscript is also likely affected by the author’s gender, age, affiliation or ethnicity. This, of course, will distract from the science.
There are some journals in my field that do double blind reviews (Behavioral Ecology, Evolutionary Applications), and I wish others would follow.

ESEB Drug resistance poster session (22)

Sometimes the most interesting part of a symposium is the poster session. I sure think there will be some great posters about drug resistance in our symposium! The poster session takes place on Tuesday night.

I will try to write something about every poster in our poster session. But some of this will be done on the plane on my way to Lisbon.

Nicole Hawkins describes the evolution of resistance to azoles (agricultural fungicides) from standing genetic variation

Nicole Hawkins writes: “For my poster, I will be presenting an example of resistance in agriculture, in a fungal plant pathogen, with an interesting resistance mechanism in which a second paralogue of the target site, having almost been lost from the population, re-emerged under selection by fungicides. (A nice example of selection from standing variation…)”

Yue Wu studies evolutionary escape in fluctuating environments

Yue Wu proposes a model which uses reaction norms to describe the fitness of bacterial strains, depending on genotype (sensitive and resistant) and the environment (drug concentration). Using this model, she studies evolutionary escape in fluctuating environments.

Yue Wu works at the University of New South Wales in Australia.

Nina Wale looks at mixed malaria infections

Malaria infections are often mixed, i.e., containing both drug resistant and drug sensitive strains. Aggressive malaria treatment with high doses of drugs may prevent the de novo evolution of resistance, but such aggressive treatment may not be optimal for mixed infections, because aggressive treatment can make it more likely that already present resistant strains outcompete the wildtype. Nina Wale from Penn State looks at whether reduced nutrient availability can prevent the resistant strains from growing to high numbers and causing disease. She writes that “Compounds that alter the host environment represent a novel, potentially ‘evolution proof’ class of drugs that could be used in combination with existing drugs to slow the evolution of drug resistance.”

Maya Groner talks about drug resistance in sea lice

Sea lice are a problem on salmon farms. Treatment is with chemicals, but the sea lice evolve to become resistant. Maya Groner models the evolution of resistance in sea lice, and studies how the rate of evolution depends on the genetic architecture (one or many loci) and on treatment and temperature. Maya Groner is at the University of Prince Edward Island in Canada.

George Shireff studies resistant HIV strains in the Swiss epidemic

It is well known that HIV can evolve to become drug resistant during treatment. It is also known that drug-resistant HIV strains can be transmitted to other people. However, it is unclear whether transmission of the resistant strains is as likely as transmission of the wildtype strains. George Shireff from the ETH in Zurich uses data from the Swiss cohort study and finds that resistant strains are much less likely to be transmitted.

Sarah Cobey studies balancing selection for resistance

Many of us are infected, asymptomatically, with Streptococcus pneumoniae or pneumococcus. Antibiotic resistant strains have appeared in the last two decades and now co-exist with susceptible strains. Sarah Cobey studies how immune-mediated competition may explain this coexistence.
Sarah Cobey is one of the organizers of the drug resistance symposium. She recently started her own group at the University of Chicago.

Victoria Furio on intrinsic resistance in Pseudomonas species

Victoria Furio studies how low-level or intrinsic resistance varies between species of Pseudomonas. She finds that differences in intrinsic resistance are substantial and that these difference are likely due to historic selection pressures. She also finds that the differences in intrinsic resistance play a role in how the different species can evolve to become completely resistant to clinical doses of antibiotics.
Victoria Furio is in Oxford and works with Craig MacLean (one of our invited speakers).

Alexey Mikaberidze on the spatial dynamics of fungicide resistance

Alexey Mikaberidze studies the invasion, persistence and spread of fungicide resistance in agricultural plant populations. He is especially interested in the different spatial scales on which the host, the parasite and the chemical control interact.

Alexey Mikaberidze works at the ETH in Zurich.

Claudia Seiler looks at heavy metals and drug resistance

Heavy metals are relevant for drug resistance because bacteria that become resistant to heavy metals are often also resistant to antibiotics. Bacteria, antibiotics and heavy metals meet each other in aquatic environments. By studying at Pseudomonas and Aeromonas strains from the Western Bug River (nice name for a river!) Claudia Seiler found that heavy metals in the environment increase the risk of antibiotic resistance.

Alexander Nijevitch studies Cag+ and Cag- Heliobacter pylori strains

This is a study on treatment in 41 young patients who are infected with H. pylori. Some of the H. pylori strains are Cag-, that is, they have lost the CagA pathogenicity island. Treatment with antibiotics was successful in 33 patients, but not successful in the remaining 8 patients. Compared to the 33 successful cases, the 8 patients with unsuccessful treatment were more likely to be infected with Cag- strains.

Uri Obolski models the effect of stress-induced mutation for drug resistance

Uri Oboski from Tel Aviv University looks at the effect of stress-induced mutation or stress-induced horizontal gene transfer. He finds that, if stress-induced mutation is relevant then treatment with multiple drugs at the same time may not be a good strategy.

Jianhua Zhang studies the evolution of azole resistance in a mold

Aspergillus fumigatus is a mold that can infect the human lung. 5% of the strains in The Netherlands are resistant to azoles, which are normally used to treat A. fumigatus infections. Most of the resistant strains have an insertion in one gene and a point mutation in another gene. Jianhua Zhang uses experimental evolution to determine under which conditions such resistance is likely to evolve. Jianhua Zhang is at the University of Wageningen (The Netherlands)

Melanie Ghoul on the evolutionary loss of bacteriocin production

Lungs of CF patients are often colonized by Pseudomonas aeruginosa, and once there, the infection usually lasts for decades. P. aeruginosa produce bacteriocins which help it to colonize new environments. However, during the long infection time of a patient, P. aeruginosa may lose its ability to produce bacteriocins and its resistance to bacteriocins. Melanie Ghoul from Oxford studies patient derived and non-patient derived strains to study the evolutionary loss of bacteriocin production and resistance.

Camilo Barbosa on different resistance mechanisms in P. aeruginosa

Pseudomonas aeruginosa can grow in very diverse environments, such as the roots of plants and the lungs of humans. P. aeruginosa can acquire resistance to treatment in many different ways, for example, through the use of efflux pumps or the forming of biofilms. Camilo Barbosa from the University of Kiel (Germany) uses experimental evolution to study the importance of different resistance mechanisms.

Frédéric Chevalier confirms the locus of oxamniquine resistance

Frédéric Chevalier is interested in the genetic basis of oxamniquine resistance in the parasitic fluke Schistosoma mansoni. Using a novel technique, termed extreme QTL, he confirmed the location of the oxamniquine resistance locus. The method starts with a cross between a resistant and a susceptible strain, and a subsequent cross between the F1 progeny. The F2s where used to infect hamsters and half of the hamsters were treated with the drug oxamniquine. Exomes from F2 flukes from treated and untreated hamsters were sequenced to high depth.

Frédéric Chevalier on sequencing exomes of larval stages of schistosomes

Schistosomes are parasitic flukes. The adults are usually not available for analysis, and the larvae are too small to do traditional sequencing of the entire genome. Frédéric Chevalier from the Texas Biomedical Research Institute describes a method to sequence accurately and economically the exome of the larval stages.

Martina Bradic on the genetic basis of drug resistance in Trichomonas vaginalis

Trichomonas vaginalis is the most widespread non-viral sexually transmitted pathogen in the world. Around 10% of isloates are resistant to common drugs (5-nitroimidazole). The genetic basis of resistance is unknown. Using double digest Restriction-Site Associated DNA (ddRAD) sequencing Martina Bradic is trying to uncover the genetic basis of drug resistance.
Martina Bradic works at NYU.

Joana Serra on the effect of low levels of antibiotics

Low levels of antibiotics may stimulate growth of bacteria and select for high level drug resistance. Such low levels may be present in nature or human body compartments during treatment. Joana Serra looks at the effect of low lecels of antibiotics on Stenotrophomonas maltophilia.
Joana Serra works in the Center for Biodiversity, Functional & Integrative Genomics in Portugal.

The ESEB drug resistance symposium (22)

Last minute changes to the program

Because two of our speakers (Cally Roper and Daniel Rankin) unfortunately had to cancel their talks, we are adding new talks to the symposium. Originally, when we decided who to invite to talk in the symposium, we each read & graded the submitted abstracts without knowing who the author was. Now that we can accept a few more talks, we are going back to our ranking and invite the people next on the list.

New: Matti Jalasvuori on preventing evolutionary rescue

Matti Jalasvuori from the University of Jyväskylä, is interested in the role of horizontal gene transfer for evolutionary rescue. The question is whether horizontal gene transfer can allow a bacterial strain to survive a lethal dose of antibiotics in the absence of pre-existing variation in the strain itself. Next, he asks whether this process can be prevented by using specific viruses.

New: Samuel Tazzyman will talk about resistance genes on plasmids

Many important resistance genes can move from bacterium to bacterium on plasmids. Samuel Tazzyman from the ETH in Zurich makes models to determine under which conditions plasmids are a favorable location for resistance genes.

New: Laura Pollitt talks about the evolution of clearance rates in Malaria

Artimisinin is the main drug used to treat malaria these days. However, the malaria parasites are evolving artimisinin resistance. This resistance comes in the form of slower clearance rates when treated. Laura Pollitt is looking at the evolution of clearance rates in an experimental system. She also considers the role of mixed infections (with resistant and susceptible parasites) and the dose of the drugs used.

Laura Pollitt works at Pennsylvania State University.

The original post

I am one of the organizers of the drug resistance symposium next week in Lisbon during the ESEB conference. Here is a short preview of the day. Hope to see you there!

The day starts with a plenary talk by Juliette de Meaux about adaptation in Arabidopsis. After the coffee break our symposium starts.

Morning session

10:30 Invited speaker: Craig MacLean on intrinsic resistance

Craig MacLean will talk about why some bacteria are intrinsically more antibiotic resistant then others. He also asks whether this intrinsic resistance helps the bugs to evolve complete resistance.

There is also a poster related to this talk by Victoria Furio and Craig MacLean.

Craig MacLean works at the University of Oxford.

11:18 Alison Hill on drugs characteristics and drug resistance in HIV

Alison Hill talks about how characteristics of drugs determine the risk that resistance evolves in HIV. She shows how non-adherence (i.e., if patients do not take all prescribed doses) can lead to treatment failure and drug resistance for some drugs, whereas non-adherence leads to treatment failure without drug resistance in other cases.

Alison Hill recently defended her PhD thesis at Harvard. She is also a co-author of the talk by Stefany Moreno in our symposium.

11:42 Jeremy Dettman on evolution of Pseudomonas aeruginosa in CF patients

Jeremy Dettman will talk about the analysis of Pseudomonas aeruginosa whole genomes from cystic fibrosis (CF) patients. CF patients are often infected with this bug for many years, so that it is likely that the bacterium adapts to the patient environment.

Jeremy Dettman works in Ottawa.

Early-afternoon session

CANCELLED Invited speaker: Cally Roper on the origins and spread of malaria drug resistance

Cally Roper works on drug resistance in malaria. She is interested in the genetics of drug resistance and how different drug resistance mutations spread through Africa. Have a look at her drug resistance geography website here: http://www.drugresistancemaps.org/maps/haplotype/dhfr/

She will also talk about the policy consequences of her work. Cally Roper works in London as a Senior Lecturer at the London School of Hygiene and Tropical Medicine.

14:48 Ana Sousa talks about the fitness effects of resistance mutations

Ana Sousa looks at the distribution of fitness effects of resistance mutation in environments without drugs. She compares the observed distribution of effects with predictions from a simple fitness landscape model.

Ana Sousa works in Portugal at the Gulbenkian Institute with Isabel Gordo.

15:12 Alex Hall about bacteriaphage and drug resistance

Alex Hall will talk about how selection pressure by bacteriaphage may change the outcome of competition between drug-resistant and drug-susceptible bacteria. He will describe results from experiments with populations of Escherichia coli in the presence and absence of bacteriaphage.

Mid-afternoon session

15:45 Daniel Rozen from Leiden about killer bugs

Daniel Rozen asks why bacteria produce antibiotics, and whether there is co-evolution happening between antibiotic-producing bacteria and their enemies.

Daniel Rozen is an assistant professor in Leiden. He has previously worked in England, USA (with Richard Lenski) and in Wageningen (with Arjan de Visser, who is also a speaker in our symposium).

16:09 Clara Torres Barceló on the costs and benefits of an SOS response pathway

Clara Torres Barceló looked at the effects of having or not having a particular stress response pathway. She finds that there is a cost of having the pathway when bacteria are grown without antibiotics. She finds no difference in adaptive potential between strains with and without the stress response pathway.

Clara Torres Barceló works in Montpellier, but the work she presents at ESEB was done in Oxford.

16:33 Kristan Schneider on resistance in two malaria species

Kristan Schneider will talk about why drug resistance evolves faster in one species of malaria (P. falciparum) as compared to another species (P. vivax). He will talk about a modeling approach that focuses on host-to vector transmission and the presence of dormant liver-stage parasites.

Kristan Schneider is a professor in Mittweida, Germany.

CANCELLED Daniel Rankin about resistance to antivirulence drugs

Daniel Rankin asks what would happen if we’d treat bacteria with antivirulence drugs (e.g., drugs that block quorum sensing). The hope is that resistance to these drugs would not evolve. However, he finds that under some conditions, increased virulence may evolve.

Daniel Rankin is at the University of Zurich.

Late-afternoon session

17:45 Arjan de Visser on experimental evolution of an enzyme

Arjan de Visser studies the evolution of a single enzyme in an experimental setting. He is interested in the distribution of fitness effects of new mutations and the epistatic interactions between such mutations. He also looked at the effect of the population size and finds that smaller populations sometimes reach higher levels of resistance.   

Arjan de Visser works in Wageningen (NL).

18:09 Stefany Moreno-Gamez about spatial structure and the evolution of drug resistance

Disclaimer: I am one of the co-authors on this talk. (I saw Stefany practice the talk – it’ll be great!)

Stefany Moreno will talk about how bugs (such as HIV and bacteria) can evolve to become resistant to multiple drugs. Specifically, she asks whether drug resistance is more likely to evolve if there are compartments in the patient where only one of the drugs is present. She finds that such compartmentalization makes it much easier for the bug to become multi-drug resistant.

Stefany Moreno is currently finishing up her Master’s Degree in the MEME program in Groningen.

18:33 Adin Ross-Gillespie on quorum quenching

This is the second talk in our symposium about antivirulence drugs. An example of an antivirulence drug, is a drug that blocks communication between bacteria – such drug blocks quorum sensing and the strategy is referred to as “quorum quenching”. Adin Ross-Gillespie will talk about a quorum quenching method in which public goods are quenched outside the producer cells.

Adin Ross Gillespie is a postdoc at the University of Zurich.

18:57 Stéphanie Bedhomme on evolution after horizontal gene tranfer

Resistance genes are often acquired by horizontal gene transfer. Genes that are acquired by horizontal gene transfers are often maladapted to the organism, for example, because they don’t use the preferred codons of the organism. Stéphanie Bedhomme studied what happens (at a genotypic and phenotypic level) to a horizontally transferred and maladapted gene in a new host.

Stéphanie Bedhomme also has a poster on a viral evolution project. She works in Barcelona at the IDIBELL Bellvitge Biomedical Research Institute.

Evening: Poster session

After the talks there will be a poster session. See poster abstracts here: https://www.eseb2013.com/abstracts?symposium=22&type=poster

My itinerary for ESEB 2013

I usually set goals for conferences (see here), but not a specific itinerary. Inspired by other bloggers (such as Jeremy Fox on Dynamic Ecology), I decided to plan my itinerary for the ESEB conference next week. ESEB stands for the European Society for Evolutionary Biology, and the ESEB conference takes place every other year in a different city. This year it’s in Lisbon!

I am sure it’ll be a great conference!

Monday Aug 19th

Arrival, some sightseeing, maybe a work meeting with a collaborator. Registration and then to the welcome reception! I hope to see all the speakers & poster presenters of the drug resistance symposium there!

Tuesday Aug 20th

On this day I have no difficult choices to make 🙂

The day starts with a plenary talk by Juliette de Meaux, who will talk about “reconciling molecular and evolutionary biology” using Arabidopsis as a model system.

Then I am off to Symposium 22: The evolution and genetics of drug resistance which I co-organize with Sarah Cobey, Fredrik Inglis and Gabriel Perron.  You can find the schedule here. During the Tuesday poster session I’ll probably hang around the Symposium 22 posters most of the time.

I will try to write a separate post about all the great talks & posters of our symposium. I hope to see many of you there!

Wednesday Aug 21st

The day starts with a plenary by Dieter Ebert on the “population genetics of host-parasite coevolution.”

Then I will head to Symposium 10 on genomics and experimental evolution, with talks about adaptation in bacteria in hosts and in the lab.

After lunch I will move to Symposium 13 on rapid evolution, and look forward especially to Richard Neher’s talk on “HIV coevolution with the host immune system” and Hildegard Uecker’s talk on “evolutionary rescue in structured populations”. Unfortunately, I will have to miss this talk by Sally Otto and this one by Claudia Bank, both on “adaptive mutations in/to different environments.”

There is a poster session in the afternoon, where I will certainly go see this poster by Ricardo Ramiro about adaptation to the gut of the mouse, and this poster by Frederic Hopital about detecting selection in chickens.

I also plan to look at this poster about diversity in SIV (George Shireff), this one about experimental evolution in mice (Mirian Linnenbrink), and two posters about the evolutionary advantage of sex (one by Su-Chan Park and one by Daniel Weissman).

Thursday Aug 22nd

Thursday starts with a plenary talk about evolution in cancer by Mel Greaves.

The rest of the morning I’ll spend at Symposium 1 which focuses on experimental evolution and fitness landscapes.

Thursday afternoon is free for sightseeing or organized tours!

Friday Aug 23rd

The plenary speaker of this day is Trudy Mackay. I have never seen her talk, so I am excited to see this famous geneticist speak about the genotype-phenotype map of fruit flies. There is a great little video about her on YouTube.

After the plenary I will go back to Symposium 1 which focuses on experimental evolution and fitness landscapes, where I will also stay after lunch.

I am still undecided for the rest of Friday afternoon.

Later on Friday there is another poster session. I plan to go see this poster on fixation probabilities (Ivo Chelo) and many others in the experimental evolution symposium (Symp 1).

Saturday Aug 24rd

The last day of the conference. The plenary speaker is Virpi Lummaa and she talks about longevity in humans.

I’ll then go to Symposium 8 on epigenetic variation.

Saturday afternoon is filled with more plenaries about speciation (Roger Butlin), species selection (Rochard FitzJohn) and a talk by Rolf Hoekstra with the great title: “♀ ♂ + –“. At night there is the conference dinner.

Your itinerary?

The ESEB website is really nice and I encourage everyone to spend some time with it before flying to Portugal. I’d love to hear where others are planning to go! I hope there will be a pdf version of the entire program soon.

I will be following the #ESEB2013 hashtag on Twitter to find out about the sessions I’ll be missing. Let’s hope there will be wifi!