Many Gordon Research Conferences now start with a Gordon Research Seminar. The GRSeminar is a smaller meeting only for the graduate students and postdocs who will attend the GRConference. Last summer I went to the Microbial Population Biology GRConference and the GRSeminar that occurred before it.
I thought the GRSeminar was a really nice way to start the week, because there were fewer people and no famous professors (except two invited speakers) so the graduate students and postdocs could focus on getting to know each other. Although the GRSeminar only lasted for about 24 hours, I still think it had a very positive effect on the rest of the week.
At the end of the GRConference I was asked to be the chair of the next GRSeminar on Microbial Population Biology that will accompany the GRConference on the same topic in 2015. Three people offered to help me with organizing the next GRSeminar (Krishna Swamy, Elizabeth Jerison and Helena Mendes-Soares) so we’ll be working as a team. Michael Travisano is the chair of the 2015 GRConference. Last week we heard that the GRC organization approved our request to have another GRSeminar, so I’ll be traveling to LA in January to learn all I need to know to be a good GRSeminar chair.
An editorial I wrote with Bob Shafer and Susan Holmes (both Stanford) got published this week in Journal of Infectious Disease. See here.
The editorial is about a recent paper by Joel Wertheim and colleagues who analyze 80,000 HIV sequences to characterize the worldwide HIV epidemic.
I wrote a blog post about it here.
A short review on F1000 said: “This is an editorial commentary that provides an excellent summary of the use and limitations of HIV viral phylogenetics to understand transmission and sexual networks.”
Last week, we got news that our paper on “Loss and recovery of genetic variation in adapting HIV populations” is accepted for publication in PLoS Genetics! My coauthors on this paper are Sergey Kryazhimskiy and John Wakeley. You can find an earlier version of the paper on the arXiv, and a related blog post on Haldane’s Sieve.
In a nutshell, this is what the paper is about: we analyze longitudinal data on 30 patients in which the virus evolves to become drug resistant. We see that
1. known resistance mutations mostly fix one at a time,
2. these fixations are associated with a reduction in genetic diversity due to hitchhiking,
3. the fixations involve both soft and hard sweeps (see pictures), and
4. recovery of genetic diversity is slow for synonymous sites and faster for non-synonymous sites.
Soft selective sweep in HIV. The K103N substitution is caused by an A to T or A to C mutation. In this patient both alleles are present. A clear example of a “multiple-origin soft sweep”.
Selective sweep in HIV. An NNRTI drug resistance mutation (K103N) goes to fixation in patient virus. The mutation (A to T) apparently occurred on one haplotype (genetic background) and as it went to fixation, genetic variation on was lost.
The video I wrote about earlier on this website (here) won the NESCent film festival! The NESCent film festival, which showcased the movies sent to the “third annual Evolution Video Competition” took place at the Evolution conference in Snowbird, Utah.
Thanks to my colleagues Tobias Pamminger, Susanne Foitzik and Dirk Metzler for the ongoing ant collaboration.
Together with Sarah Cobey I am hosting a NESCent working group on “Trends in the evolution of human viruses.” See NESCent website.
Abstract: Many of the most exciting concepts in biology, including selection and neutrality, asexual and sexual reproduction, stochastic and deterministic dynamics, and the interplay of ecology and evolution can be studied through the lens of host-pathogen interactions. Some of the best studied pathogens are viruses that infect humans, although research has focused disproportionately on a few viruses that constitute only a small fraction of the infectious disease burden on humans. The aim of this working group is to broaden our perspective on host-pathogen interactions by synthesizing observations of the evolution of the most prevalent human viruses and asking whether commonalities and differences between evolutionary patterns can be readily explained by current theory. In particular, we will seek to augment the traditional emphasis on genotype and sequence-level analysis with information on viral phenotypes. We will also investigate whether the phylodynamic framework, which proposes that viral phylogenies are chiefly shaped by immune pressure and epidemic dynamics, provides a good approximation of the dominant evolutionary modes of less well studied viruses. Our findings will help identify gaps in the study of viral evolution and aggregate observations for the development and testing of theory.
Sarah Cobey is an assistant professor at the University of Chicago. Before that she was a post doc at the Harvard School of Public Health. I met Sarah in 2005 when we were both part of the Young Scientists Summer Program of IIASA in Vienna. Her website is here.
My review paper on HIV drug resistance for Infectious Disease Reports is out (see here). It is part of a special issue entitled “Current perspectives in HIV/AIDS“. You can download the paper here: Pennings2013IDR.
Abstract: Access to combination antiretroviral treatment (ART) has improved greatly over recent years. At the end of 2011, more than eight million HIV-infected people were receiving ART in low-income and middle-income countries. ART generally works well in keeping the virus suppressed and the patient healthy. However, treatment only works as long as the virus is not resistant against the drugs used. In the last decades, HIV treatments have become better and better at slowing down the evolution of drug resistance, so that some patients are treated for many years without having any resistance problems. However, for some patients, especially in low-income countries, drug resistance is still a serious threat to their health. This essay will review what is known about transmitted and acquired drug resistance, multi-class drug resistance, resistance to newer drugs, resistance due to treatment for the prevention of mother-to-child transmission, the role of minority variants (low-frequency drug-resistance mutations), and resistance due to pre-exposure prophylaxis.
On Friday May 31st I gave a Pecha Kucha talk about HIV drug resistance at the de Young museum. I put a little more info on my blog. Here is the presentation: