Skip to content


HIV Adaptive Dynamics

How does the virus adapt so rapidly to immune surveillance and why does it not infect a broader set of target cells?

Questions being studied include:
  1. How does a severe population bottleneck at infection affect the virus's adaptation to the immune system?
  2. How does the virus manage to cross the fitness valleys it encounters when switching from one target cell type to another?
  3. How does an extremely high recombination rate affect the virus's ability to adapt to immune surveillance?
HIV cryo-electron tomograph


  • da Silva, J. and S.K. Wyatt. 2014. Fitness valleys constrain HIV-1's adaptation to its secondary chemokine coreceptor. Journal of Evolutionary Biology 27: 604-615.
  • da Silva, J. 2012. Antibody selection and amino acid reversions. Evolution 66: 3079-3087.
  • da Silva, J. 2012. The dynamics of HIV-1 adaptation in early infection. Genetics 190: 1087-1099.
  • da Silva, J., M. Coetzer, R. Nedellec, C. Pastore, and D. E. Mosier. 2010. Fitness epistasis and constraints on adaptation in a human immunodeficiency virus type 1 protein region. Genetics 185: 293-303.
  • da Silva, J., 2010 An adaptive walk by human immunodeficiency virus type 1 through a fluctuating fitness landscape. Evolution 64: 1160-1165.
  • da Silva, J., 2009 Amino acid covariation in a functionally important human immunodeficiency virus type 1 protein region is associated with population subdivision. Genetics 182: 265-275. 
  • da Silva, J., 2006 Site-specific amino acid frequency, fitness and the mutational landscape model of adaptation in human immunodeficiency virus type 1. Genetics 174: 1689-1694.

Haplodiploidy and the Origin of Eusociality

Whether haplodiploidy in the hymenoptera promotes eusociality is still an open question.

The question of whether haplodiploidy favours the evolution of eusociality has been debated for 50 years. With haplodiploidy, females are more closely related to their full sisters than to their own offspring, which may promote eusociality via kin selection. However, females are also less related to their brothers than to their own offspring, making them on average as related to their siblings as to their offspring. Nevertheless, haplodiploidy may still promote eusociality because a haploid male carrying an allele for reproductive altruism passes the allele to all of his daughters, in contrast to a diploid male. Therefore, haploid male carriers produce more altruist daughters and the amount of help provided by these to their mother that is required to cause the spread of the altruism allele is less than with diploidy. This hypothesis is being investigated with population genetic models of the origin of reproductive altruism.

honey bee

The Evolution of Sexes (Anisogamy)

The classic model of the evolution of dimorphic gametes is being extended and tested with new data from the Volvocine algae.

The enduring theory of the evolution of anisogamy is known as the disruptive selection model. In this model, anisogamy evolves from isogamy through the disruptive selection on gamete size resulting from the fitness trade-off between gamete size and number when development favours a large zygote. Game-theoretic formulations of this theory have assumed that zygote survival is a sigmoidal function of zygote size. Models have also implicitly assumed that linkage disequilibrium between a mating type locus and a gamete size locus arises by genetic drift. These assumptions are being analysed in a population genetic model of the evolution of anisogamy.

Wilson's bird-of-paradise

The Evolution of Sex: Hill-Robertson Interference and Red Queen Dynamics

The evolution of sex and recombination is one of the most vexing problems in evolutionary biology.

Early assessments and more recent work point to one general genetic mechanism favouring recombination: Hill-Robertson interference. This is the tendency of beneficial mutations to occur on chromosomes with deleterious mutations in finite populations because higher fitness chromosomes quickly spread to fixation and lower fitness chromosomes are quickly removed by selection. The resulting negative linkage disequilibrium among polymorphisms reduces the rate of adaptation. Recombination may hasten adaptation by randomising the association among beneficial and deleterious alleles, thus increasing the variance in fitness among individuals. In this way an allele at a locus that causes recombination may hitchhike to fixation with the high-fitness chromosomes that it generates. However, this advantage of recombination is transient in a static environment because the supply of beneficial mutations will eventually be exhausted. A continuous advantage of recombination requires a continuous supply of beneficial alleles. The most plausible source of this supply is the antagonistic coevolution of hosts and parasites, termed Red Queen dynamics. Models are being developed to test the plausibility of Hill-Robertson interference with Red Queen dynamics as a general explanation for the evolution of costly sex.


  • da Silva, J., and J. D. Galbraith, 2017 Hill–Robertson interference maintained by Red Queen dynamics favours the evolution of sex. Journal of Evolutionary Biology 30: 994-1010.
The Red Queen with Alice
Evolutionary Genetics

Department of Genetics & Evolution
School of Biological Sciences
The University of Adelaide
SA 5005


Jack da Silva
T: +61 8 8313 8083
F: +61 8 8313 4362