// The Read Group \\

Research

Current

Previous

(the following is arbitary - and only up good through 2006. Update to follow.)

Worm life histories

Experimental demonstration that host immunity affects sexuality in parasitic nematodes (Gemmill et al. 1997, West et al. 2001)
Development of optimality models of age to maturity in gastrointestinal nematodes that made successfully predicted the quantitative relationship between life expectancy and prepatent period in gastrointestinal worms (Gemmill et al. 1999, Read et al. 2000). This relationship explains more than half the variance in prepatent period in the GI worms of mammals (which range from a few days to many months), and is one of only a very few quantitatively successful life history models.
Experimental demonstration that age to maturity in gastrointestinal worms is determined by host immune status [although to be fair, not in the way we expected it to be!] (Guinnee et al. 2003)
Experimental demonstration that host-specificity in a gastrointestinal worm is not mediated by thymus-dependent immunity (Gemmill et al. 2000).
Demonstration, using cross species data, that as predicted by population dynamical models, hosts living at higher densities have more macroparasites (Arneberg et al. 1998)

For overview of this work, see Read et al. 2000.

Pathogen sex allocation

Quantitative verification of sex allocation theory as applied to pathogens - so far as we know, the first quantitative demonstration that optimality models can make successful predictions in the infectious disease context (Read et al. 1995, West et al. 2000).
Extension of sex allocation theory in the malaria context to incorporate wide range of population genetic structures and fertility insurance (Shutler and Read 1998, Nee et al. 2002, West et al. 2002)
Determination of the halve lives of male and female gametocytes in P. chabaudi (Reece et al. 2003).

For reviews of our sex ratio work, see West et al. 2001, Read et al. 2002.

Malaria virulence

Characterisation of clonal variation of virulence in a rodent malaria (Mackinnon and Read 1999)
Experimental demonstration of positive relationships between virulence and transmission in malaria parasites (Mackinnon and Read 1999)
Experimental demonstration that P. chabaudi virulence-transmission relationship are qualitatively similar in immunised and naïve mice (Mackinnon and Read 2003)
Experimental demonstration that serial passage increases virulence - even when there is experimentally imnposed selection for avirulence (Mackinnon and Read 1999). Thus, there is evidence of factors thought to drive virulence up (within-host competition) but not of factors thought to counter this selection (host death).
Experimental demonstration that malaria parasite strains differ in their virulence to mosquitoes (Ferguson and Read 2002, Ferguson et al. 2003).
Experimental demonstration that virulence in the vertebrate host is unrelated to virulence in the vector (Ferguson et al. in press).
Experimental demonstration that inoculating dose has an effect on rodent malaria virulence, but that the effect is small compared to intrinsic clone differences in virulence (Timms et al. 2001).

For overviews of this work, see Mackinnon and Read in press, Read et al. 2002, in press

In-host competition in malaria parasites

Demonstration that there is intense competition between clonal lineages of malaria parasites proliferating within a host (Taylor et al. 1997, de Roode et al 2003)
Demonstration that competitive ability within a host need not translate in to transmission success: numerically suppressed clones can transmit better than they would have in the absence of competition (Taylor et al. 1997, Taylor and Read 1998).
Demonstration that mixed clone infections could be more infectious (Taylor et al. 1997) - though not always (de Roode et al. 2003).
Experimental demonstration that mixed clone infections can be virulent (Taylor et al. 1998) - but not always (de Roode et al. 2003).
Development of Quantitative PCR methods to determine clone dynamics in mixed clone infections [with R. Carter’s group] (Cheesman et al. 2003).

For overviews of this work, see Read and Taylor 2001 and Read et al. 2000.

Phenotypic effects chemotherapy and vaccination on malaria parasites

Experimental demonstration that subcurative doses of antimalarial drugs can induce surviving parasites to produce more transmission stages. In our hands, this had the effect of negating any transmission-blocking advantages of chemotherapy (Buckling et al. 1997, 1999, Buckling and Read 1999)
Experimental demonstration of strain-specific transmission blocking immunity in rodent malaria (Buckling and Read 2001)

Immunity

Experimental demonstration of strain-specific immunity in invertebrates (Little et al. 2003)
Andrea and Gráinne to provide many more highlights over the next few years.

Hypotheses/Theory

An argument that vaccination can prompt virulence evolution, so as to degrade the public health benefits of vaccines seen in clinical trials and possibly make things worse than the pre-vaccine era in the medium term (Gandon et al. 2001, 2002, 2003)
The argument that chemotherapy could promote life history evolution in parasites, in clinically-beneficial and -harmful ways (Skorping and Read 1998).
The idea of reproductive restraint in malaria parasites (Taylor and Read 1997)
An adaptive explanation (yet to be falsified) of the apparently pointless and very hazardous migrations under taken through host tissues by nematode worms (Read and Skorping 1995).
The question of why helminth immunogenetics, as opposed to host immunogenetics, was receiving no attention (Read and Viney 1996).
Extension of sex allocation theory in the malaria context to incorporate wide range of population genetic structures and fertility insurance (Shutler and Read 1998, Nee et al. 2002, West et al. 2002)
Making explicit the argument that the evolution of sex may well have multiple causes (Lively et al. 1999) - for a very large series of replies/abuse this article generated, see J. Evol. Biol. 12 1013-1055.