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Evol Med Public Health. 2013 Jan;2013(1):135-47. doi: 10.1093/emph/eot011. Epub 2013 Jun 4.

Stress and sex in malaria parasites: Why does commitment vary?

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1
Institute of Evolutionary Biology, School of Biological Sciences, Ashworth Laboratories, University of Edinburgh, Edinburgh, UK; Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA; Department of Molecular Biology, 246 Carl Icahn Lab, Washington Road, Princeton University, Princeton, NJ, USA; Center for Infectious Disease Dynamics, Departments of Biology and Entomology, Pennsylvania State University, Millennium Science Complex, University Park, PA, USA and Centre for Immunity, Infection & Evolution. Institutes of Evolution, Immunology and Infection Research, School of Biological Sciences, Ashworth Laboratories, University of Edinburgh, Edinburgh, UK.

Abstract

For vector-borne parasites such as malaria, how within- and between-host processes interact to shape transmission is poorly understood. In the host, malaria parasites replicate asexually but for transmission to occur, specialized sexual stages (gametocytes) must be produced. Despite the central role that gametocytes play in disease transmission, explanations of why parasites adjust gametocyte production in response to in-host factors remain controversial. We propose that evolutionary theory developed to explain variation in reproductive effort in multicellular organisms, provides a framework to understand gametocyte investment strategies. We examine why parasites adjust investment in gametocytes according to the impact of changing conditions on their in-host survival. We then outline experiments required to determine whether plasticity in gametocyte investment enables parasites to maintain fitness in a variable environment. Gametocytes are a target for anti-malarial transmission-blocking interventions so understanding plasticity in investment is central to maximizing the success of control measures in the face of parasite evolution.

KEYWORDS:

Plasmodium; commitment; gametocyte; phenotypic plasticity; stress; transmission

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