Cell Biology for Immune Evasion: Organizing Antigenic Variation, Surfaces, Trafficking, and Cellular Structures in Trypa

For any pathogen to maintain an infection for a protracted period, there is a necessity for precise adaptation to the host environment to avoid the twin perils of elimination by the host defense system or by death of the host from a fatal impact on host p

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Cell Biology for Immune Evasion: Organizing Antigenic Variation, Surfaces, Trafficking, and Cellular Structures in Trypanosoma brucei Ka Fai Leung, Paul T. Manna, Cordula Boehm, Luke Maishman, and Mark C. Field

Abstract

For any pathogen to maintain an infection for a protracted period, there is a necessity for precise adaptation to the host environment to avoid the twin perils of elimination by the host defense system or by death of the host from a fatal impact on host physiology. There is also a need to maintain a sufficiently robust infection, and hence cell number, so that the probability of transmission is maximized, but again avoiding overwhelming host resources. For African trypanosomes, which, in the case of Trypanosoma brucei gambiense, can survive within certain mammalian hosts for many years or even decades, these constraints are clearly very well met. Here we will consider several cellular systems and current thinking on how these contribute toward immune evasion and survival; specific areas are maintaining the parasite surface proteome, motility, and control of gene expression of virulence-associated surface molecules. Our focus is essentially restricted to African trypanosomes, due in part to the overwhelmingly greater understanding we have of the cell biology of these trypanosomatids.

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Introduction

Trypanosomes are members of the Excavata supergroup, a likely early branching group of Eukaryotes, which may even lie close to the root of the eukaryotic lineage. This accident of evolution makes the host of unique or unusual features in these organisms easier to comprehend as they have had some billion years to go their own way. The trypanosomes however that interest us the most are those who have

K.F. Leung • P.T. Manna • C. Boehm • L. Maishman • M.C. Field (*) Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK e-mail: [email protected] S. Magez and M. Radwanska (eds.), Trypanosomes and Trypanosomiasis, DOI 10.1007/978-3-7091-1556-5_1, # Springer-Verlag Wien 2014

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completed a circular journey, and have returned to humans, our livestock, and crop plants to share an intimate, and frequently damaging, relationship. Presently our understanding of these organisms is, rightly, biased towards those that do directly infect or impact humans, although interest in the nonparasitic species is increasing with a welcome resurgence in protistology. It is still too early to make sweeping conclusions, but initial data suggest that much of the biology of trypanosomes is highly conserved across the group. African trypanosomes, Trypanosoma brucei spp. are the causative agent of human African trypanosomiasis and nagana, a related disease in cattle. The many Leishmania species and the South American trypanosome, T. cruzi, cause leishmaniasis of varying severity and Chagas’ disease, respectively, while additional species such as Phytomonas are important plant pathogens. Hence the reach of these parasites is both deep in terms of the levels of morbidity th