**Part 5**

**Malaria Immunology** 

172 Malaria Parasites

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**10** 

*Kenya* 

Sam M. Kinyanjui

**The Immunology of Malaria** 

*KEMRI-Wellcome Trust Research Programme, Kilifi,* 

The main impetus for trying to understand immunity to malaria is the need to develop effective malaria vaccines. Despite years of knowing that humans can be immune to malaria the mechanisms underlying this immunity are yet to be properly understood. This is, in part, attributable to the complexity of the malaria parasite and its life cycle resulting in a complex parasite-host relation. The outcome of a malaria infection is a consequence of interactions between host, parasite and environmental factors. As such attempts to correlate outcome with a single immunological parameter often results in spurious associations that do not hold in different circumstances. This situation is exacerbated by the lack of natural animal models for human malaria from which observations could reliably be extrapolated. Consequently, much of our understanding of malaria immunity is based on extrapolation of

As is the case with immunity to other infections, immunity to malaria is the result of a combination of genetic resistance, non-adaptive immunity, and acquired or adaptive immunity. This chapter will mainly focus on immunity to *Plasmodium falciparum* malaria because it accounts for largest proportion of disease and practically all malaria mortality.

Population genetics studies suggest that a large proportion of the variability in malaria incidence among people residing in a malaria endemic area may be attributable to genetic factors (Mackinnon *et al* 2005). This indicates that in addition to the well known genetic variations in red cell components there are a number of other genetic variations, albeit with less obvious phenotype, that also affect susceptibility to malaria. The discovery of these variations has accelerated in the recent while thanks to advances in molecular biology techniques especially the capacity to do high throughput DNA sequencing (Williams 2009).

**2.1 Protection against malaria by haemoglobinopathies and other red cell mutations**  Haldane in 1949 was the first to hypothesize that certain red cell mutations reached unexpectedly high prevalence in malaria endemic areas because these mutations protect against malaria and hence confer survival advantage over non-carriers (Haldane 1949, Piel *et al* 2010, Weatherall 1997). This hypothesis has since been confirmed through a number of studies that have reported over 80% protection against severe malaria among sickle cell

in vitro observations or deduced from phenomenological observations.

**2. Genetic resistance to malaria** 

**1. Introduction** 
