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Unlike many acute viral diseases that produce
life-long resistance to reinfection, Plasmodium elicits immunity only after
several years of continuous exposure, during which recurring infections and
illness occur (Taylor- Robinson, 2010). Robert Koch first reported a scientific
basis for naturally acquired protection against malaria (Koch, 1900). Using
cross-sectional studies of stained blood films, Koch deduced that protection
against malaria was acquired only after heavy and uninterrupted exposure to the
parasite. But it is not clear that as to how this protection comes about, and
there is only little knowledge on the key determinants of protection (Doolan et
al., 2009). Natural immunity against malaria develops only gradually over many
years of repeated and multiple infections in endemic areas (Marsh and
Kinyanjui,2006; Langhorne et al., 2008; Crompton et ai, 2010). The
identification of immune correlates of protection among the abundant
non-protective host responses remains a research priority. While evasion and
modulation of the host immune response clearly occurs throughout the Plasmodium
life cycle, immune mechanisms to control blood-stage parasites are acquired and
maintained by individuals living in malaria endemic areas, allowing parasite

densities to be kept below the threshold for the
induction of acute disease and providing protection against severe malaria
pathology (Lundie, 2011). In human host, it appears that natural immunity is
acquired only to blood stages. Conversely, naturally acquired immunity to
pre-erythrocytic stages is not believed to occur and this is likely due to the
small infectious

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load, the immunotolerant
state of the liver as well as host impairment of the liver-stage infection in
individuals with blood stage disease (Portugal et al., 2011). Once established,
anti-malarial immunity appears to be a ‘regional phenomenon’, as seen in labor
migrants or refugees who lose protection against re-infection when moving to
geographically separate places (Struik and Riley, 2004). The notion of ‘P.
falciparum diversity’ provides a rationalefor the observed slow acquisition of
natural immunity and strongly cautions against over-simplified vaccine
strategies that originate from clonal laboratory isolates

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