Clinical Immunity to Malaria

Abstract

Under appropriate conditions of transmission intensity, functional immunity to malaria appears to be acquired in distinct stages. The first phase reduces the likelihood of severe or fatal disease; the second phase limits the clinical impact of 'mild' malaria; and the third provides partial but incomplete protection against pathogen burden. These findings suggest clinical immunity to mortality and morbidity is acquired earlier, with greater ease, and via distinct mechanisms as compared to anti-parasite immunity, which is more difficult to achieve, takes longer and is only ever partially efficacious. The implications of this view are significant in that current vaccination strategies aim predominantly to achieve anti-parasite immunity, although imparting clinical immunity is the public health objective. Despite enormous relevance for global public health, the mechanisms governing these processes remain obscure. Four candidate mechanisms might mediate clinical immunity, namely immunity to cytoadherence determinants, tolerance to toxins, acquired immunity to toxins, and immunoregulation. This review addresses the targets and determinants of clinical immunity, and considers the implications for vaccine development.

National Malaria Prevalence in Cambodia: Microscopy Versus Polymerase Chain Reaction Estimates

“…Although not significant, the trend of lower parasitemia with increasing age in Domain 1 suggests the development of some clinical immunity to malaria. 26,27 By contrast, for individuals with vivax infections (Panel B), the geometric mean parasitemia was 50-fold lower and almost similar between age groups (84 parasites/μL in the 0-14 years age group versus 45 parasites/μL in the ≥ 15 years age, P ¼ 0.9). Our parasitemia data are consistent with those of Baird and others, who demonstrated that the development of immunity to malaria was slower for P. vivax compared with P. falciparum.…”

Advancement Towards an Approved Vaccine to Target Plasmodium Falciparum Malaria

“…29,30 As a generalisation, recurrent exposure invokes non-sterile immunity by which people have a low level parasitaemia but show few or no symptoms of disease; this is often referred to as stable malaria. 31,32 Although the adult immune system can control infections, an asymptomatic individual may act as a reservoir of infection. Moreover, immunity abates rapidly unless a person is infected repeatedly, making maintenance of immunity imperfect.…”

“…Moreover, immunity abates rapidly unless a person is infected repeatedly, making maintenance of immunity imperfect. [31][32][33] Persons with waning immunity or irregular infection thus have unstable malaria. 4 These reasons highlight further the requirement for an effective vaccine which would induce sterile immunity, i.e.…”

Malária: Dos velhos fármacos aos novos alvos moleculares

“…No entanto, se houver falha da medicação ou atraso da mesma, a parasitemia pode aumentar e a malária grave pode acontecer principalmente nas infecções por P. falciparum. Menos frequentemente, o P. vivax também provoca a forma clínica grave, assim como P. ovale e P. malariae (GREENWOOD, B. et al, 1987;MARSH et al, 1995;SCHOFIELD;MUELLER, 2006;WEINBERG;MOON, 2009). Por outro lado, indivíduos com grau leve da infecção ou sem complicações, tipicamente apresentam febre e sintomas como: arrepios, suores, dor de cabeça, vômito, diarréia, anemia, icterícia e inchaço do baço (esplenomegalia) (BAUMEISTER et al, 2006;CHAKRAVORTY;CRAIG, 2005;DEPLAINE et al, 2011;GROBUSCH;KREMSNER, 2005;KIRK et al, 2005;SALIBA, 2007;KRAEMER;SMITH, 2006;LAISHRAM et al, 2012;LAUER et al, 1997;ROWE et al, 2009).…”