Immunity to non-cerebral severe malaria is acquired after one or two infections

  title={Immunity to non-cerebral severe malaria is acquired after one or two infections},
  author={Sunetra Gupta and Robert W. Snow and Christl Ann Donnelly and Kevin Marsh and Chris I Newbold},
  journal={Nature Medicine},
In areas of stable transmission, clinical immunity to mild malaria is acquired slowly, so it is not usually effective until early adolescence. Life-threatening disease is, however, restricted to a much younger age group, indicating that resistance to the severe clinical consequences of infection is acquired more quickly. Understanding how rapidly immunity develops to severe malaria is essential, as severe malaria should be the primary target of intervention strategies, and predicting the result… 

Gradual acquisition of immunity to severe malaria with increasing exposure

It is found that immunity to severe disease was acquired more gradually with exposure than previously thought and the model suggests that physiological changes, rather than exposure, may alter the symptoms of disease with increasing age.

Immunological processes underlying the slow acquisition of humoral immunity to malaria

A large body of epidemiological evidence suggests that antibodies to Plasmodium antigens are inefficiently generated and rapidly lost in the absence of ongoing exposure, which suggests a defect in the development of B cell immunological memory.

Acquired Immunity to Malaria

This review summarizes what is understood about naturally acquired and experimentally induced immunity against malaria with the help of evolving insights provided by biotechnology and places these insights in the context of historical, clinical, and epidemiological observations.

Does malaria suffer from lack of memory?

This article critically review and challenge this interpretation of the epidemiological and experimental evidence that immunity to malaria is, to an extent, defective and that one component of this defective immune response is the inability to induce or maintain long‐term memory responses.

Age Interactions in the Development of Naturally Acquired Immunity to Plasmodium falciparum and Its Clinical Presentation

Reducing exposure to P. falciparum antigens through chemoprophylaxis early in life can delay immunity acquisition, and infants appear to acquire immunity faster than older children, but have a higher risk of developing severe forms of malaria and anaemia.

Adaptive Immunity to Plasmodium Blood Stages

Why better, sterilizing, immunity to malaria does not develop with an emphasis on the fate of memory B and T cell populations in infection is discussed.

Gammaherpesvirus Co-infection with Malaria Suppresses Anti-parasitic Humoral Immunity

The data demonstrates that an acute gammaherpesvirus infection can negatively impact the development of an anti-malarial immune response, and suggests that acute infection with EBV should be investigated as a risk factor for non-cerebral severe malaria in young children living in areas endemic for Plasmodium transmission.

Malaria : Multiclonal infections and protective immunity

It is suggested that persistence of antigenically diverse P. falciparum infections is important for protective immunity and that clearance of multiclonal infections might contribute to the rebound in clinical disease observed after IPT was stopped in some studies.

Functional antibody responses to the Plasmodium falciparum merozoite

The quantitative and qualitative differences in antibody responses to a panel of merozoite antigens in children with uncomplicated or severe malaria were evaluated using a set of assays including ELISA, Invasion Inhibition Assays (IIA), NH4SCN-ELISA and Surface Plasmon Resonance (SPR).

Correction: Age Interactions in the Development of Naturally Acquired Immunity to Plasmodium falciparum and Its Clinical Presentation

Reducing exposure to P. falciparum antigens through chemoprophylaxis early in life can delay immunity acquisition, and provides insight on the interplay between immunity and exposure-reduction interventions.



Acquired immunity and postnatal clinical protection in childhood cerebral malaria

It is clear that although the delayed peak in incidence of cerebral malaria (with age) can be generated by assuming that subsequent exposures carry a higher risk of disease, such an explanation is not compatible with the observation that severe disease rates are low among infants and young children in areas of high transmissibility.

Risk of severe malaria among African infants: direct evidence of clinical protection during early infancy.

Examination of hospital admissions in four geographically and demographically well-defined areas with differing intensities of P. falciparum transmission provides direct evidence for the very early acquisition of clinical immunity and for the existence of a period of clinical protection, which together may explain why the cumulative risk of malarial disease throughout childhood appears to decline with increasing transmission intensity.

Epidemiological significance of repeated infections with homologous and heterologous strains and species of Plasmodium.

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The use of immunofluorescent methods may provide a clearer understanding of the mechanism of partial immunity as it affects reinfection and the relationship of this partial immunity to the epidemiology and chemotherapy of the disease in endemic areas is of importance.

Malaria infection in infancy in rural Malawi.

Intervention strategies to reduce the risk of early infant infection need to be targeted toward mothers of infants at high risk in a rural area of Malawi with intense malaria transmission.

Parasite antigens on the infected red cell surface are targets for naturally acquired immunity to malaria

It is shown that the PfEMPI variants expressed during episodes of clinical malaria were less likely to be recognized by the corresponding child's own preexisting antibody response than by that of children of the same age from the same community.

Plasmodium falciparum malaria in the first year of life in an area of intense and perennial transmission

There were marked increases in P. falciparum prevalence, parasite densities, overall fever incidence and the incidence of malaria fevers with age for the first 6 months of life, and there was no initial period of protection against infection in neonates.

High incidence of asymptomatic malara infections in a birth cohort of children less than one year of age in Ghana, detected by multicopy gene polymerase chain reaction.

The level of malaria-specific IgG at birth was positively correlated with risk of infection in children 6-12 months of age, indicating that maternally derived anti-malarial IgG is correlated with exposure to malaria infection.

Infant parasite rates and immunoglobulin M seroprevalence as a measure of exposure to Plasmodium falciparum during a randomized controlled trial of insecticide-treated bed nets on the Kenyan coast.

It was demonstrated that parasite prevalence, IgM seropositivity, and the force of transmission were all significantly reduced by 50%.