Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2002-3-21
pubmed:abstractText
In areas of endemic parasite transmission, protective immunity to Plasmodium falciparum malaria is acquired over several years with numerous disease episodes. Acquisition of Abs to parasite-encoded variant surface Ags (VSA) on the infected erythrocyte membrane is important in the development of immunity, as disease-causing parasites appear to be those not controlled by preexisting VSA-specific Abs. In this work we report that VSA expressed by parasites from young Ghanaian children with P. falciparum malaria were commonly and strongly recognized by plasma Abs from healthy children in the same area, whereas recognition of VSA expressed by parasites from older children was weaker and less frequent. Independent of this, parasites isolated from children with severe malaria (cerebral malaria and severe anemia) were better recognized by VSA-specific plasma Abs than parasites obtained from children with nonsevere disease. This was not due to a higher infection multiplicity in younger patients or in patients with severe disease. Our data suggest that acquisition of VSA-specific Ab responses gradually restricts the VSA repertoire that is compatible with parasite survival in the semi-immune host. This appears to limit the risk of severe disease by discriminating against the expression of VSA likely to cause life-threatening complications, such as cerebral malaria and severe anemia. Such VSA seem to be preferred by parasites infecting a nonimmune host, suggesting that VSA expression and switching are not random, and that the VSA expression pattern is modulated by immunity. This opens the possibility of developing morbidity-reducing vaccines targeting a limited subset of common and particularly virulent VSA.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3444-50
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11907103-Adult, pubmed-meshheading:11907103-Age Factors, pubmed-meshheading:11907103-Anemia, pubmed-meshheading:11907103-Animals, pubmed-meshheading:11907103-Antibodies, Protozoan, pubmed-meshheading:11907103-Antibody Specificity, pubmed-meshheading:11907103-Antigen-Antibody Reactions, pubmed-meshheading:11907103-Antigens, Protozoan, pubmed-meshheading:11907103-Child, pubmed-meshheading:11907103-Child, Preschool, pubmed-meshheading:11907103-Cloning, Molecular, pubmed-meshheading:11907103-Erythrocytes, pubmed-meshheading:11907103-Humans, pubmed-meshheading:11907103-Immunity, Active, pubmed-meshheading:11907103-Malaria, Cerebral, pubmed-meshheading:11907103-Malaria, Falciparum, pubmed-meshheading:11907103-Merozoite Surface Protein 1, pubmed-meshheading:11907103-Plasmodium falciparum, pubmed-meshheading:11907103-Protozoan Proteins, pubmed-meshheading:11907103-Severity of Illness Index
pubmed:year
2002
pubmed:articleTitle
Plasmodium falciparum variant surface antigen expression varies between isolates causing severe and nonsevere malaria and is modified by acquired immunity.
pubmed:affiliation
Center for Medical Parasitology, Rigshospitalet and University of Copenhagen, Copenhagen, Denmark. mncmp@rh.dk
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't