Allelic variants of the Plasmodium falciparum merozoite surface antigen 2 (MSA-2) in a geographically restricted area of Irian Jaya

Marshall, Vikki M.; Anthony, Ronald L.; Bangs, Michael J.; Purnomo, Purnomo; Anders, Robin F.; Coppel, Ross L.

doi:10.1016/0166-6851(94)90004-3

Cited by 50 publications

(33 citation statements)

References 12 publications

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“…Several parasites express different epitopes during the process of colonization of the host. Plasmodium falciparum escapes the immune defences of the host by producing variations in the intragenic repetitive sequences in the genes that encode surface antigens such as MSA1 (Frontali, 1994) and MSA2 (Felger et al, 1994;Marshall et al, 1994;Anders et al, 1993 ;McColl et al, 1994) and in an Hsp70 homologue found throughout the asexual blood cycle and in gametocytes (Bianco et al, 1986). The results reported in this paper suggest that evading the host defences by incorporating highly immunogenic cytosolic proteins (enolase, Hsp70, etc.)…”

Section: Discussionmentioning

confidence: 74%

The highly immunogenic enolase and Hsp70p are adventitious Candida albicans cell wall proteins

Eroles¹,

Sentandreu²,

Elorza³

et al. 1997

Microbiology

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Screening cDNA libraries with polyclonal antibody preparations against Candida albicans yeast or mycelial cell walls resulted in isolation of several positive clones. Some of them encoded enolase; others encoded a protein of the 70 kDa heat-shock protein family (Hsp70p), etc. The presence of these cytosolic proteins in the cell wall of actively growing C. albicans was discovered by analytical (SDS-PAGE and Western blot) and cytological (indirect immunofluorescence) experiments. Supplementation of cell cultures with papulacandin B, an antibiotic that inhibits formation of the -glucan skeleton, resulted in the release of enolase to the supernatant fluids; this release was prevented when 0.6 M KCI was present as an osmotic stabilizer. The cell wall of C. albicans incorporated exogenously added proteins (enolase and Escherichia coli and C albicans cytosolic proteins). The presence in the C. albicans cell wall of enolase, Hsp70p, and probably other intracellular proteins that are highly immunogenic might help the fungal cells to evade the host defences, and consequently could represent a survival mechanism for C. albicans in vivo.

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Section: Discussionmentioning

confidence: 74%

The highly immunogenic enolase and Hsp70p are adventitious Candida albicans cell wall proteins

Eroles¹,

Sentandreu²,

Elorza³

et al. 1997

Microbiology

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“…Haplotypes occur at all eight vertices. Certain haplotypes were observed 10 times or less (3,25,29,31,32,41,46,48,74, and 90). The majority of haplotypes occurring 10 or more times differ from haplotype 42 by one or two steps.…”

Section: Discussionmentioning

confidence: 98%

“…These include the sporozoite stage of the parasite lifecycle, the circumsporozoite protein, and the two blood-stage merozoite surface proteins MSP-1 and MSP-2. [28][29][30][31][32][33] These proteins differ from TRAP in that they all contain major repeating epitopes or blocks of repeats. The sequence variation in these antigens has been examined in a variety of ways that have included RFLP and hybridization analysis of PCR products, as well as sequencing of PCR products both cloned and uncloned.…”

Section: Discussionmentioning

confidence: 99%

Natural polymorphism in the thrombospondin-related adhesive protein of Plasmodium falciparum.

Robson

Dolo

Hackford

et al. 1998

The American Journal of Tropical Medicine and Hygiene

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Abstract. We have developed a typing system using natural sequence variation in the thrombospondin-related adhesive protein (TRAP) gene of Plasmodium falciparum. This method permits a haplotype to be assigned to any particular TRAP gene. We have applied this method to a hospital-based, case control-study in Mali. Previous sequence variation and conservation in TRAP has been confirmed. Particular TRAP haplotypes can be used as geographic hallmarks. Because of the high level of conflict between characters, we have examined the phylogenetic relationships between parasites using a network approach. Having received patient samples from urban and periurban areas of Bamako, the majority of haplotypes were closely related and distinct from TRAP sequences present in other continents. This suggests that the structure of TRAP can only tolerate a limited number of sequence variations to preserve its function but that this is sufficient to allow the parasite to evade the host's immune system until a long-lived immune response can be maintained. It may also reflect host genetics in that certain variants may escape the host immune response more efficiently than others. For vaccine design, sequences from the major regional variants may need to be considered in the production of effective subunit vaccines.The thrombospondin-related adhesive protein (TRAP) gene of Plasmodium falciparum was first described in 1988. 1 The gene derives its name from the deduced protein sequence that contains two amino acid motifs found in the adhesive host glycoprotein thrombospondin. 2 One of these motifs is based on the amino acid sequence Glu-Trp-Ser-ProCys-Ser-Val-Thr-Cys-Gly-Lys-Gly-Thr-Arg-Ser-Arg-LysArg, which has been demonstrated to allow TRAP to bind to sulfatide. 3 The protein is present in sporozoites and erythrocytic-stage parasites. 4, 5 Antibodies against TRAP inhibit sporozoite invasion. 3 Recent data demonstrate that TRAP is expressed in mature, salivary gland sporozoites but not in hemocoel sporozoites, suggesting that TRAP may be one of the unidentified accessory molecules required for infection of the vertebrate host. 6 Data from a longitudinal and prospective study showed that the immune response to TRAP is long-lived in adults and older children but short-lived in young children. 7 There were seasonal fluctuations of the levels of specific antibodies, as well as age-dependent quantitative differences. 7 These data, together with that for the TRAP homolog sporozoite surface protein 2 (SSP2) from P. yoelii, suggesting that adoptive transfer of a CD8 ϩ cytotoxic T cell clone recognizing SSP2 gave complete protection against P. yoelii infection, suggest that TRAP would be an important component of a multi-subunit malaria vaccine. 8 Further evidence for this has been the identification of a cytotoxic T lymphocyte response to certain conserved epitopes in TRAP. 9,10 A major problem in the design of any malaria vaccine is which antigens to choose and which variants of these antigens are relevant. We have previously shown that TRAP is ...

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“…[17][18][19] There is no nucleotide sequence information on several antigens from single isolates. Marked diversity has been found in genes encoding MSP1, 20 MSP2, [21][22][23] and AMA1, 8,24 and the total repertoire of these proteins is estimated to be in the hundreds. More limited studies are available of the diversity of MSP3 25 and GLURP.…”

Section: Introductionmentioning

confidence: 99%

“…9 We have previously reported on MSP2 diversity in a collection of blood samples from four cross-sectional surveys of patients in the Oksibil region of Irian Jaya. 21,23 No individual was reinfected with a parasite expressing the same MSP2 allele, and there was a complete change in the type of MSP2 alleles circulating over the period of the study. These data were interpreted as being consistent with the existence of allelic specific immunity to MSP2.…”

Section: Introductionmentioning

confidence: 99%

Alterations in Plasmodium falciparum genotypes during sequential infections suggest the presence of strain specific immunity.

Eisen

Saul²,

Fryauff³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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Abstract. Many of the asexual stage Plasmodium falciparum proteins that are the targets of host protective responses are markedly polymorphic. The full repertoire of diversity is not defined for any antigen. Most studies have focused on the genes encoding merozoite surface proteins 1 and 2 (MSP1, MSP2). We explored the extent of diversity of some of the less studied merozoite surface antigens and analyzed the degree of complexity of malaria field isolates by deriving nucleotide sequences of several antigens. We have determined the genotype of apical membrane antigen 1 (AMA1) in a group of 30 field samples, collected over 29 months, from individuals living in an area of intense malaria transmission in Irian Jaya, identifying 14 different alleles. AMA1 genotyping was combined with previously determined MSP2 typing. AMA1 had the greatest power in distinguishing between isolates but methodological problems, especially when mixed infections are present, suggest it is not an ideal typing target. MSP1, MSP3, and glutamate-rich protein genotypes were also determined from a smaller group of samples, and all results were combined to derive an extended antigenic haplotype. Within this subset of 10 patients, nine different genotypes could be discerned; however, five patients were all infected with the same strain. This strain was present in individuals from two separate villages and was still present 12 months later. This strain was predominant at the first time point but had disappeared at the fourth time point. This significant change in malaria genotypes could be due to strain-specific immunity developing in this population.

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Allelic variants of the Plasmodium falciparum merozoite surface antigen 2 (MSA-2) in a geographically restricted area of Irian Jaya

Cited by 50 publications

References 12 publications

The highly immunogenic enolase and Hsp70p are adventitious Candida albicans cell wall proteins

The highly immunogenic enolase and Hsp70p are adventitious Candida albicans cell wall proteins

Natural polymorphism in the thrombospondin-related adhesive protein of Plasmodium falciparum.

Alterations in Plasmodium falciparum genotypes during sequential infections suggest the presence of strain specific immunity.

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