Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLASMODIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources
PubMed2002

Molecular phylogenetic analysis of the avian malarial parasite Plasmodium (Novyella) juxtanucleare.

Plasmodium (Novyella) juxtanucleare is a widely distributed parasite that primarily infects chickens (Gallus gallus domesticus). All species of Novyella are characterized by very small schizonts, which in the case of P. juxtanucleare are always found juxtaposed to the erythrocyte nucleus, hence its name. Nearly complete small-subunit ribosomal RNA sequences have been obtained from 2 isolates of this species, and comparisons with other Plasmodium species have been made. Phylogenetic analysis reveals that this parasite is closely related to other avian-infecting Plasmodium species and that molecular relationships among the avian-infecting plasmodia do not correspond to their morphology-based subgeneric classifications.

Animals↗
PubMed2003

Rapid phagocytosis and melanization of bacteria and Plasmodium sporozoites by hemocytes of the mosquito Aedes aegypti.

Mosquitoes are vectors of many deadly and debilitating pathogens. In the current study, we used light and electron microscopies to study the immune response of Aedes aegypti hemocytes to bacterial inoculations, Plasmodium gallinaceum natural infections, and latex bead injections. After challenge, mosquitoes mounted strong phagocytic and melanization responses. Granulocytes phagocytosed bacteria singly or pooled them inside large membrane-delimited vesicles. Phagocytosis of bacteria, Plasmodium sporozoites, and latex beads was extensive; we estimated that individual granulocytes have the capacity to phagocytose hundreds of bacteria and thousands of latex particles. Oenocytoids were also seen to internalize bacteria and latex particles, although infrequently and with low capacity. Besides phagocytosis, mosquitoes cleared bacteria and sporozoites by melanization. Interestingly, the immune response toward 2 species of bacteria was different; most Escherichia coli were phagocytosed, but most Micrococcus luteus were melanized. Similar to E. coli, most Plasmodium sporozoites were phagocytosed. The immune response was rapid; phagocytosis and melanization of bacteria began as early as 5 min after inoculation. The magnitude and speed of the cellular response suggest that hemocytes, acting in concert with the humoral immune response, are the main force driving the battle against foreign invaders.

Aedes↗
PubMed2006

NK cell responses to Plasmodium infection and control of intrahepatic parasite development.

Various components of innate and adaptive immunity contribute to host defenses against Plasmodium infection. We investigated the contribution of NK cells to the immune response to primary infection with Plasmodium yoelii sporozoites in C57BL/6 mice. We found that hepatic and splenic NK cells were activated during infection and displayed different phenotypic and functional properties. The number of hepatic NK cells increased whereas the number of splenic NK cells decreased. Expression of the Ly49 repertoire was modified in the spleen but not in the liver. Splenic and hepatic NK cells have a different inflammatory cytokines profile production. In addition, liver NK cells were cytotoxic to YAC-1 cells and P. yoelii liver stages in vitro but not to erythrocytic stages. No such activity was observed with splenic NK cells from infected mice. These in vitro results were confirmed by the in vivo observation that Rag2(-/-) mice were more resistant to sporozoite infection than Rag2(-/-) gamma c(-/-) mice, whereas survival rates were similar for the two strains following blood-stage infection. Thus, NK cells are involved in early immune mechanisms controlling Plasmodium infection, mostly at the pre-erythrocytic stage.

Animals↗
PubMed2006

CD8+ T lymphocyte-mediated loss of marginal metallophilic macrophages following infection with Plasmodium chabaudi chabaudi AS.

The splenic architecture is essential for the quick resolution of a primary infection with Plasmodium. A critical component of this architecture is the marginal zone (MZ), an area of the spleen that separates the reticuloendothelial red pulp of the spleen from the lymphoid white pulp compartment. There are two unique macrophage populations found in the MZ: MZ macrophages (MZM) found on the outer border of the MZ, and marginal metallophilic macrophages (MMM) found on the inner border, adjacent to the white pulp. We investigated the homeostasis of MMM and MZM following infection with Plasmodium chabaudi and demonstrated that a complete loss of both MMM and MZM occurred by the time of peak parasitemia, 8 days after infection. The loss was not induced by up-regulation of the inflammatory cytokines TNF or IFN-gamma. In contrast, following only CD8+ T cell depletion (not dendritic cell), MMM but not MZM were retained, implicating CD8+ T cells in the P. chabaudi-induced loss of MMM. Retention of MMM occurred in mice deficient in CD95, CD95-ligand, and perforin, indicating that these signals are involved in the death pathway of MMM. These data have significant implications for the understanding of the immune-mediated pathology of the spleen as a result of infection with Plasmodium.

Animals↗
PubMed1993

Evaluation of a nonisotopic DNA assay kit for diagnosing Plasmodium falciparum malaria in Madagascar.

This study evaluated a nonisotopic DNA assay kit for diagnosing Plasmodium falciparum malaria in an area of Madagascar where all Plasmodium species of human malaria are present and where malaria is endemic. Blood samples from 440 healthy children and 20 healthy adults were processed and assayed in a single day in a blind protocol. The parasitemia levels of the four Plasmodium species were determined by microscopic examinations and by counts of numbers of malaria parasites per 1,000 white blood cells. Relative to P. falciparum infections, the DNA assay results agreed with those of microscopy for 207 positive and 239 negative samples; two samples were scored as positive by the DNA probe that were not detected by microscopy, and 12 samples were scored as positive by microscopy but were not detected by the assay. Relative to microscopy, the sensitivity of the assay was 95%, the specificity was 99%, and the effective sensitivity threshold of the DNA probe assay was approximately 30 parasites/mm3 of blood. The assay did not detect infections with either P. vivax, P. malariae, or P. ovale alone, but detected mixed infections of P. falciparum with either P. vivax or P. ovale. With this nonisotopic DNA probe assay, we were able to process large numbers of samples efficiently and to detect P. falciparum malaria infections with high sensitivity and specificity in a population that did not display overt disease symptoms.

Adolescent↗
PubMed1997

A genetic study of a melanization response to Sephadex beads in Plasmodium-refractory and -susceptible strains of Anopheles gambiae.

A previously selected Plasmodium-refractory strain of Anopheles gambiae melanotically encapsulates many species of Plasmodium. Genetic studies of this strain have shown that this refractory phenotype is controlled by a limited number of genes, and the existence of two such genes, Pif-B and Pif-C, has been demonstrated. Further work to determine the molecular basis for this mode of refractoriness led to the discovery that the host-parasite interaction is mimicked by the mosquito's response to carboxymethyl (CM)-Sephadex beads injected into the thorax. These small beads are melanized within 24 hr in refractory mosquitoes but are rarely melanized in susceptible ones. Because of the considerable potential in using bead melanization as a model for Plasmodium refractoriness, we performed a genetic analysis of the differential response to beads. Reciprocal crosses of susceptible (4arr) and refractory (L35) mosquitoes and an analysis of F1 phenotypes were done. The F1 progeny had a phenotype similar to that of the parental refractory mosquitoes; therefore, dominant refractory allele(s) must be present in the refractory strain. Males from the reciprocal crosses had identical phenotypes, indicating that X-linked loci did not have a visible effect on the melanizing phenotype. To further study the mode of inheritance of the melanizing trait, a backcross of F1 females to 4arr males was done. The phenotypic distribution of the backcross progeny was bimodal, and the melanization phenotypes were similar to those of the susceptible and refractory parents. These data suggest that a small number of loci are responsible for the differential response to CM-Sephadex beads, and that one chromosomal region contributes strongly to the melanizing trait. Because the 4arr strain carries mutations in the pink eye (X) and red eye (III) genes, possible linkage of the melanizing phenotype to these two genes was tested. No linkage with either marker was detected. The pattern of inheritance of the melanizing phenotype is similar to that of the refractory phenotype of Pif-B; therefore, the genetic basis of the two responses may be the same.

Animals↗
PubMed1999

Immunocapture diagnostic assays for malaria using Plasmodium lactate dehydrogenase (pLDH).

We have developed two diagnostic assays based on the specific detection of Plasmodium lactate dehydrogenase (pLDH) activity. These assays exploit a panel of monoclonal antibodies that capture the parasite enzyme and allow for the quantitation and speciation of human malaria infections. An immunocapture pLDH activity assay (ICpLDH) allows for the rapid purification and measurement of pLDH from infected blood using the NAD analog APAD, which reacts specifically with Plasmodium LDH isoforms. An immunochromatographic test (the OptiMAL assay) was also formatted and allowed the detection of parasite infections of approximately 200 parasites/microl of blood. By using a combination of antibodies, both tests can not only detect but differentiate between P. falciparum and non-P. falciparum malaria. Both assays show a sensitivity comparable with other commercial nonmicroscopic tests; importantly, we found very few instances of false-positive samples, especially with samples from patients recently cleared of malaria infection. Furthermore, we find that when one uses the quantitative ICpLDH assay, the levels of pLDH activity closely mirror the levels of parasitemia in both initial diagnosis and while following patient therapy. We conclude that diagnostic tests based on the detection of pLDH are both sensitive and practical for the detection, speciation, and quantitation of all human Plasmodium infections and can also be used to indicate drug-resistant infections.

Animals↗
PubMed1988

Plasmodium relictum as a cause of avian malaria in wild-caught magellanic penguins (Spheniscus magellanicus).

Avian malaria (Plasmodium relictum) caused significant mortality in wild-caught Magellanic penguins (Spheniscus magellanicus) in 1986 at the Blank Park Zoo in Des Moines, Iowa (USA). In early winter, wild birds were captured off the southern coast of Chile and flown to Detroit, Michigan for a 38 day quarantine. After quarantine, 18 birds were dispersed to Lansing, Michigan, six to a facility in Maine, and 46 to Des Moines, Iowa. Upon arrival in Des Moines, several penguins became weak and inactive, had to be force-fed, and died after 2 days. Gross lesions at postmortem included splenomegaly, hepatomegaly, and pulmonary edema. Histopathological examination revealed numerous intraendothelial schizonts in spleen, lung, liver, heart and kidney. Schizonts were generally 16 to 28 micron by 11 to 16 micron and contained merozoites of two distinct sized (macromerozoites, nuclei 1.0 micron; micromerozoites, nuclei 0.5 micron). Based on the morphology of the abundant exoerythrocytic forms, a tentative diagnosis of avian malaria (Plasmodium sp.) was made. Subsequent transmission electron microscopic examination of schizonts in formalized tissue revealed merozoites with tear-shaped rhoptries. Antimalarial therapy was initiated early but deaths continued for 5 mo. Mortality, which eventually totaled 83%, occurred in three distinct waves, each separated by a hiatus of approximately 1 mo. Despite examinations of repeated blood smears, intraerythrocytic Plasmodium relictum was not detected until late in the outbreak. Diagnosis was based on morphologic characteristics including schizonts with eight to 12 merozoites/segmenter and round gametocytes that displaced and turned the infected erythrocyte nucleus. In addition to malaria, penguins showed evidence of aspergillosis, bacterial enteritis (Escherichia coli; Proteus sp.; and Edwardsiella sp.), and helminthiasis (Contracaecum sp. and Tetrabothrius sp.). Based on gross and histological lesions, disease prevalence in this group of penguins was malaria 58%, aspergillosis 61%, enteritis 60%, helminthiasis 26%. Epidemiologic investigation including group transport history, disease prevalence in co-quarantined birds not sent to Des Moines and climatological data implicated Des Moines as the likely site for initial exposure, although information is not conclusive. Stress and concurrent disease certainly contributed to the severe mortality in this group of penguins infected with P. relictum.

Animals↗
PubMed1998

Chronosexuality of Plasmodium species of Central African Muridae.

A host harbouring many parasite species of the same genus is a phenomenon frequently observed in numerous parasitic infections. This is the case for the Plasmodium parasites of Muridae in Central Africa, where three different parasite species are found in the same rodent host species. It is highly likely that these three Plasmodium species are transmitted simultaneously by the same vector. We and others have shown that the maturation periods of the various asexual and sexual stages in the rodent, differ amongst the three parasites. In this article we propose that these differences are the product of complex adaptations which result, for all three Plasmodium species, in a maximum peak of infectivity to the insect vector occurring around 3 a.m., the period of highest activity of the nocturnal host rodent.

Animals↗
PubMed1999

[Rapid resolution of Plasmodium ovale malarial attacks using artesunate (Arsumax)].

This randomized, non-comparative clinical trial without placebo was carried out to assess the efficacy and tolerance of artesunate for treatment of acute Plasmodium ovale malarial attacks. Thirty Cameroonese patients were included. All presented acute Plasmodium ovale malarial attacks with parasitemia in excess of 500 asexual forms per mm3. Four days after treatment with artesunate, all 30 patients were asymptomatic with no parasitemia. Reduction rates were 93.9 p. 100 for asexual forms and 75.4 p. 100 for gametocytes. Parasite clearance was achieved within 38.8 hours and fever disappeared within 36.6 hours. Tolerance was excellent in 29 patients. The remaining patient briefly complained of mild vertigo. A transient decrease in reticulocyte levels was observed in one patient initially presenting anemia. Artesunate appears to achieve rapid and complete resolution of acute Plasmodium ovale malarial attacks. Since artesunate eliminates both asexual forms and gametocytes, it also acts on transmission by limiting the duration of survival of asexual forms.

Acute Disease↗
PubMedDate not supplied

[Mechanisms and dynamics of drug resistance in Plasmodium falciparum].

The emergence of chloroquine resistance has been associated with a dramatic increase in malaria mortality in some human populations from endemic regions. Plasmodium falciparum drug resistant malaria originates from chromosomal mutations. Analysis using molecular, genetic and biochemical approaches has shown that 1) impaired intake of chloroquine by the parasite vacuole is a common characteristic of resistant strains, the chloroquine-resistance mechanism regulates the access of chloroquine to hematin, this phenotype correlates with Pfmdr1 and Pfcg2 gene mutations; 2) one to four point mutations of dihydrofolate reductase, the enzyme target of antifolinics (pyrimethamine and proguanil), give moderate to high levels of resistance to these drugs but there is a fitness cost to resistance; 3) the mechanism of resistance to sulfonamides and sulfones involves mutations of dihydropteroate synthase, their enzyme target; 4) treatment with sulphadoxine-pyrimethamine (SP) selected for the variants Ile(51), Arg(59) and Asn(108) of DHFR and for the variants Ser(436), Gly(437), and Glu(540) of DHPS; 5)clones that were resistant to some traditional antimalarial agents acquired resistance to new ones at high frequency (accelerated resistance to multiple drugs--ARMD). Amino-alcohol (quinine, mefloquine, halofantrine) mechanisms of resistance are still unclear. Population genetic studies have confirmed that selfing is more frequent in Plasmodium falciparum where the transmission rate is lower in some regions such as Papua-New Guinea, whereas isolates from individuals on the Thai-Burmese border, an area of hypoendemic transmission, revealed a higher number of genotypes per infected person. It has been suggested that intense intra-host competition between co-infecting clones, low numbers of genes required to encode resistance, and high drug usage all encourage the emergence of drug resistance. On the other hand, the greater effective recombination in high transmission areas may breakdown multiple drug resistance when it is coded for by two unlinked loci. Epidemiological studies have established that the frequency of chloroquine resistant mutants varies among parasite isolate populations while resistance to antifolinics is highly prevalent in most malarial endemic countries (more than 92% of Kenyan field isolates have undergone at least one point mutation). Established and strong drug pressure as well as low antiparasitic immunity probably explains the multidrug-resistance encountered in forests of Southeast Asia and South America. In Africa, frequent genetic recombinations in Plasmodium originate from a high level of malaria transmission, and falciparum chloroquine-resistant prevalence seems to stabilise at an equal level as chloroquine-sensitive malaria. Clinical studies demonstrated that control of clinical symptoms is better when chloroquine is used with sulphadoxine-pyrimethamine (SP) than when SP is used alone, and the cure rate also tends to be higher with the triple combination regimen.

Animals↗
PubMed1999

Biosynthesis of glycosylphosphatidylinositols of Plasmodium falciparum in a cell-free incubation system: inositol acylation is needed for mannosylation of glycosylphosphatidylinositols.

The structures of glycosylphosphatidylinositols (GPIs) in Plasmodium have been described [Gerold, Schuppert and Schwarz (1994) J. Biol. Chem. 269, 2597-2606]. A detailed understanding of GPI synthesis in Plasmodium is a prerequisite for identifying differences present in biosynthetic pathways of parasites and host cells. A comparison of the biosynthetic pathway of GPIs has revealed differences between mammalian cells and parasitic protozoans. A cell-free incubation system prepared from asexual erythrocytic stages of Plasmodium falciparum, the causative agent of malaria in humans, is capable of synthesizing the same spectrum of GPIs as that found in metabolically labelled parasites. The formation of mannosylated GPIs in the cell-free system is shown to be inhibited by GTP and, unexpectedly, micromolar concentrations of GDP-Man. Lower concentrations of GDP-Man affect the spectrum of GPIs synthesized. The inositol ring of GPIs of P. falciparum is modified by an acyl group. The preferred donor of this fatty acid at the inositol ring is myristoyl-CoA. Inositol acylation has to precede the mannosylation of GPIs because, in the absence of acyl-CoA or CoA, mannosylated GPIs were not detected. Inositol myristoylation is a unique feature of plasmodial GPIs and thus might provide a potential target for drug therapy.

Acetylglucosamine↗
PubMed1999

Genome plasticity and sexual differentiation in Plasmodium.

Spontaneous subtelomeric deletions of Plasmodium chromosomes have been observed both in natural infections and in laboratory maintained parasites. In the latter case, functions dispensable for asexual parasite multiplication and encoded at the extremities of the chromosomes are easily lost. In particular, spontaneous subtelomeric deletions have been characterised which affect gametocytogenesis both in Plasmodium berghei maintained in laboratory animals and in Plasmodium falciparum propagated in in vitro cultures. In order to identify these genetic determinants, and, potentially, other genes located subtelomerically, we designed a transfection system able to induce and select for controlled, site-specific subtelomeric deletions.

Animals↗
PubMed1999

Protective immunity against Plasmodium berghei malaria after administration of interleukin-12.

Interleukin-12 (IL-12) has been shown to induce protection in mice against Plasmodium cyanomolgi and in rhesus monkey against Plasmodium yeolii. This study is to investigate whether recombinant IL-12 can induce protection in BALB/c mice against Plasmodium berghei. Five mice were given intraperitoneal injection of 7.5 micrograms/kg body weight recombinant mouse IL-12 two days prior to challenge with 5 x 10(4) of P. berghei, while mice in the control group were injected with 0.5 ml of normal saline prior to challenge. In both groups, the parasitaemia appeared on the fourth day after the infection. There was a slight reduction in the parasite burden in mice given IL-12 and the mice also survived longer compared to controls. Statistical significance of the difference could not be determined due to the small sample size. Nevertheless, the results of the study suggested that IL-12 may be able to protect mice against P. berghei infection.

Animals↗
PubMed2000

[Drug resistance of Plasmodium falciparum in coastal regions of Madagascar].

Chloroquine is still the drug of choice for first-line treatment of uncomplicated malaria in Madagascar. However development and spread of chloroquine-resistance could compromise this therapeutic strategy in the future. The purpose of this 1997 study was to compare the efficacy of combined treatment using sulfadoxine and pyrimethamine and single-agent treatment using chloroquine for management of uncomplicated malaria. Study data were collected at four sites in coastal areas of Madagascar where transmission of malaria is perennial. Prevalence of malaria ranged from 15 p. 100 to 22 p. 100 in school children and from 24 p. 100 to 72 p. 100 in outpatient consulting spontaneously at community health centers. All four Plasmodium species affecting man were identified. Plasmodium falciparum was involved in 83 p. 100 of cases. In vivo testing of the susceptibility of Plasmodium falciparum to chloroquine was performed in 149 patients according to the standard simplified 7-day protocol of the WHO. The 35 tests in school children demonstrated no evidence of resistance. However type R1 + R2 resistance was noted in 17 of the 114 tests performed on outpatients, i.e. 14.9 p. 100. In vitro testing demonstrated chloroquine resistance in four of the 90 specimens tested, i.e. 4.4 p. 100. With regard to combined sulfadoxine/pyrimethamine treatment, 45 of 46 in vivo tests in outpatients showed no evidence of resistance. Combination treatment was more effective than single-agent treatment (p = 0.02) and could offer an effective alternative for future use.

Adolescent↗
PubMed1998

[Cloning and sequencing of the gene coding the sexual stage antigen Pfs48/45 of Plasmodium falciparum].

AIM: To express the antigen Pfs48/45 in vitro and provide an antigen for the development of the transmission-blocking vaccine. METHODS: According to the published nucleotide sequence of Pfs48/45 of Plasmodium falciparum isolate NF54, a pair of oligonucleotides was designed and used as primers(P1, P2). The gene encoding the gametocyte/gamete-specific membrane protein Pfs48/45 of P. falciparum isolate FCC1/HN has been amplified by using polymerase chain reaction (PCR) technique. The PCR product was purified and directly sequenced by the dideoxynucleotide terminator method with 5'-end primer P1. At the same time, the purified PCR product was digested with BamHI and EcoRI and cloned into the plasmid pcDNA3, then the recombinant clones were transformed into E. coli strain TG1. The recombinant plasmid pcDNA3-Pfs48/45 was screened and identified by PCR amplification and restriction analysis. RESULTS: 1. The gene fragment Pfs48/45 was specifically amplified from the genomic DNA of Plasmodium falciparum isolate FCC1/HN; 2. The sequence demonstrated that the that the 5'-end nucleotide and predicted aminoacid sequence of Pfs48/45 from FCC1/HN isolate was basically identical with that from NF54 isolate. We found that the sequence of the Pfs48/45 gene from the isolate FCC1/HN differs from the published sequence(isolate NF54) only at positions 307 and 372(T-->C). The substitution of T-->C at the position of 372 generates a new restriction site Taq I. The PCR product digested by Taq I generates DNA fragment of 984 bp and 379 bp, suggesting that the PCR product is the gene encoding the transmission blocking antigen Pfs48/45; 3. The gene fragment of Pfs48/45 was directly inserted into the BamHI and EcoRI site of plasmid pcDNA3. CONCLUSION: The nucleotide sequence of Pfs48/45 of Plasmodium falciparum isolate FCC1/HN from south China was similar to that of isolate NF54. The recombinant plasmid pcDNA3-Pfs48/45 was successfully constructed, providing a means to evaluate the role and biological function of this sexual-stage-specific protein of Pfs48/45.

Amino Acid Sequence↗
PubMed1999

[Cloning and sequence analysis of histidine-rich protein-II gene fragment of Plasmodium falciparum yunnan strain].

AIM: To determine the nucleotide sequence of the partial gene of the histidine-rich protein II (HRP II) the Plasmodium falciparum PFD-3/YN and find out the differences of the HRP II gene sequence between this isolate and other isolates. METHODS: The histidine-rich protein-II gene fragment was amplified by polymerase chain reaction and cloned into M13 bacteriophage. M13-HRP II single strand DNAs of three positive clones were extracted, respectively. The nucleotide sequence of the HRP II gene fragment was determined by the dideoxy chain termination method. Using PCGENE software to compare and analyze the HRP II gene sequence among the different isolates. RESULTS: Different degrees of diversity of the HRP II gene sequences were found among Plasmodium falciparum PFD-3/YN(from China) and two other isolates (7G8 from Brazil and D10 from Gambia). The HRP II in the three isolates exhibited 70.3% homology in amino acid sequences and 68.6% homology in the nucleic acid sequences. CONCLUSION: There were differences in HRP II gene sequence among the Plasmodium falciparum PFD-3/YN and two other isolates (7G8 and D10).

Amino Acid Sequence↗
PubMed1999

Sequence analysis of the MSP 1 gene of Plasmodium falciparum isolates from Hainan, China.

AIM: To obtain the complete sequence and analyze the diversity of the MSP 1 molecule from the Chinese isolates of Plasmodium falciparum. METHODS: Genomic DNA was prepared directly from blood samples spotted on filter papers from 2 malaria patients from Baoting County, Hainan Province. PCR amplification of the target gene was carried out using 5 pairs of oligonucleotides specific for the MSP 1 gene. Direct sequencing of the target gene fragments was performed using ABI PRISM Dye Terminator Cycle Sequencing Ready Reaction Kit (Perkin Elmer) in a automatic ABI PRISM 310 Genetic Analyzer. RESULTS: For the first time, two complete sequences of the MSP1 gene from two Chinese isolates of Plasmodium falciparum were obtained. A comparison with the previously reported sequences identified them as members of the MAD20 allelic family. The deduced amino acid sequences of the MSP1 from this two Chinese isolates were identical with each other except for Blocks 2, 4 and 8. CONCLUSION: The sequences of the MSP 1 from two Chinese isolates of P. falciparum belong to the MAD20 allelic family. Minor variations through the whole sequences exist compared with the MAD20 sequence. The results provide the first evidence of the diversity of the MSP 1 molecule from Chinese isolates of Plasmodium falciparum.

Amino Acid Sequence↗