Cytofluorograf Detection of Plasmodium yoelii, Trypanosoma gambiense, and Trypanosoma equiperdum by Laser Excited Fluorescence of Stained Rodent Blood

1977 ◽  
Vol 63 (4) ◽  
pp. 593 ◽  
Author(s):  
Peter R. Jackson ◽  
Donald G. Winkler ◽  
Stephen L. Kimzey ◽  
Frank M. Fisher
Keyword(s):  
Plasmodium Yoelii ◽  
Trypanosoma Equiperdum ◽  
Trypanosoma Gambiense

scholarly journals Genome sequence, transcriptome, and annotation of rodent malaria parasite Plasmodium yoelii nigeriensis N67

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Cui Zhang ◽  
Cihan Oguz ◽  
Sue Huse ◽  
Lu Xia ◽  
Jian Wu ◽  
...  
Keyword(s):  
Dna Sequences ◽  
Malaria Parasite ◽  
Vaccine Development ◽  
De Novo ◽  
Gene Families ◽  
Plasmodium Yoelii ◽  
Control Measures ◽  
Effective Control ◽  
Malaria Parasites ◽  
Rodent Malaria

Abstract Background Rodent malaria parasites are important models for studying host-malaria parasite interactions such as host immune response, mechanisms of parasite evasion of host killing, and vaccine development. One of the rodent malaria parasites is Plasmodium yoelii, and multiple P. yoelii strains or subspecies that cause different disease phenotypes have been widely employed in various studies. The genomes and transcriptomes of several P. yoelii strains have been analyzed and annotated, including the lethal strains of P. y. yoelii YM (or 17XL) and non-lethal strains of P. y. yoelii 17XNL/17X. Genomic DNA sequences and cDNA reads from another subspecies P. y. nigeriensis N67 have been reported for studies of genetic polymorphisms and parasite response to drugs, but its genome has not been assembled and annotated. Results We performed genome sequencing of the N67 parasite using the PacBio long-read sequencing technology, de novo assembled its genome and transcriptome, and predicted 5383 genes with high overall annotation quality. Comparison of the annotated genome of the N67 parasite with those of YM and 17X parasites revealed a set of genes with N67-specific orthology, expansion of gene families, particularly the homologs of the Plasmodium chabaudi erythrocyte membrane antigen, large numbers of SNPs and indels, and proteins predicted to interact with host immune responses based on their functional domains. Conclusions The genomes of N67 and 17X parasites are highly diverse, having approximately one polymorphic site per 50 base pairs of DNA. The annotated N67 genome and transcriptome provide searchable databases for fast retrieval of genes and proteins, which will greatly facilitate our efforts in studying the parasite biology and gene function and in developing effective control measures against malaria.

Variable expression of virulence in the rodent malaria parasitePlasmodium yoelii yoelii

Parasitology ◽  
1980 ◽  
Vol 81 (1) ◽  
pp. 211-219 ◽  
Author(s):  
G. Knowles ◽  
D. Walliker
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Marked Decrease ◽  
Plasmodium Yoelii ◽  
Intermediate Level ◽  
Rodent Malaria ◽  
Variable Expression ◽  
Plasmodium Yoelii Yoelii

SUMMARYThe expression of the virulence character in the virulent line (YM) ofPlasmodium yoelii yoeliiwas investigated. The level of virulence was measured by counting the parasitaemia of the mature red blood cells. Several sub-clones were isolated from the virulent line YM and each was tested for its level of virulence. Out of 10 sub-clones 1 showed a marked decrease in virulence. However, transmission of this sub-clone through mosquitoes fully restored its virulence. A clone isolated from the progeny of a cross between mild and virulent parents had an intermediate level of virulence. A sub-clone isolated from this intermediate virulent line exhibited greatly reduced virulence. Mosquito transmission of this sub-clone also restored its virulence to a level comparable with the virulent line YM.

UP REGULATION OF UBIQUITIN C-TERMINAL HYDROLASE IN THE RESPONSE OF THE MOSQUITO ANOPHELES STEPHENS TO PLASMODIUM YOELII INFECTION

2002 ◽  
Vol 9 (3) ◽  
pp. 23-27
Author(s):  
XU Xiao-chun ◽  
QU Feng-yi ◽  
SONG Gum-hong ◽  
XU Jian-nong
Keyword(s):  
Plasmodium Yoelii

Plasmodium yoelii: Influence of antimalarial treatment on acquisition of immunity in BALB/c and DBA/2 mice

2007 ◽  
Vol 116 (3) ◽  
pp. 266-272 ◽  
Author(s):  
Shi-hong Ma ◽  
Li Zheng ◽  
Ying-jie Liu ◽  
Sheng-yu Guo ◽  
Hui Feng ◽  
...  
Keyword(s):  
Plasmodium Yoelii ◽  
Antimalarial Treatment

Trypanosoma gambiense: Immune responses of neonatal rats receiving antibodies from the female

1978 ◽  
Vol 44 (1) ◽  
pp. 82-91 ◽  
Author(s):  
Tan Takayanagi ◽  
Misako Takayanagi ◽  
Yoshisada Yabu ◽  
Hirotsugu Kato
Keyword(s):  
Immune Responses ◽  
Neonatal Rats ◽  
Trypanosoma Gambiense

scholarly journals Plasmodium yoelii Sporozoites with Simultaneous Deletion of P52 and P36 Are Completely Attenuated and Confer Sterile Immunity against Infection

2007 ◽  
Vol 75 (8) ◽  
pp. 3758-3768 ◽  
Author(s):  
Mehdi Labaied ◽  
Anke Harupa ◽  
Ronald F. Dumpit ◽  
Isabelle Coppens ◽  
Sebastian A. Mikolajczak ◽  
...  
Keyword(s):  
Host Cell ◽  
Genetic Manipulation ◽  
Parasitophorous Vacuole ◽  
Plasmodium Yoelii ◽  
Blood Stage ◽  
Mammalian Host ◽  
Electron Microscopic ◽  
Rodent Host ◽  
Blood Stage Infection ◽  
Stage Infection

ABSTRACT Malaria infection starts when sporozoites are transmitted to the mammalian host during a mosquito bite. Sporozoites enter the blood circulation, reach the liver, and infect hepatocytes. The formation of a parasitophorous vacuole (PV) establishes their intracellular niche. Recently, two members of the 6-Cys domain protein family, P52 and P36, were each shown to play an important albeit nonessential role in Plasmodium berghei sporozoite infectivity for the rodent host. Here, we generated p52/p36-deficient Plasmodium yoelii parasites by the simultaneous deletion of both genes using a single genetic manipulation. p52/p36-deficient parasites exhibited normal progression through the life cycle during blood-stage infection, transmission to mosquitoes, mosquito-stage development, and sporozoite infection of the salivary glands. p52/p36-deficient sporozoites also showed normal motility and cell traversal activity. However, immunofluorescence analysis and electron microscopic observations revealed that p52/p36-deficient parasites did not form a PV within hepatocytes in vitro and in vivo. The p52/p36-deficient parasites localized as free entities in the host cell cytoplasm or the host cell nucleoplasm and did not develop as liver stages. Consequently, they did not cause blood-stage infections even at high sporozoite inoculation doses. Mice immunized with p52/p36-deficient sporozoites were completely protected against infectious sporozoite challenge. Our results demonstrate for the first time the generation of two-locus gene deletion-attenuated parasites that infect the liver but do not progress to blood-stage infection. The study will critically guide the design of Plasmodium falciparum live attenuated malaria vaccines.

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