Plasmodium berghei

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Plasmodium berghei
Blood-borne forms
Blood-borne forms
Scientific classification Edit this classification
Domain: Eukaryota
Clade: Diaphoretickes
Clade: SAR
Clade: Alveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemospororida
Family: Plasmodiidae
Genus: Plasmodium
Species:
P. berghei
Binomial name
Plasmodium berghei
Vincke & Lips, 1948
Strains

Plasmodium berghei is a

parasite causing rodent malaria. It is in the Plasmodium subgenus Vinckeia
.

Originally, isolated from

thicket rats in Central Africa, P. berghei is one of four Plasmodium species that have been described in African murine rodents, the others being P. chabaudi, P. vinckei, and P. yoelii. Due to its ability to infect rodents and relative ease of genetic engineering, P. berghei is a popular model organism
for the study of human malaria.

Biology

Like all malaria parasites of

cerebral murine malaria, CMM). These symptoms are to a certain degree comparable to symptoms of cerebral malaria in patients infected with the human malaria parasite Plasmodium falciparum.[3]

Although sexuality is necessary in vivo in P. berghei as normal for most sexual organisms, it is a stark competitive disadvantage in vitro. Sinha et al., 2014 implement both mechanical passaging and competitive assay to demonstrate the advantage of loss of gametocyte production: During mechanical passage successive generations are found to naturally trend toward lower gametocytaemia; and nonsexuals outcompete sexuals rapidly when placed together in vitro.[4]: 575 

Immunochemistry

cerebral murine malaria.[2] Martins et al., 2016 find blockade of endothelin-1 prevents CMM and its symptoms and supplementation helps to produce it.[2] Subramaniam et al., 2015 find mice increase production of BTNL2 during infection and so it is probably protective.[2] Chertow et al., 2015 find the asymmetric dimethylarginine-to-arginine ratio is indicative of disease severity in mice with P. berghei ANKA.[5][6] This ratio is a metric of arginine bioavailability and in this disease they find it predicts degree of endothelial dysfunction.[5][6]

Strains

Some strains produce

See section above for specific molecules' interactions.

Distribution

Plasmodium berghei is found in the forests of

surdaster) and the mosquito (Anopheles dureni
).

Hosts

Plasmodium berghei was first identified in the thicket rat (

Meriones unguiculatus).[7] In M. musculusP. b. ANKA, downregulation of responses is necessary to prevent self-inflicted damage leading to CMM.[8][9]: 97  Specifically, Sarfo et al., 2011 finds mice produce the cytokine interleukin-10 (cIL-10) to suppress otherwise-potentially-deadly CMM damage from others of their own immune factors.[8][9]

The natural insect host of P. berghei is likely Anopheles dureni, however in laboratory conditions it has also been shown to infect An. stephensi.[citation needed]

Gene interactions

In

cerebral murine malaria. Kassa et al., 2016 finds several genes
to be of no effect:

They find one improves survival probability:

: 221 

Treatment

Some phytochemicals show efficacy against P. berghei. Bankole et al., 2016 find Markhamia tomentosa to be highly effective, comparable to chloroquine, while Monoon longifolium is also significantly effective. They find Trichilia heudelotii to be ineffective.[16]

History

This species was first described by Vincke and Lips in 1948 in the Belgian Congo.[17]

erythrocytes
; visualised using a fluorescence microscope
Infected mouse, with P. berghei in the lungs, spleen and adipose tissue. Transgenic parasites are visualized by their expression of the bioluminescent reporter protein Luciferase
A liver cell with P. berghei (a schizont with daughter parasites) expressing mCherry (red). Here the parasite membrane is stained green with an antibody, while the nuclei of liver cells and parasites are stained with DAPI (blue)

Research

Plasmodium berghei infection of laboratory mouse strains is frequently used in research as a model for human malaria.[18] In the laboratory the natural hosts have been replaced by a number of commercially available laboratory mouse strains, and the mosquito Anopheles stephensi, which is comparatively easily reared and maintained under defined laboratory conditions.

P. berghei is used as a model organism for the investigation of human

genetically manipulated
more easily than the species which infect humans, making it a useful model for research into Plasmodium genetics.

In several aspects the pathology caused by P. berghei in mice differs from malaria caused by P. falciparum in humans. In particular, while death from P. falciparum malaria in humans is most frequently caused by the accumulation of

immune cells in brain blood vessels.[18] This has led some to question the use of P. berghei infections in mice as an appropriate model of cerebral malaria in humans.[18]

P. berghei can be genetically manipulated in the laboratory using standard

genetic modification.[19][20][21] Additionally, the genome of P. berghei has been sequenced and it shows a high similarity, both in structure and gene content, with the genome of the primate malaria parasite Plasmodium falciparum.[22][23][24]

A number of genetically modified P. berghei lines have been generated which express fluorescent reporter proteins such as

bioluminescent reporters such as Luciferase. These transgenic parasites are important tools to study and visualize the parasites in the living host.[25][26]

P. berghei is used in research programs for development and screening of anti-malarial drugs and for the development of an effective vaccine against malaria.[27]

References