View source for Plasmodium berghei

{{Short description|Single celled parasite, rodent malaria}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{Speciesbox
| image = Berghei_01.png
| image_alt = Blood-borne forms
| image_caption = Blood-borne forms
| genus = Plasmodium
| species = berghei
| authority = Vincke & Lips, 1948
| synonyms = 
| synonyms_ref = 
| subdivision_ranks = Strains
| subdivision =
* [[#ANKA|ANKA]]<ref name="Torre-et-al-2018" />
* [[#NK65|NK65]]<ref name="Moxon-et-al-2020" />
}}

'''''Plasmodium berghei''''' is a [[unicellular|single]]-celled [[parasite]] causing [[rodent malaria]]. It is in the ''Plasmodium'' subgenus ''[[Vinckeia]]''.

Originally, isolated from [[thicket rat]]s in Central Africa,<ref>{{cite journal | vauthors = Conteh S, Anderson C, Lambert L, Orr-Gonzalez S, Herrod J, Robbins YL, Carter D, Karhemere SB, Pyana P, Büscher P, Duffy PE| title = ''Grammomys surdaster'', the Natural Host for ''Plasmodium berghei'' Parasites, as a Model to Study Whole-Organism Vaccines Against Malaria | journal = The American Journal of Tropical Medicine and Hygiene | volume = 96 | issue = 4 | pages = 835–841 | date = April 2017 | pmid = 28115674 | pmc = 5392629 | doi = 10.4269/ajtmh.16-0745 }}</ref> ''P. berghei'' is one of four ''[[Plasmodium]]'' species that have been described in African [[Murinae|murine]] rodents, the others being ''[[Plasmodium chabaudi|P. chabaudi]]'', ''[[Plasmodium vinckei|P. vinckei]]'', and ''[[Plasmodium yoelii|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.<ref name=":0">{{cite journal | vauthors = Kamil M, Kina UY, Atmaca HN, Unal S, Deveci G, Burak P, Aly AS | title = Endoplasmic reticulum localized TMEM33 domain-containing protein is crucial for all life cycle stages of the malaria parasite | journal = Molecular Microbiology | volume = 121 | issue = 4 | pages = 767–780 | date = April 2024 | pmid = 38238886 | doi = 10.1111/mmi.15228 | doi-access = free }}</ref>

== Biology ==
Like all malaria parasites of [[mammal]]s, including the four human [[malaria]] parasites, ''P. berghei'' is transmitted by ''[[Anopheles]]'' mosquitoes and it infects the liver after being injected into the bloodstream by a bite of an infected female mosquito. After a short period (a few days) of development and multiplication, these parasites leave the liver and invade [[erythrocytes]] (red blood cells). The multiplication of the parasite in the blood causes the pathology such as [[anaemia]] and damage of essential organs of the host such as lungs, liver, spleen. ''P. berghei'' infections may also affect the brain and can be the cause of cerebral complications in laboratory mice ([[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]]''.<ref>{{cite journal | vauthors = Franke-Fayard B, Fonager J, Braks A, Khan SM, Janse CJ | title = Sequestration and tissue accumulation of human malaria parasites: can we learn anything from rodent models of malaria? | journal = PLOS Pathogens | volume = 6 | issue = 9 | pages = e1001032 | date = September 2010 | pmid = 20941396 | pmc = 2947991 | doi = 10.1371/journal.ppat.1001032 | doi-access = free }}</ref>

Although [[Sexual reproduction|sexuality]] is necessary ''in vivo'' in ''P. berghei'' as normal for most sexual organisms, it is a stark [[intraspecific competition|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 [[natural selection|naturally trend]] toward lower [[gametocytaemia]]; and nonsexuals outcompete sexuals rapidly when placed together ''in vitro''.<ref name="Josling-Llinas-2015">{{cite journal | vauthors = Josling GA, Llinás M | title = Sexual development in Plasmodium parasites: knowing when it's time to commit | journal = Nature Reviews. Microbiology | volume = 13 | issue = 9 | pages = 573–587 | date = September 2015 | pmid = 26272409 | doi = 10.1038/nrmicro3519 | publisher = [[Nature Portfolio]] | s2cid = 2182486 }}</ref>{{rp|575}}

=== Immunochemistry ===
[[Endothelin 1]] has an uncertain role in producing [[cerebral murine malaria]].<ref name="Moxon-et-al-2020">{{cite journal | vauthors = Moxon CA, Gibbins MP, McGuinness D, Milner DA, Marti M | title = New Insights into Malaria Pathogenesis | journal = Annual Review of Pathology | volume = 15 | issue = 1 | pages = 315–343 | date = January 2020 | pmid = 31648610 | doi = 10.1146/annurev-pathmechdis-012419-032640 | publisher = [[Annual Reviews (publisher)|Annual Reviews]] | s2cid = 204882296 }}</ref> Martins ''et al.'', 2016 find blockade of endothelin-1 ''prevents'' CMM and its symptoms and supplementation helps to ''produce'' it.<ref name="Moxon-et-al-2020" /> Subramaniam ''et al.'', 2015 find mice increase production of [[BTNL2]] during infection and so it is probably protective.<ref name="Moxon-et-al-2020" /> Chertow ''et al.'', 2015 find the [[asymmetric dimethylarginine]]-to-[[arginine]] ''ratio'' is indicative of disease severity in mice with ''P. berghei'' ANKA.<ref name="Ngai-et-al-2020">{{cite journal | vauthors = Ngai M, Weckman AM, Erice C, McDonald CR, Cahill LS, Sled JG, Kain KC | title = Malaria in Pregnancy and Adverse Birth Outcomes: New Mechanisms and Therapeutic Opportunities | journal = Trends in Parasitology | volume = 36 | issue = 2 | pages = 127–137 | date = February 2020 | pmid = 31864896 | doi = 10.1016/j.pt.2019.12.005 | publisher = [[Cell Press]] | s2cid = 209446589 }}</ref><ref name="Kayano-et-al-2016">{{cite journal | vauthors = Kayano AC, Dos-Santos JC, Bastos MF, Carvalho LJ, Aliberti J, Costa FT | title = Pathophysiological Mechanisms in Gaseous Therapies for Severe Malaria | journal = Infection and Immunity | volume = 84 | issue = 4 | pages = 874–882 | date = April 2016 | pmid = 26831465 | pmc = 4807480 | doi = 10.1128/iai.01404-15 | publisher = [[American Society for Microbiology]] | s2cid = 29927044 | veditors = Andrews-Polymenis HL }}</ref> This ratio is a metric of arginine [[bioavailability]] and in this disease they find it predicts degree of endothelial dysfunction.<ref name="Ngai-et-al-2020" /><ref name="Kayano-et-al-2016" />

=== Strains ===
Some strains produce [[cerebral murine malaria]] and some do not.<ref name="Moxon-et-al-2020" />
* {{ visible anchor |ANKA}} produces CMM.<ref name="Moxon-et-al-2020" /> Martins ''et al.'', 2016 find endothelin-1 production is vital to CMM disease progression.<ref name="Torre-et-al-2018" /> Subramaniam ''et al.'', 2015 find mice respond to ANKA by increasing BTNL2.<ref name="Moxon-et-al-2020" /> Chertow ''et al.'', 2015 find arginine metabolism indicative of disease severity.<ref name="Ngai-et-al-2020" /><ref name="Kayano-et-al-2016" />
* {{ visible anchor |NK65}} notably does not produce CMM.<ref name="Moxon-et-al-2020" /> Martins ''et al.'', 2016 find NK65 ''can'' produce CMM under supplementation of endothelin-1.<ref name="Moxon-et-al-2020" />
See section above for specific molecules' interactions.

== Distribution ==
''Plasmodium berghei'' is found in the forests of [[Central Africa]], where its natural cyclic hosts are the thicket rat (''[[Grammomys]] [[Grammomys surdaster|surdaster]]'') and the [[mosquito]] (''[[Anopheles dureni]]'').

== Hosts ==
''Plasmodium berghei'' was first identified in the thicket rat (''[[Grammomys]] [[Grammomys surdaster|surdaster]]''). It has also been described in ''[[Leggada bella]]'', ''[[Praomys jacksoni]]'' and ''[[Thamnomys]] [[Thamnomys surdaster|surdaster]].''{{citation needed|date=January 2016}} In research laboratories, various rodents can be infected, such as mice (''[[Mus musculus]]''), rats and gerbils (''[[Meriones unguiculatus]]'').<ref name="JunaidKhaw2017">{{cite journal | vauthors = Junaid QO, Khaw LT, Mahmud R, Ong KC, Lau YL, Borade PU, Liew JW, Sivanandam S, Wong KT, Vythilingam I| title = Pathogenesis of Plasmodium berghei ANKA infection in the gerbil (Meriones unguiculatus) as an experimental model for severe malaria | journal = Parasite | volume = 24 | pages = 38 | year = 2017 | pmid = 29034874 | pmc = 5642054 | doi = 10.1051/parasite/2017040 }} {{open access}}</ref> In ''M. musculus'' ⇔ ''P. b.'' ANKA, downregulation of responses is necessary to prevent self-inflicted damage leading to CMM.<ref name="Xu-et-al-2016">{{cite journal | vauthors = Xu Z, Zhang X, Lau J, Yu J | title = C-X-C motif chemokine 10 in non-alcoholic steatohepatitis: role as a pro-inflammatory factor and clinical implication | journal = Expert Reviews in Molecular Medicine | volume = 18 | pages = e16 | date = September 2016 | pmid = 27669973 | doi = 10.1017/erm.2016.16 | publisher = [[Cambridge University Press]] (CUP) | s2cid = 28322523 }}</ref><ref name="Fillatreau-O-Garra-2014">{{cite book | vauthors = Fillatreau S, O'Garra A |series=[[Current Topics in Microbiology and Immunology]]| title=Interleukin-10 in Health and Disease | journal=International Journal of Molecular Sciences | publisher=[[Springer Berlin Heidelberg]] | publication-place=[[Berlin]], [[Heidelberg]] | year=2014 | volume=20 | issue=3 | page=649 | doi=10.1007/978-3-662-43492-5 | pmid=30717382 | pmc=6387150 | isbn=978-3-662-43491-8 | issn=0070-217X}}</ref>{{rp|97}} Specifically, Sarfo ''et al.'', 2011 finds mice produce the cytokine [[interleukin 10|interleukin-10]] (cIL-10) to suppress otherwise-potentially-deadly CMM damage from others of their own immune factors.<ref name="Xu-et-al-2016" /><ref name="Fillatreau-O-Garra-2014" />

The natural insect host of ''P. berghei'' is likely ''[[Anopheles dureni]]'', however in laboratory conditions it has also been shown to infect ''[[Anopheles stephensi|An. stephensi]]''.{{citation needed|date=January 2016}}

=== Gene interactions ===
In ''[[Mus musculus]]'' ⇔ the ''P. b.'' ANKA strain various [[gene]]s affect the incidence of [[cerebral murine malaria]]. Kassa ''et al.'', 2016 finds several [[gene]]s to be of no effect:
* [[Apolipoprotein A-I]] (''[[APOA1]]'')<ref name="Torre-et-al-2018">{{cite journal | vauthors = Torre S, Langlais D, Gros P | title = Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei | journal = Mammalian Genome | volume = 29 | issue = 7–8 | pages = 488–506 | date = August 2018 | pmid = 29922917 | doi = 10.1007/s00335-018-9752-9 | publisher = [[Springer Science+Business Media]] | s2cid = 49309005 | id = [[International Mammalian Genome Society]] }}</ref>
* [[Low density lipoprotein receptor]] (''[[LDLR]]'')<ref name="Torre-et-al-2018" />
* [[Low density lipoprotein receptor-related protein 1]] (''[[LRP1]]'')<ref name="Torre-et-al-2018" />
* [[Very low density lipoprotein receptor]] (''[[VLDLR]]'')<ref name="Torre-et-al-2018" />
They find one improves survival probability:
* [[Apolipoprotein E]] (''[[APOE (gene)|APOE]]'')<ref name="Torre-et-al-2018" />

''[[Anopheles gambiae|An. gambiae]]''{{'}}s [[hemocyte]]s transcribe a wide array of molecular responses to ''Plasmodium'' infections.<ref name="Smith-et-al-2014">{{cite journal | vauthors = Smith RC, Vega-Rodríguez J, Jacobs-Lorena M | title = The Plasmodium bottleneck: malaria parasite losses in the mosquito vector | journal = Memórias do Instituto Oswaldo Cruz | volume = 109 | issue = 5 | pages = 644–661 | date = August 2014 | pmid = 25185005 | pmc = 4156458 | doi = 10.1590/0074-0276130597 | publisher = [[FapUNIFESP]] ([[SciELO]]) }}</ref><ref name="Willis-et-al-2012">{{cite book | veditors = Gilbert LI | vauthors = Willis JH, Papandreou NC, Iconomidou VA, Hamodrakas SJ | title=Insect Molecular Biology and Biochemistry | chapter=5 Cuticular Proteins | publisher=[[Elsevier]] | year=2012 | isbn=978-0-12-384747-8 | oclc=742299021 | pages=x+563}}</ref>{{rp|138}}<ref name="Clayton-et-al-2014">{{cite journal | vauthors = Clayton AM, Dong Y, Dimopoulos G | title = The Anopheles innate immune system in the defense against malaria infection | journal = Journal of Innate Immunity | volume = 6 | issue = 2 | pages = 169–181 | year = 2014 | pmid = 23988482 | pmc = 3939431 | doi = 10.1159/000353602 | publisher = [[Karger Publishers]] }}</ref><ref name="Hillyer-Strand-2014">{{cite journal | vauthors = Hillyer JF, Strand MR | title = Mosquito hemocyte-mediated immune responses | journal = Current Opinion in Insect Science | volume = 3 | pages = 14–21 | date = September 2014 | pmid = 25309850 | pmc = 4190037 | doi = 10.1016/j.cois.2014.07.002 | publisher = [[Elsevier]] | id = [[NIH Manuscript Submission|NIHMSID]] 615755 | bibcode = 2014COIS....3...14H }}</ref><ref name="Cheng-et-al-2016">{{cite journal | vauthors = Cheng G, Liu Y, Wang P, Xiao X | title = Mosquito Defense Strategies against Viral Infection | journal = Trends in Parasitology | volume = 32 | issue = 3 | pages = 177–186 | date = March 2016 | pmid = 26626596 | pmc = 4767563 | doi = 10.1016/j.pt.2015.09.009 | publisher = [[Cell Press]] }}</ref><ref name="Hillyer-2010">{{cite book | veditors = Söderhäll K | vauthors = Hillyer JF | title=Invertebrate Immunity | chapter=Mosquito Immunity |series=[[Advances in Experimental Medicine and Biology]]| publisher=[[Springer Nature]] | publication-place=[[Boston, MA]] | year=2010 | volume=708 | isbn=978-1-4419-8058-8 | issn=0065-2598 | doi=10.1007/978-1-4419-8059-5_12 | pages=218–238| pmid=21528701 }}</ref>{{rp|221}} In response to this species, Baton ''et al.'', 2009 find this includes increased expression of the ''[[prophenoloxidase]]'' gene, cascading to increase [[phenoloxidase]] and thereby [[melanization]].<ref name="Smith-et-al-2014" /><ref name="Willis-et-al-2012" />{{rp|138}}<ref name="Clayton-et-al-2014" /><ref name="Hillyer-Strand-2014" /><ref name="Cheng-et-al-2016" /><ref name="Hillyer-2010" />{{rp|221}}

== Treatment ==
Some [[phytochemical]]s show efficacy against ''P. berghei''. Bankole ''et al.'', 2016 find ''[[Markhamia]] [[Markhamia tomentosa|tomentosa]]'' to be highly effective, comparable to [[chloroquine]], while ''[[Monoon longifolium]]'' is also significantly effective. They find ''[[Trichilia]] [[Trichilia heudelotii|heudelotii]]'' to be ineffective.<ref name="Dkhil-et-al-2021">{{cite journal | vauthors = Dkhil MA, Al-Quraishy S, Al-Shaebi EM, Abdel-Gaber R, Thagfan FA, Qasem MA | title = Medicinal plants as a fight against murine blood-stage malaria | journal = Saudi Journal of Biological Sciences | volume = 28 | issue = 3 | pages = 1723–1738 | date = March 2021 | pmid = 33732056 | pmc = 7938113 | doi = 10.1016/j.sjbs.2020.12.014 | publisher = [[Elsevier]] | s2cid = 232241302 | id = [[Saudi Biological Society]] | bibcode = 2021SJBS...28.1723D }}</ref>

TMEM33 is an endoplasmic reticulum localized protein that is essential for all life cycle stages of ''Plasmodium berghei''.<ref name=":0" /> It is an important regulator of intracellular calcium homeostasis.<ref>{{cite journal | vauthors = Arhatte M, Gunaratne GS, El Boustany C, Kuo IY, Moro C, Duprat F, Plaisant M, Duval H, Li D, Picard N, Couvreux A, Duranton C, Rubera I, Pagnotta S, Lacas-Gervais S, Ehrlich BE, Marchant JS, Savage AM, van Eeden FJ, Wilkinson RN, Demolombe S, Honoré E, Patel A| title = TMEM33 regulates intracellular calcium homeostasis in renal tubular epithelial cells | journal = Nature Communications | volume = 10 | issue = 1 | pages = 2024 | date = May 2019 | pmid = 31048699 | pmc = 6497644 | doi = 10.1038/s41467-019-10045-y | bibcode = 2019NatCo..10.2024A }}</ref> In humans and other eukaryotes, TMEM33 is a stress-inducible ER transmembrane protein, and is the regulator of UPR response elements.<ref>{{cite journal | vauthors = Sakabe I, Hu R, Jin L, Clarke R, Kasid UN | title = TMEM33: a new stress-inducible endoplasmic reticulum transmembrane protein and modulator of the unfolded protein response signaling | journal = Breast Cancer Research and Treatment | volume = 153 | issue = 2 | pages = 285–297 | date = September 2015 | pmid = 26268696 | pmc = 4559576 | doi = 10.1007/s10549-015-3536-7 }}</ref> UPR regulators and ER stress response elements play an important role in the blood stage infection and mosquito transmission of ''Plasmodium berghei''.<ref name=":0" /> Targeted deletions of TMEM33 show reduced parasitemia and mortality, indicating its potential as a drug target.<ref name=":0" />

The autophagy-related genes of ''Plasmodium berghei'', ''Pb''ATG5, ''Pb''ATG8, and ''Pb''ATG12 respond to 5-fluorouracil and chloroquine treatment, resulting in their upregulation and leading to apoptosis.<ref>{{cite journal | vauthors = Unal S, Kina UY, Kamil M, Aly AS, Palabiyik B | title = Drug-induced ER stress leads to induction of programmed cell death pathways of the malaria parasite | journal = Parasitology Research | volume = 123 | issue = 7 | pages = 263 | date = July 2024 | pmid = 38976068 | pmc = 11230985 | doi = 10.1007/s00436-024-08281-3 }}</ref>

== History ==
This species was first described by Vincke and Lips in 1948 in the [[Belgian Congo]].<ref name="Vinke1948">Vincke, I.H. and Lips, M. (1948) Un nouveau plasmodium d'un rongeur sauvage du Congo: ''Plasmodium berghei'' n.sp. Annales de la Société Belge de Médecine Tropicale 28, 97-104</ref>

[[Image:Berghei 02.png|thumb|150px|left|Live ''P. berghei'' expressing [[Green Fluorescent Protein|GFP]] (green) in [[erythrocytes]]; visualised using a fluorescence microscope]]
[[Image:Berghei 03.png|thumb|150px|left|Infected mouse, with ''P. berghei'' in the lungs, spleen and [[adipose tissue]]. Transgenic parasites are visualized by their expression of the [[bioluminescence|bioluminescent]] reporter protein [[Luciferase]]]]
[[File:Liver stage malaria parasite.jpg|thumb|220px|left|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.<ref name=Craig2012>{{cite journal | vauthors = Craig AG, Grau GE, Janse C, Kazura JW, Milner D, Barnwell JW, Turner G, Langhorne J| title = The role of animal models for research on severe malaria | journal = PLOS Pathogens | volume = 8 | issue = 2 | pages = e1002401 | date = February 2012 | pmid = 22319438 | pmc = 3271056 | doi = 10.1371/journal.ppat.1002401 | doi-access = free }}</ref> 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 [[malaria]] because of its similarity to the ''Plasmodium'' species which cause human malaria. ''P. berghei'' has a very similar life-cycle to the species that infect humans, and it causes disease in mice which has [[medical sign|signs]] similar to those seen in human malaria. Importantly, ''P. berghei'' can be [[genetic manipulation|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 [[red blood cells]] in the blood vessels of the brain, it is unclear to what extent this occurs in mice infected with ''P. berghei''.<ref name=Craig2012/> Instead, in ''P. berghei'' infection, mice are found to have an accumulation of [[immune cells]] in brain blood vessels.<ref name=Craig2012/> This has led some to question the use of ''P. berghei'' infections in mice as an appropriate model of cerebral malaria in humans.<ref name=Craig2012/>

''P. berghei'' can be genetically manipulated in the laboratory using standard [[genetic engineering]] technologies. Consequently, this parasite is often used for the analysis of the function of malaria genes using the technology of [[genetic modification]].<ref name="Janse2006">{{cite journal | vauthors = Janse CJ, Ramesar J, Waters AP | title = High-efficiency transfection and drug selection of genetically transformed blood stages of the rodent malaria parasite Plasmodium berghei | journal = Nature Protocols | volume = 1 | issue = 1 | pages = 346–356 | date = 2006 | pmid = 17406255 | doi = 10.1038/nprot.2006.53 | s2cid = 20096737 }}</ref><ref>{{cite journal | vauthors = Janse CJ, Kroeze H, van Wigcheren A, Mededovic S, Fonager J, Franke-Fayard B, Waters AP, Khan SM| title = A genotype and phenotype database of genetically modified malaria-parasites | journal = Trends in Parasitology | volume = 27 | issue = 1 | pages = 31–39 | date = January 2011 | pmid = 20663715 | doi = 10.1016/j.pt.2010.06.016 }}</ref><ref>{{cite book|author1=Khan SM |author2=Kroeze H |author3=Franke-Fayard B |author4=Janse CJ |title=Malaria |chapter=Standardization in Generating and Reporting Genetically Modified Rodent Malaria Parasites: The RMGMDB Database |date=2013 |volume=923 |pages=139–50 |pmid=22990775 |doi=10.1007/978-1-62703-026-7_9|series=[[Methods in Molecular Biology]]|isbn=978-1-62703-025-0 }}</ref> 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]]''.<ref>{{cite journal | vauthors = Hall N, Karras M, Raine JD, Carlton JM, Kooij TW, Berriman M, Florens L, Janssen CS, Pain A, Christophides GK, James K, Rutherford K, Harris B, Harris D, Churcher C, Quail MA, Ormond D, Doggett J, Trueman HE, Mendoza J, Bidwell SL, Rajandream MA, Carucci DJ, Yates JR, Kafatos FC, Janse CJ, Barrell B, Turner CM, Waters AP, Sinden RE| title = A comprehensive survey of the Plasmodium life cycle by genomic, transcriptomic, and proteomic analyses | journal = Science | volume = 307 | issue = 5706 | pages = 82–86 | date = January 2005 | pmid = 15637271 | doi = 10.1126/science.1103717 | s2cid = 7230793 | bibcode = 2005Sci...307...82H }}</ref><ref>{{cite journal | vauthors = Kooij TW, Janse CJ, Waters AP | title = Plasmodium post-genomics: better the bug you know? | journal = Nature Reviews. Microbiology | volume = 4 | issue = 5 | pages = 344–357 | date = May 2006 | pmid = 16582929 | doi = 10.1038/nrmicro1392 | s2cid = 38403613 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Otto TD, Böhme U, Jackson AP, Hunt M, Franke-Fayard B, Hoeijmakers WA, Religa AA, Robertson L, Sanders M, Ogun SA, Cunningham D, Erhart A, Billker O, Khan SM, Stunnenberg HG, Langhorne J, Holder AA, Waters AP, Newbold CI, Pain A, Berriman M, Janse CJ| title = A comprehensive evaluation of rodent malaria parasite genomes and gene expression | journal = BMC Biology | volume = 12 | pages = 86 | date = October 2014 | pmid = 25359557 | pmc = 4242472 | doi = 10.1186/s12915-014-0086-0 | doi-access = free }}</ref>

A number of genetically modified ''P. berghei'' lines have been generated which express fluorescent reporter proteins such as [[Green Fluorescent Protein]] (GFP) and [[mCherry]] (red) or [[bioluminescent]] reporters such as [[Luciferase]]. These transgenic parasites are important tools to study and visualize the parasites in the living host.<ref name="Amino2005">{{cite journal | vauthors = Amino R, Ménard R, Frischknecht F | title = In vivo imaging of malaria parasites--recent advances and future directions | journal = Current Opinion in Microbiology | volume = 8 | issue = 4 | pages = 407–414 | date = August 2005 | pmid = 16019254 | doi = 10.1016/j.mib.2005.06.019 }}</ref><ref name="Franke2006">{{cite journal | vauthors = Franke-Fayard B, Waters AP, Janse CJ | title = Real-time in vivo imaging of transgenic bioluminescent blood stages of rodent malaria parasites in mice | journal = Nature Protocols | volume = 1 | issue = 1 | pages = 476–485 | year = 2006 | pmid = 17406270 | doi = 10.1038/nprot.2006.69 | s2cid = 20812965 }}</ref>

''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.<ref>{{cite journal | vauthors = Khan SM, Janse CJ, Kappe SH, Mikolajczak SA | title = Genetic engineering of attenuated malaria parasites for vaccination | journal = Current Opinion in Biotechnology | volume = 23 | issue = 6 | pages = 908–916 | date = December 2012 | pmid = 22560204 | doi = 10.1016/j.copbio.2012.04.003 }}</ref>

{{clear}}

== References ==
{{Reflist}}

{{Alveolata}}
{{Taxonbar|from=Q65021}}

== External links ==
{{Commons category}}
{{Scholia|topic}}
;General information about (the biology of) ''P. berghei'':
*[https://www.pberghei.nl/homepage/model-of-malaria www.pberghei.nl/homepage/model-of-malaria]

;Information about the genome and genes of ''P. berghei'':
*[https://www.pberghei.eu www.pberghei.eu]
*[https://plasmogem.sanger.ac.uk plasmogem.sanger.ac.uk]
*[https://www.plasmodb.org/plasmo/app www.plasmodb.org/plasmo/app]
*[https://www.ncbi.nlm.nih.gov/sites/entrez?Db=genomeprj&Cmd=Search&Term=txid5821 www.ncbi.nlm.nih.gov/sites/entrez?Db=genomeprj&Cmd=Search&Term=txid5821]

[[Category:Plasmodium|berghei]]
[[Category:Apicomplexa species|berghei]]
[[Category:Parasites of rodents]]