Disease relevance of CYTB

• Linkage between mitochondrial cytochrome b lineages and morphospecies of two avian malaria parasites, with a description of Plasmodium (Novyella) ashfordi sp. nov [1].

High impact information on CYTB

• The evolution of primate malaria parasites based on the gene encoding cytochrome b from the linear mitochondrial genome [2].
• This DNA contains two open reading frames with potential to encode cytochrome c oxidase subunit I (cox1) and cytochrome b (cob) as well as fragments of rRNA genes scattered on both strands [3].
• A combined treatment of T. gondii-infected cells with HDQ and the antimalarial agent atovaquone, which blocks the ubiquinol oxidation site of cytochrome b in complex III, resulted in synergism, with a calculated fractional inhibitory concentration of 0.16 nM [4].
• BACKGROUND: Two single-point mutations of the Plasmodium falciparum cytochrome b gene (Tyr268Asn and Tyr268Ser) were recently reported in cases of atovaquone/proguanil (Malarone) treatment failure [5].
• Mutations in cytochrome b resulting in atovaquone resistance are associated with loss of fitness in Plasmodium falciparum [6].

Biological context of CYTB

• Analyses of cytochrome b sequences from 83 independent infections identified 29 unique haplotypes, representing 2 well-differentiated Haemoproteus spp. lineages and 6 differentiated Plasmodium spp. lineages [7].
• METHODS: The prevalence of cytochrome b point mutations possibly conferring atovaquone resistance in Plasmodium falciparum isolates in atovaquone treatment-na??ve patient cohorts from Lambar??n??, Gabon and from South Western Ethiopia was assessed [8].
• Molecular modelling showed that amino acid mutations are clustered around a putative atovaquone-binding site resulting in a reduced binding affinity of atovaquone for plasmodial cytochrome b, thus resulting in drug resistance [8].

Anatomical context of CYTB

• A verification study, using a single-tube nested PCR to eliminate contamination, showed that infections as low as 1 parasite per millions of erythrocytes could be detected by amplifying a 673 bp fragment of the cytochrome b gene [9].

Associations of CYTB with chemical compounds

• Molecular modeling of the interaction of P. falciparum cytochrome b with ubiquinone led to the prediction that a loss of fitness of the malaria parasites would result from the G280D mutation due to its close proximity to the putative ubiquinone-binding site [6].
• BACKGROUND: In vitro and in vivo resistance of Plasmodium falciparum to atovaquone or atovaquone-proguanil hydrochloride combination has been associated to two point mutations in the parasite cytochrome b (cytb) gene (Tyr268Ser and Tyr268Asn) [10].

Analytical, diagnostic and therapeutic context of CYTB

• Nested cytochrome b polymerase chain reaction diagnostics underestimate mixed infections of avian blood haemosporidian parasites: microscopy is still essential [11].

References