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Abagero, B. R.

Publications and source records attributed to Abagero, B. R..

3 recordsLinked to original sources

Stage-aware transcriptomics reveals selective haplotype persistence in short-term ex vivo cultured Plasmodium vivax

Plasmodium vivax (Pv) infections are developmentally asynchronous and often polyclonal, complicating interpretation of bulk parasite transcriptomes. Here, we analyzed paired in vivo and short-term ex vivo transcriptomes from Ethiopian clinical isolates using stage deconvolution and PvMSP1 haplotyping. Ex vivo maturation modestly increased inferred schizont representation while largely preserving the proportion of trophozoites and gametocytes. After adjustment for parasite stage composition, in vivo and ex vivo transcriptomes remained globally similar, with no genes significantly differentially expressed, indicating the absence of major culture-induced transcriptional response. In contrast, short-term culture reduced multiplicity of infection, contracted within-host haplotype diversity, and non-randomly depleted specific haplotypes, consistent with a clonal bottleneck. In a subset of low-complexity infections, residual expression patterns were clustered by dominant haplotype, suggesting genotype-associated transcriptional heterogeneity independent of developmental stage. Together, these findings indicate that short-term ex vivo culture enriches late asexual stages and selectively filters clones rather than inducing a common transcriptional program. These results shows that ex vivo cultures are reliable way to study gene expression, especially for late stages. However, these needs explicitly model developmental composition and infection complexity when interpreting Pv transcriptomes from natural infections Author summaryMalaria caused by Plasmodium vivax is difficult to study because this parasite cannot yet be grown continuously in the laboratory and infections in patients often contain parasites at different developmental stages and multiple parasite lineages at the same time. In this study, we wanted to understand how much of the parasite gene-expression signal reflects true biological differences, and how much is explained by parasite development or changes that occur during short-term laboratory maturation. We compared parasites collected directly from patients in Ethiopia with matched parasite matured briefly outside the body. We found that short-term culture mainly increased the proportion of later-stage parasites, but after accounting for developmental stage, the overall gene-expression patterns remained very similar. However, culture reduced the diversity of parasite lineages within infections, suggesting that some parasite lineages survive better than others under laboratory conditions. Our findings highlight that natural Pv infections are complex mixtures of parasite stages and lineages. Accounting for this complexity will improve how researchers interpret parasite gene-expression studies and design future studies of parasite invasion, transmission, and survival.

cell biology↗

Plasmodium vivax genome evolution for erythrocyte invasion in Duffy-negative infections from East Africa

Historically, Plasmodium vivax (Pv) malaria was rare in Africa due to the lack of Duffy antigen receptor for chemokines (DARC) expression on host erythrocytes, an essential receptor for Pv Duffy Binding Protein (PvDBP1)-mediated invasion. However, increased reports of Pv cases across Africa and among Duffy-negative individuals have led to the hypothesis that the parasites have evolved alternate invasion mechanisms that are DARC-independent. To investigate potential genetic adaptations underlying this phenomenon, we performed genome-wide single nucleotide polymorphisms (SNPs) analyses of 110 Pv isolates collected from Ethiopia, comprising 38 Duffy-negative and 72 Duffy-positive infections. Pv from Duffy positives exhibited markedly higher genetic variation (477,561 SNPs) than those from Duffy negatives (197,461 SNPs). Chromosomes 1, 2, 9, 10, and 12 harbored the highest SNPs densities, consistent across both host genotypes but elevated in Duffy-positive infections. Among 43 erythrocyte-binding gene candidates, tryptophan rich antigen 3 and 34 (TRAg3 and TRAg34) and members of the merozoite surface protein 3 (MSP3) family showed the greatest nucleotide diversity per kilobase, highlighting these loci as potential mediators of host-parasite interaction shifts. Signals of positive selection differed by host Duffy genotypes. In Duffy-positive Pv, adaptive signatures were observed in genes related to drug resistance (chloroquine resistance-associated protein CG1 and 26S proteasome regulatory subunit RPN2) and erythrocyte binding (MAEBL); whereas in Duffy negative Pv, positive selection was observed in genes linked to organellar maintenance and vesicle trafficking (plastid replication repair enzyme and the AP-5 complex subunit beta 1), implicating alternative metabolic or trafficking adaptations. Amino acid substitutions in invasion ligands (PvDBP1, PvEBP/DBP2, and PvRBP2b) were common in Duffy-positive Pv but largely absent in Duffy-negative ones, with almost half of the mutations located in critical binding domains. Overall, Pv isolates in Duffy-negative hosts displayed reduced genomic diversity yet retained high conservation across the genome, suggesting strong selective constraints and limited diversification. Phylogenetic comparison revealed that Ethiopian Pv clustered closely with other East African isolates, whereas Southeast Asian and South American Pv represented more distant lineages. These findings indicate that Pv circulating in Duffy-negative populations maintains a genetically conserved background, potentially reflecting stringent evolutionary bottlenecks and/or specialized host-parasite interactions required for invasion of Duffy-negative erythrocytes.

genomics↗

Whole Genome Sequencing of Plasmodium vivax Isolates Reveals Frequent Sequence and Structural Polymorphisms in Erythrocyte Binding Genes

Plasmodium vivax malaria is much less common in Africa than the rest of the world because the parasite relies primarily on the Duffy antigen/chemokine receptor (DARC) to invade human erythrocytes, and the majority of Africans are Duffy negative. Recently, there has been a dramatic increase in the reporting of P. vivax cases in Africa, with a high number of them being in Duffy negative individuals, potentially indicating P. vivax has evolved an alternative invasion mechanism that can overcome Duffy negativity. Here, we analyzed single nucleotide polymorphism (SNP) and copy number variation (CNV) in Whole Genome Sequence (WGS) data from 44 P. vivax samples isolated from symptomatic malaria patients in southwestern Ethiopia, where both Duffy positive and Duffy negative individuals are found. A total of 236,351 SNPs were detected, of which 21.9% was nonsynonymous and 78.1% was synonymous mutations. The largest number of SNPs were detected on chromosomes 9 (33,478 SNPs; 14% of total) and 10 (28,133 SNPs; 11.9%). There were particularly high levels of polymorphism in erythrocyte binding gene candidates including reticulocyte binding protein 2c (RBP2c), merozoite surface protein 1 (MSP1), and merozoite surface protein 3 (MSP3.5, MSP3.85 and MSP3.9). Thirteen genes related to immunogenicity and erythrocyte binding function were detected with significant signals of positive selection. Variation in gene copy number was also concentrated in genes involved in host-parasite interactions, including the expansion of the Duffy binding protein gene (PvDBP) on chromosome 6 and several PIR genes. Based on the phylogeny constructed from the whole genome sequences, the expansion of these genes was an independent process among the P. vivax lineages in Ethiopia. We further inferred transmission patterns of P. vivax infections among study sites and showed various levels of gene flow at a small geographical scale. The genomic features of P. vivax provided baseline data for future comparison with those in Duffy-negative individuals, and allowed us to develop a panel of informative Single Nucleotide Polymorphic markers diagnostic at a micro-geographical scale.

genomics↗