Paul M. Sharp

University of Edinburgh

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Beatrice H. Hahn

University of Pennsylvania

Martine Peeters

Institut de Recherche pour le Développement

George M. Shaw

University of Pennsylvania

Gerald H. Learn

University of Alabama at Birmingham

Yingying Li

Shaanxi Provincial People's Hospital

Julian C. Rayner

University of Cambridge

Lindsey J. Plenderleith

University of Edinburgh

Kenneth H. Wolfe

University College Dublin

Dorothy E. Loy

University of Colorado Hospital

Ahidjo Ayouba

Institut de Recherche pour le Développement

Cooperative Institutions

University of Pennsylvania

University of Alabama at Birmingham

Université de Montpellier

Institut de Recherche pour le Développement

Agropolis International

University of Edinburgh

Max Planck Institute for Evolutionary Anthropology

Centers for Disease Control and Prevention

Inserm

Emory University

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Prehistory of HIV-1

Nature (2008)

Paul M. Sharp Beatrice H. Hahn

Pandemic

10.1038/455605a

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Citations (39)

Evidence for a High Frequency of Simultaneous Double-Nucleotide Substitutions

Science (2000)

Michalis Averof Antonis Rokas Kenneth H. Wolfe Paul M. Sharp

Point mutations are generally assumed to involve changes of single nucleotides. Nevertheless, the nature and known mechanisms of mutation do not exclude the possibility that several adjacent nucleotides may change simultaneously in a single mutational event. Two independent approaches are used here to estimate the frequency of simultaneous double-nucleotide substitutions. The first examines switches between TCN and AGY (where N is any nucleotide and Y is a pyrimidine) codons encoding absolutely conserved serine residues in a number of proteins from diverse organisms. The second reveals double-nucleotide substitutions in primate noncoding sequences. These two complementary approaches provide similar high estimates for the rate of doublet substitutions, on the order of 0.1 per site per billion years.

10.1126/science.287.5456.1283

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Citations (127)

Gene acquisition in HIV and SIV

Nature (1996)

Paul M. Sharp Elizabeth Bailes Mario Stevenson Michael Emerman Beatrice H. Hahn

Simian immunodeficiency virus

10.1038/383586a0

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Citations (99)

Understanding the origins of AIDS viruses

Nature (1988)

Paul M. Sharp Wen‐Hsiung Li

Viral evolution

10.1038/336315a0

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Citations (63)

Correction: The Malagarasi River Does Not Form an Absolute Barrier to Chimpanzee Movement in Western Tanzania

PLoS ONE (2017)

A. Piel Fiona A. Stewart Lilian Pintea Yingying Li Miguel Ángel Ramírez

[This corrects the article DOI: 10.1371/journal.pone.0058965.].

10.1371/journal.pone.0182723

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Malaria-driven adaptation of MHC class I in wild bonobo populations

Nature Communications (2023)

Emily E. Wroblewski Lisbeth A. Guethlein Aaron Anderson Weimin Liu Yingying Li

Abstract The malaria parasite Plasmodium falciparum causes substantial human mortality, primarily in equatorial Africa. Enriched in affected African populations, the B*53 variant of HLA-B, a cell surface protein that presents peptide antigens to cytotoxic lymphocytes, confers protection against severe malaria. Gorilla, chimpanzee, and bonobo are humans’ closest living relatives. These African apes have HLA-B orthologs and are infected by parasites in the same subgenus ( Laverania ) as P. falciparum , but the consequences of these infections are unclear. Laverania parasites infect bonobos ( Pan paniscus ) at only one (TL2) of many sites sampled across their range. TL2 spans the Lomami River and has genetically divergent subpopulations of bonobos on each side. Papa-B, the bonobo ortholog of HLA-B, includes variants having a B*53-like (B07) peptide-binding supertype profile. Here we show that B07 Papa-B occur at high frequency in TL2 bonobos and that malaria appears to have independently selected for different B07 alleles in the two subpopulations.

Bonobo

Pan paniscus

HLA-B Antigens

10.1038/s41467-023-36623-9

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Citations (4)

Adaptation of Plasmodium falciparum to humans involved the loss of an ape-specific erythrocyte invasion ligand

Nature Communications (2019)

William R. Proto Sasha V. Siegel Selasi Dankwa Weimin Liu Alison Kemp

Plasmodium species are frequently host-specific, but little is currently known about the molecular factors restricting host switching. This is particularly relevant for P. falciparum, the only known human-infective species of the Laverania sub-genus, all other members of which infect African apes. Here we show that all tested P. falciparum isolates contain an inactivating mutation in an erythrocyte invasion associated gene, PfEBA165, the homologues of which are intact in all ape-infective Laverania species. Recombinant EBA165 proteins only bind ape, not human, erythrocytes, and this specificity is due to differences in erythrocyte surface sialic acids. Correction of PfEBA165 inactivating mutations by genome editing yields viable parasites, but is associated with down regulation of both PfEBA165 and an adjacent invasion ligand, which suggests that PfEBA165 expression is incompatible with parasite growth in human erythrocytes. Pseudogenization of PfEBA165 may represent a key step in the emergence and evolution of P. falciparum.

10.1038/s41467-019-12294-3

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Citations (29)

Genomes of cryptic chimpanzee Plasmodium species reveal key evolutionary events leading to human malaria

Nature Communications (2016)

Sesh A. Sundararaman Lindsey J. Plenderleith Weimin Liu Dorothy E. Loy Gerald H. Learn

Abstract African apes harbour at least six Plasmodium species of the subgenus Laverania , one of which gave rise to human Plasmodium falciparum . Here we use a selective amplification strategy to sequence the genome of chimpanzee parasites classified as Plasmodium reichenowi and Plasmodium gaboni based on the subgenomic fragments. Genome-wide analyses show that these parasites indeed represent distinct species, with no evidence of cross-species mating. Both P. reichenowi and P. gaboni are 10-fold more diverse than P. falciparum , indicating a very recent origin of the human parasite. We also find a remarkable Laverania -specific expansion of a multigene family involved in erythrocyte remodelling, and show that a short region on chromosome 4, which encodes two essential invasion genes, was horizontally transferred into a recent P. falciparum ancestor. Our results validate the selective amplification strategy for characterizing cryptic pathogen species, and reveal evolutionary events that likely predisposed the precursor of P. falciparum to colonize humans.

Plasmodium (life cycle)

Subgenus

10.1038/ncomms11078

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Citations (152)

Wild bonobos host geographically restricted malaria parasites including a putative new Laverania species

Nature Communications (2017)

Weimin Liu Scott Sherrill-Mix Gerald H. Learn Erik J. Scully Yingying Li

Malaria parasites, though widespread among wild chimpanzees and gorillas, have not been detected in bonobos. Here, we show that wild-living bonobos are endemically Plasmodium infected in the eastern-most part of their range. Testing 1556 faecal samples from 11 field sites, we identify high prevalence Laverania infections in the Tshuapa-Lomami-Lualaba (TL2) area, but not at other locations across the Congo. TL2 bonobos harbour P. gaboni, formerly only found in chimpanzees, as well as a potential new species, Plasmodium lomamiensis sp. nov. Rare co-infections with non-Laverania parasites were also observed. Phylogenetic relationships among Laverania species are consistent with co-divergence with their gorilla, chimpanzee and bonobo hosts, suggesting a timescale for their evolution. The absence of Plasmodium from most field sites could not be explained by parasite seasonality, nor by bonobo population structure, diet or gut microbiota. Thus, the geographic restriction of bonobo Plasmodium reflects still unidentified factors that likely influence parasite transmission.

Bonobo

Plasmodium (life cycle)

Pan paniscus

Gorilla

10.1038/s41467-017-01798-5

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Citations (51)

Comparative Genome Analysis Provides Insights into the Evolution and Adaptation of Pseudomonas syringae pv. aesculi on Aesculus hippocastanum

PLoS ONE (2010)

Sarah Green David J. Studholme Bridget E. Laue Federico Dorati Helen C. Lovell

A recently emerging bleeding canker disease, caused by Pseudomonas syringae pathovar aesculi (Pae), is threatening European horse chestnut in northwest Europe. Very little is known about the origin and biology of this new disease. We used the nucleotide sequences of seven commonly used marker genes to investigate the phylogeny of three strains isolated recently from bleeding stem cankers on European horse chestnut in Britain (E-Pae). On the basis of these sequences alone, the E-Pae strains were identical to the Pae type-strain (I-Pae), isolated from leaf spots on Indian horse chestnut in India in 1969. The phylogenetic analyses also showed that Pae belongs to a distinct clade of P. syringae pathovars adapted to woody hosts. We generated genome-wide Illumina sequence data from the three E-Pae strains and one strain of I-Pae. Comparative genomic analyses revealed pathovar-specific genomic regions in Pae potentially implicated in virulence on a tree host, including genes for the catabolism of plant-derived aromatic compounds and enterobactin synthesis. Several gene clusters displayed intra-pathovar variation, including those encoding type IV secretion, a novel fatty acid biosynthesis pathway and a sucrose uptake pathway. Rates of single nucleotide polymorphisms in the four Pae genomes indicate that the three E-Pae strains diverged from each other much more recently than they diverged from I-Pae. The very low genetic diversity among the three geographically distinct E-Pae strains suggests that they originate from a single, recent introduction into Britain, thus highlighting the serious environmental risks posed by the spread of an exotic plant pathogenic bacterium to a new geographic location. The genomic regions in Pae that are absent from other P. syringae pathovars that infect herbaceous hosts may represent candidate genetic adaptations to infection of the woody parts of the tree.

Pathovar

Pseudomonas syringae

Genomic island

Comparative Genomics

10.1371/journal.pone.0010224

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Citations (111)