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Literature detail

Plasmodium simium: Population Genomics Reveals the Origin of a Reverse Zoonosis.

Thaís C de Oliveira1 Priscila T Rodrigues1 Angela M Early2,3 Ana Maria R C Duarte4,5 Julyana C Buery6 Marina G Bueno7,8 José L Catão-Dias7 Crispim Cerutti6 Luísa D P Rona9,10 Daniel E Neafsey2,3 Marcelo U Ferreira1
Affiliations 10 institutions
  1. Department of Parasitology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
  2. Infectious Disease and Microbiome Program, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
  3. Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA.
  4. Laboratory of Biochemistry and Molecular Biology, Superintendency for the Control of Endemics (SUCEN), State Secretary of Health, São Paulo, Brazil.
  5. Laboratory of Protozoology, Institute of Tropical Medicine of São Paulo, University of São Paulo, São Paulo, Brazil.
  6. Department of Social Medicine, Center for Health Sciences, Federal University of Espírito Santo, Vitória, Brazil.
  7. Laboratory of Wildlife Comparative Pathology, Department of Pathology, School of Veterinary Medicine and Animal Sciences, University of São Paulo, São Paulo, Brazil.
  8. Laboratory of Comparative and Environmental Virology, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro, Brazil.
  9. Department of Cell Biology, Embryology, and Genetics, Federal University of Santa Catarina, Florianópolis, Brazil.
  10. National Council for Scientific and Technological Development, National Institute of Science and Technology in Molecular Entomology, Rio de Janeiro, Brazil.
PMID 33870436 2021 J Infect Dis eng ppublish
PubMed DOI Browse context

Article

Publication summary

The population history of Plasmodium simium, which causes malaria in sylvatic Neotropical monkeys and humans along the Atlantic Coast of Brazil, remains disputed. Genetically diverse P vivax populations from various sources, including the lineages that founded the species P simium, are thought to have arrived in the Americas in separate migratory waves. We use population genomic approaches to investigate the origin and evolution of P simium. We find a minimal genome-level differentiation between P simium and present-day New World P vivax isolates, consistent with their common geographic origin and subsequent divergence on this continent. The meagre genetic diversity in P simium samples from humans and monkeys implies a recent transfer from humans to non-human primates - a unique example of malaria as a reverse zoonosis of public health significance. Likely genomic signatures of P simium adaptation to new hosts include the deletion of >40% of a key erythrocyte invasion ligand, PvRBP2a, which may have favored more efficient simian host cell infection. New World P vivax lineages that switched from humans to platyrrhine monkeys founded the P simium population that infects nonhuman primates and feeds sustained human malaria transmission in the outskirts of major cities.

Neotropical monkeys Plasmodium simium reverse zoonosis Bacterial Zoonoses Metagenomics Animals Brazil Haplorhini Malaria Monkey Diseases Plasmodium Plasmodium vivax Polymerase Chain Reaction Polymorphism, Single Nucleotide

Structured evidence records

Evidence records

3 total
Genomic Evolution 1 records
Genomic Evolution Extraction confidence 0.95
Key finding

Population genomic comparison showed minimal differentiation between Plasmodium simium and New World Plasmodium vivax, indicating a recent human-to-monkey transfer and adaptive deletion in PvRBP2a associated with simian host infection.

Virus
Not specified
Location
Not specified
Supporting text

We use population genomic approaches to investigate the origin and evolution of P simium. We find a minimal genome-level differentiation between P simium and present-day New World P vivax isolates, consistent with their common geographic origin and subsequent divergence on this continent. Likely genomic signatures of P simium adaptation to new hosts include the deletion of >40% of a key erythrocyte invasion ligand, PvRBP2a.

Genes or proteins
PvRBP2a
Analysis methods
population genomic analysis; comparative genomic analysis
Molecular Adaptation 1 records
Molecular Adaptation Extraction confidence 0.90
Key finding

Plasmodium simium shows a deletion of over 40% of the erythrocyte invasion ligand PvRBP2a, indicating adaptation for infection of simian host cells.

Virus
Not specified
Host
Not specified
Location
Not specified
Supporting text

Likely genomic signatures of P simium adaptation to new hosts include the deletion of >40% of a key erythrocyte invasion ligand, PvRBP2a, which may have favored more efficient simian host cell infection.

Genes or proteins
PvRBP2a
Mechanism types
host_cell_invasion; molecular_adaptation
Spillover Event 1 records
Spillover Event Extraction confidence 0.95
Key finding

Genomic data indicate that Plasmodium simium originated from human Plasmodium vivax lineages that recently spilled back from humans to Neotropical monkeys in Brazil.

Virus
Not specified
Location
Brazil Atlantic Coast of Brazil, Brazil
Supporting text

The meagre genetic diversity in P simium samples from humans and monkeys implies a recent transfer from humans to non-human primates - a unique example of malaria as a reverse zoonosis of public health significance.

Method
genomic sequencing; population genomics
Study design
population genomic analysis
Transmission direction
human-to-animal
Geographic raw
Atlantic Coast of Brazil
Country inferred
Brazil