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Genetic Recombination between Human and Animal Parasites Creates Novel Strains of Human Pathogen

Identifieur interne : 000B74 ( Main/Merge ); précédent : 000B73; suivant : 000B75

Genetic Recombination between Human and Animal Parasites Creates Novel Strains of Human Pathogen

Auteurs : Wendy Gibson [Royaume-Uni] ; Lori Peacock [Royaume-Uni] ; Vanessa Ferris [Royaume-Uni] ; Katrin Fischer [Royaume-Uni] ; Jennifer Livingstone [Royaume-Uni] ; James Thomas [Royaume-Uni] ; Mick Bailey [Royaume-Uni]

Source :

RBID : PMC:4376878

Descripteurs français

English descriptors

Abstract

Genetic recombination between pathogens derived from humans and livestock has the potential to create novel pathogen strains, highlighted by the influenza pandemic H1N1/09, which was derived from a re-assortment of swine, avian and human influenza A viruses. Here we investigated whether genetic recombination between subspecies of the protozoan parasite, Trypanosoma brucei, from humans and animals can generate new strains of human pathogen, T. b. rhodesiense (Tbr) responsible for sleeping sickness (Human African Trypanosomiasis, HAT) in East Africa. The trait of human infectivity in Tbr is conferred by a single gene, SRA, which is potentially transferable to the animal pathogen Tbb by sexual reproduction. We tracked the inheritance of SRA in crosses of Tbr and Tbb set up by co-transmitting genetically-engineered fluorescent parental trypanosome lines through tsetse flies. SRA was readily transferred into new genetic backgrounds by sexual reproduction between Tbr and Tbb, thus creating new strains of the human pathogen, Tbr. There was no evidence of diminished growth or transmissibility of hybrid trypanosomes carrying SRA. Although expression of SRA is critical to survival of Tbr in the human host, we show that the gene exists as a single copy in a representative collection of Tbr strains. SRA was found on one homologue of chromosome IV in the majority of Tbr isolates examined, but some Ugandan Tbr had SRA on both homologues. The mobility of SRA by genetic recombination readily explains the observed genetic variability of Tbr in East Africa. We conclude that new strains of the human pathogen Tbr are being generated continuously by recombination with the much larger pool of animal-infective trypanosomes. Such novel recombinants present a risk for future outbreaks of HAT.


Url:
DOI: 10.1371/journal.pntd.0003665
PubMed: 25816228
PubMed Central: 4376878

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PMC:4376878

Le document en format XML

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<p>Genetic recombination between pathogens derived from humans and livestock has the potential to create novel pathogen strains, highlighted by the influenza pandemic H1N1/09, which was derived from a re-assortment of swine, avian and human influenza A viruses. Here we investigated whether genetic recombination between subspecies of the protozoan parasite,
<italic>Trypanosoma brucei</italic>
, from humans and animals can generate new strains of human pathogen,
<italic>T</italic>
.
<italic>b</italic>
.
<italic>rhodesiense</italic>
(
<italic>Tbr</italic>
) responsible for sleeping sickness (Human African Trypanosomiasis, HAT) in East Africa. The trait of human infectivity in
<italic>Tbr</italic>
is conferred by a single gene,
<italic>SRA</italic>
, which is potentially transferable to the animal pathogen
<italic>Tbb</italic>
by sexual reproduction. We tracked the inheritance of
<italic>SRA</italic>
in crosses of
<italic>Tbr</italic>
and
<italic>Tbb</italic>
set up by co-transmitting genetically-engineered fluorescent parental trypanosome lines through tsetse flies.
<italic>SRA</italic>
was readily transferred into new genetic backgrounds by sexual reproduction between
<italic>Tbr</italic>
and
<italic>Tbb</italic>
, thus creating new strains of the human pathogen,
<italic>Tbr</italic>
. There was no evidence of diminished growth or transmissibility of hybrid trypanosomes carrying
<italic>SRA</italic>
. Although expression of
<italic>SRA</italic>
is critical to survival of
<italic>Tbr</italic>
in the human host, we show that the gene exists as a single copy in a representative collection of
<italic>Tbr</italic>
strains.
<italic>SRA</italic>
was found on one homologue of chromosome IV in the majority of
<italic>Tbr</italic>
isolates examined, but some Ugandan
<italic>Tbr</italic>
had
<italic>SRA</italic>
on both homologues. The mobility of
<italic>SRA</italic>
by genetic recombination readily explains the observed genetic variability of
<italic>Tbr</italic>
in East Africa. We conclude that new strains of the human pathogen
<italic>Tbr</italic>
are being generated continuously by recombination with the much larger pool of animal-infective trypanosomes. Such novel recombinants present a risk for future outbreaks of HAT.</p>
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