Long-term transmission of defective RNA viruses in humans and Aedes mosquitoes.
In 2001, dengue virus type 1 (DENV-1) populations in humans and mosquitoes from Myanmar acquired a stop-codon mutation in the surface envelope (E) protein gene. Within a year, this stop-codon strain had spread to all individuals sampled. The presence of truncated E protein species within individual viral populations, along with a general relaxation in selective constraint, indicated that the stop-codon strain represents a defective lineage of DENV-1. We propose that such long-term transmission of defective RNA viruses in nature was achieved through complementation by coinfection of host cells with functional viruses.
Aaskov
John
J
School of Life Sciences, Queensland University of Technology, 2 George Street, Brisbane, 4001, Australia.
Buzacott
Katie
K
Thu
Hlaing Myat
HM
Lowry
Kym
K
Holmes
Edward C
EC
D000330:Aedes / Q000821:virology*; D000818:Animals; D018388:Codon, Terminator; D003673:Defective Viruses / Q000235:genetics / Q000502:physiology*; D003715:Dengue / Q000635:transmission / Q000821:virology*; D003716:Dengue Virus / Q000235:genetics / Q000502:physiology*; D019143:Evolution, Molecular; D006801:Humans; D009154:Mutation; D002052:Myanmar; D014759:Viral Envelope Proteins / Q000235:genetics*
D018388:Codon, Terminator; D014759:Viral Envelope Proteins; C072281:E protein TH Sman, Dengue virus