期刊
SCIENCE
卷 311, 期 5758, 页码 236-238出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1115030
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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 vital 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 tong-term transmission of defective RNA viruses in nature was achieved through complementation by coinfection of host cells with functional viruses.
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