Literature DB >> 10092452

Lack of evolutionary stasis during alternating replication of an arbovirus in insect and mammalian cells.

I S Novella1, C L Hershey, C Escarmis, E Domingo, J J Holland.   

Abstract

The evolution of vesicular stomatitis virus (VSV) in a constant environment, consisting of either mammalian or insect cells, has been compared to the evolution of the same viral population in changing environments consisting in alternating passages in mammalian and insect cells. Fitness increases were observed in all cases. An initial fitness loss of VSV passaged in insect cells was noted when fitness was measured in BHK-21 cells, but this effect could be attributed to a difference of temperature during VSV replication at 37 degrees C in BHK-21 cells. Sequencing of nucleotides 1-4717 at the 3' end of the VSV genome (N, P, M and G genes) showed that at passage 80 the number of mutations accumulated during alternated passages (seven mutations) is similar or larger than that observed in populations evolving in a constant environment (two to four mutations). Our results indicate that insect and mammalian cells can constitute similar environments for viral replication. Thus, the slow rates of evolution observed in natural populations of arboviruses are not necessarily due to the need for the virus to compromise between adaptation to both arthropod and vertebrate cell types. Copyright 1999 Academic Press.

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Year:  1999        PMID: 10092452     DOI: 10.1006/jmbi.1999.2635

Source DB:  PubMed          Journal:  J Mol Biol        ISSN: 0022-2836            Impact factor:   5.469


  64 in total

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Review 6.  Specific and nonspecific host adaptation during arboviral experimental evolution.

Authors:  Isabel S Novella; John B Presloid; Sarah D Smith; Claus O Wilke
Journal:  J Mol Microbiol Biotechnol       Date:  2012-01-13

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9.  Modeling viral genome fitness evolution associated with serial bottleneck events: evidence of stationary states of fitness.

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Journal:  J Virol       Date:  2002-09       Impact factor: 5.103

10.  West Nile Virus fidelity modulates the capacity for host cycling and adaptation.

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