Ebola mutagenicity; Contingency planning

[Aaron Delwiche]

Albert Nanomius (nanomius at netcom.com) wrote:
: hello, I just got done reading an article in the newspaper,
: I think it was AP or NYT or something, in which the
: whole assertion was that the Ebola virus was NOT likely
: to mutate. it was in direct contradiction to your claims. it
: claimed the Ebola is DNA based and therefore involves a lot
: of "error correction" so that mutation would be unlikely.
: It said that in its current form it requires shoddy
: sanitation (such as shared needles) to propagate and is
: unlikely to advance because of this.

I found this on David Ornstein's Ebola page.  This suggests that Ebola is 
an RNA virus:

>                  Regulation of a Runaway Replicator 
>  
>                   By Myles Axton (myles at wi.mit.edu) 
>  
> -------------------------------------------------------------------- 
> This is a description of the microbiological processes behind Ebola. 
>   Myles has kindly written this piece for us. He says that "I am a 
>  biologist but not a specialist virologist. Perhaps this summary of 
>    the replication strategy of a filovirus would be of use here. I 
>    wrote it myself and am personally entirely responsible for any 
>                  errors or omissions it contains." 
> -------------------------------------------------------------------- 
>  
> Ebola virus particles are lethally elegant helically coiled tubes 
> made of four distinct virally-encoded proteins covered in plasma 
> membrane looted from host cells. Two further viral proteins lie 
> along the membrane, and spikes of another viral protein with 
> carbohydrate decoration protrude through the membrane. The whole 
> tube is 80nm wide and of variable length. Tubes 970nm long are 
> maximally infectious. In the 20nm interior of the tube lies the 
> viral code, a single linear strand of negative-sense (-) RNA about 
> 12 700 monomer units long, (a molecular mass of 4.2x10E6). This (-) 
> RNA is a reference copy of the or assembly instructions, for just 
> seven proteins that execute the virus=B9s strategy. Without its 
> tubular armor, the viral RNA would be non-infectious and rapidly 
> broken up by ubiquitous RNAse enzymes. 
>  
> Once inside a susceptible cell such as a human macrophage (the big 
> eaters that scavenge the blood for invaders) the virus is unwrapped 
> and an information bomb explodes. The viral L protein is an RNA 
> dependent RNA copying machine. that uses the (-) viral template to 
> transcribe each of the viral genes into a positive strand (+) RNA 
> message commanding the host cell to synthesize a specific viral 
> protein. Each gene on the (-) RNA is flanked by control sequences 
> directing the independent copying of each gene to a separate 
> message. This permits one copy of template to direct synthesis of 
> different amounts of message to make the seven proteins in the 
> correct relative amounts for virus assembly. 
>  
> When sufficient viral proteins have been made, the entire viral code 
> is copied from end to end to produce a full-length (+) strand 
> template. The (+) strand is itself copied. New (-) strand viral 
> genomes are immediately packaged into viral protein coats and 
> rapidly leave the cell by budding out of the cell membrane. The 
> switch from making gene-length messages to replicating the whole 
> genome is fascinating, perhaps when enough viral proteins have 
> accumulated, they can bind to termination sites between genes and 
> prevent the copying L enzyme from falling off until it reaches the 
> end. Sites of massive viral replication in the cytoplasm of infected 
> cells are visible to the light microscope. 
>  
> Unlike influenza, Ebola doesn=B9t hang around in the cell swapping 
> chromosomes with other strains of the virus. This is a rather rigid 
> program. Explosive replication results in degenerative changes in 
> the host cell which dies, subverted to a virus factory. 
>  
> Rules for replicating nucleic acids (RNA) 
>  
> Four kinds of monomer A,C,G,U: 
>  
>    * A pairs with and templates U 
>    * C pairs with and templates G 
>  
> Add monomers to the free 3=B9 OH end of the chain 
>  
>    * 5=B9 AGUC 3=B9 (+) strand 
>    * 3=B9 UCAG 5=B9 (-) strand 
>  
> Sources 
>  
> Murphy FA, Kiley MP and Fisher-Hoch SP (1990) Filoviridae, Marburg 
> and Ebola Viruses. (in)Virology, Fields BN et al. ed. Raven Press NY 
> USA pp933-942. 
>  
> Feldmann H, Klenk HD and Sanchez A (1993) Molecular biology and 
> evolution of filoviruses. Arch. Virol. Suppl. 7, 81-100. 
> -------------------------------------------------------------------- 
>  
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