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 virus¹s 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 doesn¹t 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:
Add monomers to the free 3¹ OH end of the chain
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.