Viruses are intracellular parasites whose genes enable replication in the presence of cellular machinery. Their genomes are composed of DNA or RNA. Some RNA viruses integrate into the chromosome of the host cell, and a reverse transcriptase converts them into DNA (retroviruses).
This lesson focused on the influenza virus as an (extraordinary) model of the impact of genetic variation on the emergence and dynamics of today's viral epidemics/pandemics.
Like most emerging pathogenic viruses, the influenza virus responsible for the flu is an RNA virus. Genetic variation in these viruses is ensured by a number of possibly associated mechanisms:
- mutations caused by numerous errors due to their generally low fidelity RNA polymerases, their lack of effective quality control mechanisms(proof reading), their rapid replication rate, their very short generation time and viral populations reaching high titres within infected tissues. This leads in the extreme to the notion of "quasi-species", which plays a key role in the adaptation of viruses to changes in environment and host, and can cause changes in pathogenicity;
- genomic modifications are also a source of diversity, with intra-species recombination events amplifying the evolutionary speed of certain viruses, or more rarely, recombination with host cell genes in retroviruses. In viruses with segmented genomes, intra-species reassortment of viral segments results in considerable genetic variability.
Influenza viruses evolve through a combination of mutations giving rise to minor serotypic variations that account for recurrent annual epidemics, and reassortments of segments between different serotypes responsible for sudden pandemic episodes.
