We are interested in the evolution and diversity of viral lifestyles. Viruses are the epitome of parasitism. Viral life cycle alternates between a metabolically inactive entity responsible for transmission, the virion, and a metabolically active entity responsible for genome replication, transcription, translation and virion generation, the virocell. A virus must infect a cellular host so that the ensemble becomes a virocell. The interactions between viruses and hosts from the very beginning of cellular life itself have generated an enormous diversity of viral life cycles and several gradients of virus-host interactions: from acute to chronic, latent or silent; from lethal to benign or asymptomatic; from extremely to slightly productive. We aim at understanding the origin and evolution of viral lifestyle diversity by means of experimental and bioinformatic approaches.
What is codon usage bias? Each amino acid is encoded by a variable number of so-called synonymous codons. Being synonymous does not mean that the use of one codon instead of another has no consequences on the biology of organisms. Indeed, synonymous codons are not used at random, and each species has its own codon preferences, which can vary from a gene to another, even within the same genome.
The codon usage among human viruses is modified by selection and/or mutations and is usually poorly adapted to human preferences. This creates a differential during translation between the present codons and the tRNA populations available in the cell. There may thus be an impact of codon usage preferences on protein translation in terms of amount and quality of the synthesised protein, The consequences are especially important for the viruses, since all viruses fully depend on the host machinery to produce viral proteins.
The papillomaviruses, used as a model in our team, infect the mucosa and the skin of a large host spectrum, from fishes to placental mammals. More than 250 genotypes of Human papillomaviruses (HPVs) have been described. The vast majority produce asymptomatic infections while some of them are associated to a high diversity of de manifestations, from mild cutaneous lesions to cancers. Indeed, chronic infections by oncogenic HPVs are responsible for 5% of the human cancers worldwide.
HPVs are a good model to try to understand the adaptative mechanisms of the viral genomes to their hosts. We are interested in the effects of this evolutionary process on information flow, specifically on protein translation, and on its consequences at the molecular and cellular levels, especially its impact on oncogenic processes. As a prospect, we are interested in the differential impact of infection-linked cancers according to the socioeconomic development status.
We are based in Montpellier, and belong to the Health Ecology Evolution Department within the MIVEGEC laboratory (Infectious diseases and Vectors: Ecology, Genetics, Evolution and Control) , a joint research unit by the CNRS (the French National Center for Scientific Researc), the IRD (French National Research Institute for Development) and the University of Montpellier.