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Our group focuses more specifically on two viruses: HIV-1 and influenza A viruses, respectively responsible for AIDS and flu.

  • Worldwide, the AIDS pandemic started to flow back thanks to prevention and treatments: new infections by the human immunodeficiency virus type 1 (HIV-1) decreased by 35% since year 2000, the number of deaths due to AIDS decreased by 42% since its peak in 2004, and access to antiretroviral treatments increased by 84% since year 2010 (http://www.unaids.org/).
  • Nowadays, highly active antiretroviral treatments (HAART) are very efficient, but they still have serious limitations:
    • They do not allow eradication of the virus and patients have to be treated for life.
    • They are toxic.
    • Under sub-optimal treatment conditions, the virus progressively acquires mutations that provide resistance to the antivirals.
    • An increasing number of people are infected by HIV isolates that are resistant to the currently available antivirals.
  • Our aim is improve our knowledge of the molecular mechanisms of the HIV-1 replication and the innate cellular defense against this virus, in order to identify potential new pharmacological targets and innovative antiviral strategies. Our group is particularly interested in several key steps of HIV-1 replication where RNA plays a central role.

Seasonal flu is estimated to kill 250,000 to 500,000 people yearly, amongst which about 2,000 to 3,000 in France. In 2015, it nevertheless killed 24,000 people in France alone. There are three types of flu viruses: A, B and C. Flu cases are due to type B and mainly type A viruses, the latter ones being occasionally at the origin of severe pandemics, like the Spanish flu pandemic (1918-1920, 30 to 100 millions deaths) or the Asian (1957, 1 to 4 millions deaths) and the Hong-Kong one (1968, 1 million deaths).

  • Influenza viruses belong to the orthomyxoviridae family. Their negative strand genomic RNA is made of 7 (in the case of influenza C viruses) or 8 (in the case of influenza A and B viruses) segments of which one copy is packaged into infectious viral particles.
  • Our aim is to elucidate the molecular mechanisms that allow selective packaging of one copy of each RNA fragments as well as those regulating the genetic reassortment events that can occur between two influenza A viruses that infect the same cell.

Our work is supported by l’ANRS, SIDACTION and ANR.

Former team members (since 1992)