Andrea Cimarelli obtained his PhD at the University of Pavia, Italy, in 1996. He then performed his postdoctoral training at Columbia University, New York, in the laboratory of Dr. J. Luban, where he studied the mechanis m underlaying the assembly of virion particles of HIV. In 2000 he joined the laboratory of Dr. J.L. Darlix at the Virology Unit of INSERM at the Ecole Normale Superièure de Lyon. From 2005 he directs a group of research focused on the study of human lentiviruses in the Unit of Human Virology, INSERM U758, at the Ecole Normale Supérieure de Lyon. From 2013 the laboratory joined the Centre Internationale de Recherche en Infectiologie (CIRI) of Lyon.
Investigating and targeting the replication of the human lentiviruses HIV-1 and HIV-2
Human immunodeficiency viruses (HIVs) are the causal agents of the acquired immunodeficiency syndrome (AIDS). This disease is characterized by a progressive failure of the immune system that exposes the body to opportunistic infections leading to a fatal outcome in the absence of antiviral treatment. Still nowadays, the HIV/AIDS epidemic remains an enormous public health problem throughout the world that requires a convergence of multidisciplinary efforts that range from a fundamental understanding of the virus biology to the elaboration of appropriate political and socio-economical decisions.
Our laboratory studies from a basic virological point of view how HIV-1 and HIV-2 infect their target cells and how this process modifies the behavior of the infected cell and thus affects the cell’s functions during antiviral immune responses. To this end, we focus collectively on myeloid cells that play a central role in the regulation of the immune system.
At present our research efforts revolve around two major axes that explore different aspects of the host-pathogen relationship established during primate lentiviral infection of myeloid cells (monocytes, macrophages and dendritic cells). Our laboratory is interested in these cells for different reasons: because they play a key role in immune responses, because they constitute an important viral reservoir, and also because, despite being infected, they display a significant resistance against the virus. Given that in some of these studies we make use of lentiviral derived vectors, some of these findings in basic virology can also be exploited to ameliorate the efficacy of gene transfer for gene therapy purposes.
1) Understanding how the virus completes the early phases of infection
To complete its life cycle, viruses rely on complex interactions with the intracellular environment. Our lab aims at elucidating some of these interactions that may modulate the behavior of HIV in its target cells.
2) Exploring the consequences of lentiviral infection on the physiology of infected cells
Once a cell is infected, its physiology is seldom unscanted. Given that myeloid cells are at the core of immune responses, we believe that HIV may profoundly affet the functionality of antiviral responses by modifying the natural physiology of myeloid cells. By comparing close HIV viruses of different pathogenic properties we aim at determining the specificities of such changes