Carine Van Lint
Academic Editor

Carine Van Lint


After performing her PhD thesis at the National Institutes of Health (NIH, Bethesda, USA) from 1991 to 1994 and a postdoctoral fellowship in New York from 1994 to 1997, Carine Van Lint joined the Faculty of Sciences of the "Université Libre de Bruxelles" as the head of the Laboratory of Molecular Virology. As a biochemist, Carine Van Lint has developed for the last 25 years a specific interest for pathogenic retroviruses. Her laboratory is mainly studying the role played by epigenetic modifications (such as histone acetylation, histone methylation and DNA methylation) and by non-epigenetic regulatory elements in transcriptional latency and reactivation of HIV-1 (Human Immunodeficiency Virus type 1 - the ethiologic agent of the acquired immunodeficiency syndrome (AIDS)), BLV (Bovine Leukemia Virus - the etiologic agent of a chronic lymphoproliferative disease termed enzootic bovine leucosis) and HTLV-1 (Human T-cell leukemia virus 1 - the etiologic agent of an aggressive lymphoproliferative disease (Adult T-cell Leukemia/Lymphoma) and a neurological degenerative syndrome (tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM)).

HIV Infectious Diseases Microbiology Molecular Biology Oncology Virology

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Work details

Research Director

Université Libre de Bruxelles
October 1996
Service of Molecular Virology
The Laboratory of Molecular Virology is studying the role played by epigenetic modifications (histone acetylation, histone methylation and DNA methylation) in transriptional latency and reactivation from latency of three retroviruses : HIV-1 (Human Immunodeficiency Virus type 1), HTLV-I (Human T-cell leukemia virus I) and BLV (Bovine Leukemia Virus).Infection by these retroviruses is characterized by viral latency in the large majority of infected cells and by the absence of viremia (in the cases of HTLV-I and BLV). These features are thought to be due to the transcriptional repression of viral expression in vivo, but the molecular mechanisms involved in such a repression are not fully elucidated. The epigenetic modifications could be one mechanism by which these viruses escape the host immune response and, in the case of HTLV-I/BLV, allow tumor development.


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