Angela Ciuffi Lab

Angela Ciuffi, PhD, MER & PD
Tel. +41 21 314 4099
Mobile: +41 79 556 2633
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HIV-Host Cell Interaction

Integration, Transcription, Latency and Innate Immunity

The human immunodeficiency virus or HIV is the etiological agent of AIDS (Acquired ImmunoDeficiency Syndrome). This virus, which infected more than 77 million of people and killed more than 40 million people, is transmitted through the exchange of contaminated fluids (unprotected sex, blood contacts, mother-to-child transmission). 

Throughout its replication cycle, HIV uses the cellular machinery. This is how it gets into the cell, integrates into the genome of the host cell, and produces new particles that bud out of the host cell. HIV has developed several strategies to reproduce effectively and to promote its own replication, by exploiting host cell resources on one hand and by blocking host cell defenses (innate immunity) on the other hand.

There is today an effective antiviral treatment allowing blocking disease progression, making HIV a chronic infection rather than a deadly infection. Nevertheless, this treatment does not allow eliminating the virus, that persists in the organism via viral reservoirs, and that requires a life-long treatment. These viral reservoirs, constituted in part by latently infected CD4+ T cells, are considered to date as a major obstacle to HIV cure.

Our field of expertise is fundamental virology, in particular HIV and its interaction with the host cell. Our ultimate goal is a better understanding of HIV biology in order to contribute to the identification of new therapeutic strategies aiming at eradicating HIV. More specifically, our research focuses on the four following  topics: 

(i)    HIV replication dynamics (transcriptome and proteome analyses during HIV progression throughout the host cell).
(ii)    HIV integration (proteins involved in HIV integration, integration site selection, genomic features of integration sites and impact on viral expression).
(iii)    HIV latency (transcriptome analyses of primary CD4+ T cells, entering or exiting latency upon reactivation with different stimulating compounds, at population and single cell level). 
(iv)    Host innate immunity (identification and characterization of HIV restriction factors). 

Keywords: HIV virus, integration, latency, innate immunity, transcriptome (RNA-Seq), single cell, virology
 

Funding

These projects are supported by the Swiss National Science Foundation, the FP7 European Program (n°305762: Hit Hidden HIV), the Novartis Foundation for Medical-Biological Research, and the Swiss HIV Cohort Study, which includes more than 9000 individuals who have provided consent for genetic analyses. 

 Last updated on 18/10/2018 at 12:26