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Titre : | Étude de limpact des protéines SERINC5 sur la réplication et linfectivitédu VIH-2 |
Auteurs : | Basma SERGHINI, Auteur ; François Dufrasne, Promoteur |
Type de document : | Travail de fin d'études |
Editeur : | Bruxelles : Institut Paul Lambin, 2020 |
Langues: | Français |
Index. décimale : | TFE - Biologie médicale |
Résumé : |
The Acquired Immunodeficiency Syndrome (AIDS) is a disease that emerged cognizant in the 20th century and is caused by human immunodeficiency viruses (HIVs). HIVs originated from simian host infected by simian immunodeficiency viruses (SIVs) and are part of the Retroviridae family. Those viruses harbor an envelope from the host cell, and their genome is composed of two copies of RNA. HIVs show an affinity for cells that express the CD4 receptor on their surface, for example lymphocytes T cells, dendritic cells, monocytes and macrophages. By infecting these cells, HIVs induce the destruction of the immune cells. Therefore, the immune system weakens and the infected person is more susceptible to be infected by opportunistic pathogens.
Two types of HIV were discovered: HIV-1 and HIV-2. HIV-1 is widespread in the worldwide while HIV-2 is restricted to several countries in West Africa, as well as in Portugal, France, India and United States of America. These two types of retroviruses are transmitted through sexual intercourse, blood-borne or from mother to child. Intriguingly and interestingly, more than 60% of HIV-2-infected individuals do not progress to the AIDS stage of the disease and do not need antiretroviral therapy, in striking contrast to HIV-1-infected persons who all (>99%) are under therapy. It seems that HIV-2 is less pathogenic and is more controlled by the host immune system but the molecular mechanisms underpinning this disease outcomes are not well understood. Recent studies have shown the presence of new restriction factors able to dampen the replication of HIVs in immune cells, the SERINC proteins. It is a family of proteins that comprises five members, SERINC1-5, but only SERINC5 efficiently inhibits HIV-1 infectivity. However, SERINC5 is antagonized by Nef, an accessory protein produced by HIVs and SIVs. Although several studies have demonstrated that HIV-1 Nef is able to antagonize SERINC5, little is known about the capacity of HIV-2 Nef to antagonize this restriction factor. The aim of this work is thus to assess the potential impact of SERINC5 proteins on the replication and infectivity of HIV-2 and HIV-2 that was deleted in the nef gene (HIV-2 Δnef). We aim to compare the results with HIV-1 and HIV-1 Δnef. We confirmed that SERINC5 is able to restrict the infectivity of both retroviruses. In absence of Nef, HIV-1 infectivity was drastically reduced by SERINC5 proteins. However and interestingly, we observed that the infectivity of HIV-2 Δnef viruses is also decreased by SERINC5 but in a lesser extent than HIV-1 Δnef. These results show that HIV-2 is less sensitive to the SERINC5 restriction than HIV-1 and may also suggest that HIV-2 would use another protein to antagonize SERINC5 when Nef is lacking. One candidate could be the HIV-2 envelope glycoprotein. Unfortunately, no conclusion can be drawn because several other experiments would have been necessary to confirm this hypothesis. |
Accès : | Identifiez-vous avant d'accéder au document électronique |
Disponible en ligne : | Oui |
Lieu du stage : | Pôle de microbiologie médicale (MBLG), Institut de recherche expérimentale et clinique (IREC), UCLouvain |
Département : | Biologie médicale |
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TFE biologie médicale Adobe Acrobat PDF |