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HIV fusion is correlated to the ability of gp41 to switch from a latent to a fusogenic structure. The latter has been partly elucidated. In this work, molecular modelling techniques were used to predict a 3-D model of the gp41 latent structure, and a model of its transconformation process. These results were partly obtained by homology to the Influenza HA2 protein. HA2 latent and fusogenic structures were studied and compared. Features crucial for the transconformation and fusion have been identified. The gp41 sequence was then analysed and characterized thoroughly. A complete trimeric 3-D model of the gp41 fusogenic structure was predicted by homology to the SIV gp41 structure, and characterized. Thanks to the results obtained from these various analyses and to the comparison of HA2 and gp41 sequences, similarities related to their transconformation and their role in fusion have been brought to the fore. Fusogenic structures of both proteins show notably "imperfections" which would reflect the structural flexibility of some regions. Based on these similarities, a trimeric 3-D model of the gp41 N- terminal part could be predicted for the latent state and validated. We also put forward hypotheses about the role of the gp41 ectodomain C-terminal part which is not described in our 3-D model. Finally, a model of gp41 transconformation was proposed. To our knowledge, it agrees with results presented in the literature.

Immunological diseases --- proteins --- Melting. --- Models

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monkeys --- viruses. --- viruses --- Viroses --- proteins --- Immunological diseases --- Protoplast fusion --- Immunogenetics

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IMMUNITY --- IMMUNOLOGY --- IMMUNOBIOLOGY --- IMMUNOLOGICAL DISEASES --- INFECTIOUS DISEASES --- ANTIBODIES --- ANTIGENS --- LYMPHOID SYSTEM --- TEXTBOOKS

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Pathological haematology --- Immunologic diseases. --- Immune diseases --- Immune disorders --- Immune system --- Immunologic disorders --- Immunological diseases --- Diseases

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immune system --- immunity --- medical sciences --- Immunology --- Immunological techniques --- Immunological diseases --- Human pathology --- Immune response