Abstract
Late steps of HIV-1 life cycle are determinant for optimal dissemination of the virus to new target cells. These steps include assembly of structural precursors, budding of the new particle and maturation into fully infectious virions. Each step is finely tuned and timely regulated to allow the appropriate assembly of structural components, the efficient recruitment of viral and cell partners and the timely regulated proteolytic processing of the protein precursors. Despite the huge number of studies devoted to the definition of molecular mechanisms regulating these steps, a number of question remains to be answered before they are clearly apprehended. The elucidation of the role played by each viral proteins, nucleic acids as well as host-encoded factors will provide new clues in the understanding of the retroviral assembly/maturation process and will allow further development of new antiviral compounds. This review reports the most recent progress as well as the questions that remain to be answered in the field of HIV-1 assembly, release and maturation. Finally, we also describe the data available on the design and use of new antiretroviral drugs targeting these specific steps of the retroviral replication.
Highlights
HIV-1 assembly, release and maturation are steps of primary importance for the production of infectious particles capable to disseminate in new target cells
This review reports the most recent progress as well as the questions that remain to be answered in the field of HIV-1 assembly, release and maturation
The capacity of HIV-1 to produce fully mature proteins addressed to appropriate cellular compartments, the competence of these viral proteins to multimerize and to interact with viral nucleic acids and the faculty of these complexes to recruit cellular partners required for efficient release in the extracellular space is of crucial importance for viral dissemination
Summary
HIV-1 assembly, release and maturation are steps of primary importance for the production of infectious particles capable to disseminate in new target cells. The capacity of HIV-1 to produce fully mature proteins addressed to appropriate cellular compartments, the competence of these viral proteins to multimerize and to interact with viral nucleic acids and the faculty of these complexes to recruit cellular partners required for efficient release in the extracellular space is of crucial importance for viral dissemination. Even they have attracted a considerable effort since the discovery of HIV-1, the mechanisms involved in the assembly of infectious particles remain incompletely defined. The understanding of protein-protein and protein-nucleic acids contacts as well as interactions with cellular lipids engaged during retroviral assembly more than ever represents a major challenge for the future development of new HIV-1 inhibitors
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