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oai:repisalud.isciii.es:20.500.12105/65402024-09-27T08:47:13Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud author Suarez, Henar author Rocha-Perugini, Vera author Alvarez, Susana author Yanez-Mo, Maria funder Fundación Ramón Areces funder Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 2018-10-26T07:59:27Z 2018-10-26T07:59:27Z 2018 Front Immunol. 2018; 9:1811 1664-3224 http://hdl.handle.net/20.500.12105/6540 30127789 10.3389/fimmu.2018.01811 Frontiers in Immunology Despite the great research effort placed during the last decades in HIV-1 study, still some aspects of its replication cycle remain unknown. All this powerful research has succeeded in developing different drugs for AIDS treatment, but none of them can completely remove the virus from infected patients, who require life-long medication. The classical approach was focused on the study of virus particles as the main target, but increasing evidence highlights the importance of host cell proteins in HIV-1 cycle. In this context, tetraspanins have emerged as critical players in different steps of the viral infection cycle. Through their association with other molecules, including membrane receptors, cytoskeletal proteins, and signaling molecules, tetraspanins organize specialized membrane microdomains called tetraspanin-enriched microdomains (TEMs). Within these microdomains, several tetraspanins have been described to regulate HIV-1 entry, assembly, and transfer between cells. Interestingly, the importance of tetraspanins CD81 and CD63 in the early steps of viral replication has been recently pointed out. Indeed, CD81 can control the turnover of the HIV-1 restriction factor SAMHD1. This deoxynucleoside triphosphate triphosphohydrolase counteracts HIV-1 reverse transcription (RT) in resting cells via its dual function as dNTPase, catalyzing deoxynucleotide triphosphates into deoxynucleosides and inorganic triphosphate, and as exonuclease able to degrade single-stranded RNAs. SAMHD1 has also been related with the detection of viral nucleic acids, regulating the innate immune response and would promote viral latency. New evidences demonstrating the ability of CD81 to control SAMHD1 expression, and as a consequence, HIV-1 RT activity, highlight the importance of TEMs for viral replication. Here, we will briefly review how tetraspanins modulate HIV-1 infection, focusing on the latest findings that link TEMs to viral replication. eng Tetraspanins HIV Entry Assembly Budding Reverse transcription IMMUNODEFICIENCY-VIRUS TYPE-1 STABLE MICROTUBULE FORMATION CELL-MEDIATED TRANSFER PLASMA-MEMBRANE T-CELLS REVERSE TRANSCRIPTION TRANSMEMBRANE-4 SUPERFAMILY ENRICHED MICRODOMAINS RETROVIRAL INFECTION TRANS INFECTION Tetraspanins, Another Piece in the HIV-1 Replication Puzzle journal article URL https://repisalud.isciii.es/bitstreams/a6d9d661-8ba0-42d6-9192-92325d9e933a/download File MD5 880ae601cb71b6504dab14258ca688c8 969582 application/pdf TetraspaninsAnotherPiece_2018.pdf URL https://repisalud.isciii.es/bitstreams/1a9dd1f4-6f93-4115-a87b-a2ef41f59b8e/download File MD5 11a6737a05cd8fc321601b6f19db66ae 54538 text/plain TetraspaninsAnotherPiece_2018.pdf.txt