Interferon-associated therapies toward HIV control: The back and forth
Identifieur interne : 000418 ( Main/Curation ); précédent : 000417; suivant : 000419Interferon-associated therapies toward HIV control: The back and forth
Auteurs : Nicolas Noel [France] ; Béatrice Jacquelin [France] ; Nicolas Huot [France] ; Cécile Goujard [France] ; Olivier Lambotte [France] ; Michaela Müller-Trutwin [France]Source :
- Cytokine and Growth Factor Reviews [ 1359-6101 ] ; 2018-04.
English descriptors
- mix :
Abstract
Human immunodeficiency virus (HIV) induces a persistent and incurable infection. However, the combined antiretroviral treatment (cART) has markedly changed the evolution of the infection and transformed a deadly disease into a manageable chronic infection. Withdrawal of cART generally leads though to resumption of the viral replication. The eradication of the virus from its cellular and anatomical reservoirs remains a goal-to-achieve for a cure. In this context, developing novel therapies contributing to this aim are an important field of research. Type I IFN has antiviral activity, which, before the presence of efficient anti-HIV drugs, has led to the testing of IFN-based therapeutic strategies during the early years of the pandemic. A historical overview of the results and its limitations that were put into light are reviewed here. In addition, several lessons could be drawn. For instance, the efficacy of the IFN-I depends on the timing of its administration and the context. Thus, the persistence of an endogenous IFN-signature, such as that generally observed in viremic patients, seems to be associated with a lower efficacy of IFN. Based on the lessons from previous trials, and in the context of cART and research for a cure, type I Interferon has regained interest and novel therapeutic approaches are currently tested in combination with cART, some with disappointing, other with encouraging results with regard to a reduction in the size of the HIV reservoir and/or delays in viral rebound after cessation of cART. Additional strategies are currently developed in addition to improve the antiviral function of the IFN-I, by using for instance other IFN subtypes than IFN-Iα2. In parallel, the development of innovative strategies aimed at counteracting the excessive activation of the IFN-pathways have been continued and their results are reviewed here as well. Altogether, the use of IFN-I in anti-HIV therapies has gone through distinct phases and many lessons could be drawn. Novel combinations are currently be tested that might provide interesting results.
Url:
DOI: 10.1016/j.cytogfr.2018.03.004
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Hal:pasteur-01969821Le document en format XML
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<desc> <address> <addrLine>Site de l'Hôpital de Bicêtre - Faculté de Médecine Paris Sud - 63 rue Gabriel Péri 94276 Le Kremlin-Bicêtre Cedex.Site du CEA de Fontenay-aux-Roses - 10, route du Panorama - BP 6 - 92265 Fontenay-aux-Roses.</addrLine>
<country key="FR"></country>
</address>
<ref type="url">https://www.universite-paris-saclay.fr/fr/recherche/laboratoire/centre-de-recherche-en-immunologie-des-infections-virales-et-des-maladies-auto</ref>
</desc>
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<relation name="U1184" active="#struct-303623" type="direct"></relation>
</listRelation>
<tutelles><tutelle active="#struct-92966" type="direct"><org type="institution" xml:id="struct-92966" status="VALID"> <orgName>Université Paris-Sud - Paris 11</orgName>
<orgName type="acronym">UP11</orgName>
<desc> <address> <addrLine>Bâtiment 300 - 91405 Orsay cedex</addrLine>
<country key="FR"></country>
</address>
<ref type="url">http://www.u-psud.fr/</ref>
</desc>
</org>
</tutelle>
<tutelle name="DRF/IMETI" active="#struct-300016" type="direct"><org type="institution" xml:id="struct-300016" status="VALID"> <orgName>Commissariat à l'énergie atomique et aux énergies alternatives</orgName>
<orgName type="acronym">CEA</orgName>
<desc> <address> <addrLine>Centre de SaclayCentre de GrenobleCentre de Cadaracheetc</addrLine>
<country key="FR"></country>
</address>
<ref type="url">http://www.cea.fr/</ref>
</desc>
</org>
</tutelle>
<tutelle name="U1184" active="#struct-303623" type="direct"><org type="institution" xml:id="struct-303623" status="VALID"> <idno type="IdRef">026388278</idno>
<orgName>Institut National de la Santé et de la Recherche Médicale</orgName>
<orgName type="acronym">INSERM</orgName>
<desc> <address> <addrLine>101, rue de Tolbiac, 75013 Paris </addrLine>
<country key="FR"></country>
</address>
<ref type="url">http://www.inserm.fr</ref>
</desc>
</org>
</tutelle>
</tutelles>
</hal:affiliation>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Muller Trutwin, Michaela" sort="Muller Trutwin, Michaela" uniqKey="Muller Trutwin M" first="Michaela" last="Müller-Trutwin">Michaela Müller-Trutwin</name>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-410431" status="VALID"> <orgName>HIV, Inflammation et persistance</orgName>
<desc> <address> <addrLine>Département Virologie, 25-28 rue du Docteur Roux, 75724 Paris cedex 15</addrLine>
<country key="FR"></country>
</address>
<ref type="url">https://research.pasteur.fr/fr/team/hiv-inflammation-persistence/</ref>
</desc>
<listRelation> <relation active="#struct-300027" type="direct"></relation>
</listRelation>
<tutelles><tutelle active="#struct-300027" type="direct"><org type="institution" xml:id="struct-300027" status="VALID"> <idno type="IdRef">027936643</idno>
<idno type="ISNI">0000 0001 2353 6535</idno>
<orgName>Institut Pasteur [Paris]</orgName>
<date type="start">1887-06-04</date>
<desc> <address> <addrLine>25-28, rue du docteur Roux, 75724 Paris cedex 15</addrLine>
<country key="FR"></country>
</address>
<ref type="url">https://www.pasteur.fr</ref>
</desc>
</org>
</tutelle>
</tutelles>
</hal:affiliation>
<country>France</country>
</affiliation>
</author>
</analytic>
<idno type="DOI">10.1016/j.cytogfr.2018.03.004</idno>
<series><title level="j">Cytokine and Growth Factor Reviews</title>
<idno type="ISSN">1359-6101</idno>
<imprint><date type="datePub">2018-04</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>HIV</term>
<term>Interferon</term>
<term>cure</term>
<term>immune activation</term>
<term>reservoirs 2</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"> <p>Human immunodeficiency virus (HIV) induces a persistent and incurable infection. However, the combined antiretroviral treatment (cART) has markedly changed the evolution of the infection and transformed a deadly disease into a manageable chronic infection. Withdrawal of cART generally leads though to resumption of the viral replication. The eradication of the virus from its cellular and anatomical reservoirs remains a goal-to-achieve for a cure. In this context, developing novel therapies contributing to this aim are an important field of research. Type I IFN has antiviral activity, which, before the presence of efficient anti-HIV drugs, has led to the testing of IFN-based therapeutic strategies during the early years of the pandemic. A historical overview of the results and its limitations that were put into light are reviewed here. In addition, several lessons could be drawn. For instance, the efficacy of the IFN-I depends on the timing of its administration and the context. Thus, the persistence of an endogenous IFN-signature, such as that generally observed in viremic patients, seems to be associated with a lower efficacy of IFN. Based on the lessons from previous trials, and in the context of cART and research for a cure, type I Interferon has regained interest and novel therapeutic approaches are currently tested in combination with cART, some with disappointing, other with encouraging results with regard to a reduction in the size of the HIV reservoir and/or delays in viral rebound after cessation of cART. Additional strategies are currently developed in addition to improve the antiviral function of the IFN-I, by using for instance other IFN subtypes than IFN-Iα2. In parallel, the development of innovative strategies aimed at counteracting the excessive activation of the IFN-pathways have been continued and their results are reviewed here as well. Altogether, the use of IFN-I in anti-HIV therapies has gone through distinct phases and many lessons could be drawn. Novel combinations are currently be tested that might provide interesting results.</p>
</div>
</front>
</TEI>
</record>
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