ABSTRACT
Correction to: Chapter 7 in L. Zhang, S. R. Lewin (eds.), HIV Vaccines and Cure, Advances in Experimental Medicine and Biology 1075, https://doi.org/10.1007/978-981-13-0484-2_7.
ABSTRACT
HIV persists within the body despite successful suppression of virus replication with antiretroviral therapy (ART). HIV lurks in latent and active reservoirs, leading to rebound of virus spread if ART is interrupted. The latent HIV reservoir is a natural consequence of the life cycle of HIV, with integration of HIV into the genomes of cells that are or later enter the resting state, resulting in transcriptionally quiescent provirus. Resting CD4 T cells comprise the majority of the latent reservoir, although new evidence points to additional, smaller cellular reservoirs of latent HIV. An alternate, so-called active reservoir of HIV also exists within cells such as those found the B cell follicle of lymph nodes, where expression of HIV RNA can be found, again despite the full suppression of viremia and viral replication. Multiple factors such as the degree of virus exposure, timing of ART, and host factors can influence the size and characteristics of the HIV reservoir. Constructing effective strategies for HIV eradication and measuring their impact will require a sophisticated knowledge of the HIV reservoir.
Subject(s)
Anti-HIV Agents/therapeutic use , HIV Infections/drug therapy , HIV-1/drug effects , Viremia/drug therapy , Aging/immunology , Animals , Anti-HIV Agents/pharmacology , Child , Clinical Trials as Topic , Clone Cells/virology , Drug Resistance, Viral , Female , HIV-1/classification , HIV-1/physiology , Humans , Macrophages/virology , Male , Patient Selection , Racial Groups , T-Lymphocyte Subsets/virology , Viral Load , Virus Latency , Virus ReplicationABSTRACT
Effective antiretroviral therapy (ART) blunts viraemia, which enables HIV-1-infected individuals to control infection and live long, productive lives. However, HIV-1 infection remains incurable owing to the persistence of a viral reservoir that harbours integrated provirus within host cellular DNA. This latent infection is unaffected by ART and hidden from the immune system. Recent studies have focused on the development of therapies to disrupt latency. These efforts unmasked residual viral genomes and highlighted the need to enable the clearance of latently infected cells, perhaps via old and new strategies that improve the HIV-1-specific immune response. In this Review, we explore new approaches to eradicate established HIV-1 infection and avoid the burden of lifelong ART.
