Publication
Lymph Node Cellular and viral Dynamics in Natural Hosts and impact for HIV Cure Strategies
Downloadable Content
- Persistent URL
- Last modified
- 05/15/2025
- Type of Material
- Authors
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Nicolas Huot, Institut PasteurSteven Bosinger, Emory UniversityMirko Paiardini, Emory UniversityR. Keith Reeves, Harvard UniversityMichaela Mueller-Trutwin, Institut Pasteur
- Language
- English
- Date
- 2018-04-19
- Publisher
- Frontiers Media
- Publication Version
- Copyright Statement
- © 2018 Huot, Bosinger, Paiardini, Reeves and Müller-Trutwin.
- License
- Final Published Version (URL)
- Title of Journal or Parent Work
- ISSN
- 1664-3224
- Volume
- 9
- Start Page
- 780
- End Page
- 780
- Grant/Funding Information
- MM-T received a grant from the French Agency of AIDS Research, ANRS (AO 2017-2), and a donation from the L’OREAL Foundation.
- RR is supported by National Institutes of Health (NIH) grants RO1 DE026014 and RO1 AI120828.
- MP is supported by NIH grants R01AI-110334, R01AI-116379, R33AI-104278, and R33AI116171.
- The Infectious Disease Models and Innovative Therapies (IDMIT) center in Fontenay-aux-Roses, France, is funded by the French government’s Investissements d’Avenir program for infrastructures (PIA) under grant ANR-11-INBS-0008 and the PIA grant ANR-10-EQPX-02-01.
- SB is supported by NIH grants U24-AI120134, UM1-AI124436, and R21-AI118542.
- NH was recipient of a fellowship from the French Vaccine Research Institute funded by the National Agency of Research (ANR) under reference ANR-10-LABX-77.
- Abstract
- Combined antiretroviral therapies (cARTs) efficiently control HIV replication leading to undetectable viremia and drastic increases in lifespan of people living with HIV. However, cART does not cure HIV infection as virus persists in cell ular and anatomical reservoirs, from which the virus generally rebounds soon after cART cessation. One major anatomical reservoir are lymph node (LN) follicles, where HIV persists through replication in follicular helper T cells and is also trapped by follicular dendritic cells. Natural hosts of SIV, such as African green monkeys and sooty mangabeys, generally do not progress to disease although displaying persistently high viremia. Strikingly, these hosts mount a strong control of viral replication in LN follicles shortly after peak viremia that lasts throughout infection. Herein, we discuss the potential interplay between viral control in LNs and the resolution of inflammation, which is characteristic for natural hosts. We furthermore detail the differences that exist between non-pathogenic SIV infection in natural hosts and pathogenic HIV/SIV infection in humans and macaques regarding virus target cells and replication dynamics in LNs. Several mechanisms have been proposed to be implicated in the strong control of viral replication in natural host's LNs, such as NK cell-mediated control, that will be reviewed here, together with lessons and limitations of in vivo cell depletion studies that have been performed in natural hosts. Finally, we discuss the impact that these insights on viral dynamics and host responses in LNs of natural hosts have for the development of strategies toward HIV cure.
- Author Notes
- Keywords
- PERSISTENT LCMV INFECTION
- SIMIAN-IMMUNODEFICIENCY-VIRUS
- T cells
- NONHUMAN PRIMATE HOSTS
- SIV
- INFECTED SOOTY MANGABEYS
- viral control
- Life Sciences & Biomedicine
- PLASMACYTOID DENDRITIC CELLS
- AFRICAN-GREEN MONKEYS
- Science & Technology
- NK cells
- CD4(+) T-CELLS
- natural hosts
- NONPATHOGENIC SIV INFECTION
- I INTERFERON RESPONSES
- inflammation
- RHESUS MACAQUES
- lymph nodes
- HIV
- Immunology
- Research Categories
- Biology, Microbiology
- Health Sciences, Immunology
- Biology, Virology
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