Title

Immunometabolism and HIV pathogenesis (CME)

Code

SY20

Session Type

Symposium

Track

Cross-track

Channel

Channel 3

Date Time

19 July 12:00- 12:50

Local Date Time

12:00 - 12:50 W. Europe Daylight Time

Moderator:

Clovis Steve PALMER, Burnet Institute, Jamaica

This session will provide an introduction to, and overview of, novel and evolving concepts by which intrinsic immune cellular metabolism and whole-body metabolic status impact metabolic co-morbidities and HIV reservoir persistence. A number of perspectives will be explored, looking at metabolic diseases in people ageing with HIV, immune activation/inflammation and HIV replication, and the role of glycomics in HIV pathogenesis.

2 min	Introduction Clovis Steve PALMER, Burnet Institute, Jamaica

10 min	Obesity: Immunometabolic consequences in HIV and aging Janine TREVILLYAN, Austin Health, Australia	Slides

10 min	Mechanistic insights into immunometabolic disruptions in HIV Asier SAEZ-CIRION, Institut Pasteur, France	Slides

10 min	Functional glycomics in HIV and future directions Mohamed ABDEL-MOHSEN, The Wistar Institute, University of Pennsylvania, United States	PDF

18 min	Live Q&A Mohamed ABDEL-MOHSEN, The Wistar Institute, University of Pennsylvania, United States Clovis Steve PALMER, Burnet Institute, Jamaica Asier SAEZ-CIRION, Institut Pasteur, France Janine TREVILLYAN, Austin Health, Australia

AUTHOR

Philippe Rascle

SUMMARY

This session, chaired by Clovis Steve PALMER, presented the different functions of the metabolism in HIV infection. The immune cellular metabolism and whole-body metabolic status were described as recent and important input to increase our understanding of HIV disease.

HIGHLIGHTS

Janine TREVILLYAN described the risk to develop obesity in PWH. She displayed the role of ART in this metabolism disorder via inhibitor combination (DTG/ABC/3TC or EFV/TDF/FTC). The persistent inflammation and monocyte activation are also related to significant increase of obesity risk. Asier SAEZ-CIRION demonstrated that CD8+ T cells present specific metabolism signature when comparing HIV Controllers (HIC) and Non-Controllers (NC). Differences between CD8+ T cell metabolism from HIC (glycolysis and mitochondrial metabolic pathways) and NC (glycolysis metabolic pathway) were shown. He provided convincing data about CD8+ T cell metabolic reprogramming in NC via IL-15 or GSK3β inhibition, which leads to enhanced CD8 effector activities and in vitro viral restriction. Finally, Mohamed ABDEL-MOHSEN demonstrated that metabolism markers may be associated with viral rebound, suggesting that the different glycan surface expression on infected cells can be used as biomarker of HIV persistence.

CRITICAL ASSESSMENT

The metabolism can be applied at different research fields in HIV disease. The possibility that immunometabolism may be used as biomarker, as well as for the modulation of cellular antiviral activity, has to be explored. The metabolism in HIV Non-Controllers individuals has been associated to increased risk of obesity, decreased cell activities, and viral rebound. And although keep the viremia at low level by ART is of upmost importance, ART cannot solve this metabolism disruption.