XIX International AIDS Conference

MOSY06 Immunopathogenesis and its Treatment
  Symposia Session
Venue: Session Room 9
Time: 23.07.2012, 14:30 - 16:00
Co-Chairs: Galit Alter, United States
Scott Kitchen, United States
Studies of the immunopathogenesis of HIV infection have been instrumental not only in uncovering the mechanisms and processes by which the virus causes disease but also in highlighting rational approaches for therapeutic and vaccine interventions. Much of the work has been performed in the context of unchecked viral replication. However, now that greater numbers of individuals are being treated with ART and have virus replication suppressed to near undetectable levels, it is becoming increasingly clear that pathogenic processes not directly related to viral replication are a significant cause of mortality and morbidity in HIV infected people. This symposia session is directed to clinicians and scientists interested in better understanding the recent advances in knowledge related to HIV immunopathogenesis and treatment. At the completion of the session, participants will be knowledgeable about the mechanisms that underlie these processes and the therapeutic approaches that are being explored to mitigate their effects on health.


Immunopathogenesis under antiretroviral treatment

S. Deeks, United States

Systemic inflammation

N. Sandler, United States


T. Schacker, United States

What have we learnt from cytokine therapy in HIV infection?

Y. Levy, France

Novel approaches: treatment and HIV pathogenesis

L. Trautmann, United States

Questions, answers and conclusion

Powerpoints presentations
Immunopathogenesis under antiretroviral treatment - Steven G. Deeks

Novel approaches: treatment and HIV pathogenesis - Lydie Trautmann

Rapporteur report

Track A report by Galit Alter

The Session on Immunopathogenesis and its Treatment was an exciting review of the state of our current understanding of the impact of inflammation on accelerated incidence of cardiovascular disease, etc. Dr. Steve Deeks led off the session with a comprehensive overview of our increasing understanding of the link between emerging inflammatory markers that are tightly linked to HIV associated immunopathology including: cellular activation (first proposed by Dr. Giorgie nearly 2 decades ago), serum markers (IL-6, d-dimers, etc), microbial bi-products (LPS, etc), and tissue based alterations (fibrosis, etc). Most interestingly, these markers persist at remarkably high levels despite durable suppression of viral replication by ART, suggesting irreparable damage has occurred within the immune system that results in persistent inflammatory cues that may continue to drive immunopathology in the absence of high level viremia. Importantly, early treatment resulted in a significant reduction in inflammatory markers, implicating early immunopathological events in driving this aberrant persistent underlying inflammation that may be centrally responsible for increased morbidities in HIV-infected individuals on therapy. This presentation was then followed by a more mechanistic evaluation of  interventions that have sought to dampen and/or eliminate inflammation including ART intensification, anti-inflammatories, and non-absorbable antibiotics by Dr. Netanya Sandler. Dr. Tim Schacker then followed up with a fascinating glimpse into the potential role of inflammation associated tissue fibrosis in the etiology of HIV disease progression. Interestingly, Dr. Schacker showed data that baseline levels of inflammation driven tissue fibrosis are higher in Ugandan healthy populations associated with reduced CD4+ T cell numbers, strongly implicating fibrosis as a central driver of CD4+ T cell loss, likely due to the loss of IL-7 secreted cells. This presentation was then followed by a critical review of the cytokine based therapeutic interventions, by Dr. Yves Levy, pointing to an improved therapeutic outcome with IL-7 over IL-2 centrally related to the target T cell populations modulated by these cytokines. Fundamentally, IL-2 expanded T-regs, likely counterproductive to anti-HIV activities, whereas IL-7 expanded T cell populations more broadly, capable of controlling HIV infected cells. Finally, Dr. Lydie Trautmann showed some new data on T cell functional difference between subjects off and on therapy, suggesting that while the T cell responses are abundant during uncontrolled infection, they functional "quality" is inferior to T cells in treated patients that may be less abundant. Therefore she proposed that boosting the frequency of high "quality" T cell responses during suppressive therapy may promote more effective control of viremia post therapy discontinuation.      


    The organizers reserve the right to amend the programme.

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