7th IAS Conference on HIV Pathogenesis, Treatment and Prevention (IAS 2013)

TUSY01 The Roles of Secondary Lymphoid Tissues in HIV Infection: What Do We Know and Don’t Know?
  Symposia Session
Venue: Session Room 3
Time: 02.07.2013, 11:00 - 12:30
Co-Chairs: Olivier Lambotte, France
Jean-Pierre Routy, Canada
Secondary lymphoid tissues, such as lymph nodes (LN), are the sites where the adaptive immune responses are initiated and educated; they are also a major site of HIV/SIVmac replication which disrupts the normal structure of LN and the functioning of cells within them. Recent findings have shed new lights on virus and immune system interactions at these sites. This symposium will review these findings as they relate to our understanding of structure/function relationships in secondary lymphoid tissues, potential viral reservoirs, immunopathogenesis of HIV infection, and the induction of immune responses in these tissues. In particular, this session will highlight the subsets of cells in LN susceptible to infection, including recent data on infection of T follicular helper cells, and will examine how HIV/SIV infection and the resulting inflammation lead to structural changes in LN, thus promoting loss of CD4+ T cells and limiting immune reconstitution. The implications of these findings for treatment and prevention will be discussed.


Architectural abnormalities of the lymph nodes and mechanisms of CD4 T cell depletion
T. Schacker, United States

Viral reservoirs in lymphoid tissues during pathogenic and non-pathogenic lentiviral infections
G. Silvestri, United States

Lymph node structure and HIV-1 infection: T-cell immunopathogenesis
R. Koup, United States

Follicular helper T-cells and HIV
J. Van Lunzen, Germany

Questions and answers

Rapporteur report

Track A report by Uriel Moreno-Nieves

The Roles of Secondary Lymphoid Tissues in HIV Infection : What Do We Know and Don’t Know.


In this session speakers presented data highlighting the importance of Lymphoid Tissues in HIV pathogenesis.


T. Schacker presented data showing that there is a collagen deposition in the T cell zone of lymph nodes (LN) starting early on during HIV infection and correlating with the stages of the disease. The collagen deposition disrupts the Fibroreticular Cell network (FRCn) and impairs the homeostatic  mechanisms required for T cell homing and survival.


G. Silvestri, comparing two animal models, with different outcomes of SIV disease (Sooty Mangabeys which progress to AIDS whereas Rhesus Macaques do not), first showed that some features of SM are lower viral load in the LN and increased levels of infected central memory T cells (TCM). Secondly, further analyzing the subsets of CD4+ T cells, he showed that RM naturally have higher frequency of stem cell memory CD4+ T cell (TSCM), and also that this subset is highly susceptible to HIV infection in vivo, whereas TSCM of SM appear not to be infected in vivo. This observed characteristic can have a high importance, also pointed out by M. Lichterfeld, as targeting TSCM could lead to decreased HIV reservoir.


R. Koup presented data on the acute and early SIV infection of RM. He showed that there is a massive depletion of memory CD4 T cells in LN and gut, and the depletion of CD4+ T cells in the gut leads to microbial translocation and general immune activation. Immune activation then promotes differentiation of T cells in the LN which migrate and accumulate in the germinal center (GC), resulting in GC hypertrophy. 


Finally, J. van Lunzen showed data about follicular helper T cell (TFH). He showed that HIV-specific TFH expand in chronic HIV infection, also that TFH serve as a viral reservoir and promote HIV replication.




    The organizers reserve the right to amend the programme.