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
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
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.