To elucidate the initial pathogenic events in lymphoid organs, the maj
or reservoir of virus in HIV infection, follow-ups of viral load, path
ological changes and target cells were performed in the rhesus macaque
SIVmac251 model and in the cat FIV model. Lymph nodes (LN) obtained f
rom animals sacrificed at early time points following experimental ino
culation were analysed by in situ hybridization for virus load and by
combined immunohistochemistry and in situ hybridization for virus cell
ular tropism. In the SIV model, the LN presented a high viral load at
7 days post inoculation (p.i.); at this stage, macrophages and T4 lymp
hocytes were identified as the target cells of the virus. A shift in t
he pattern of viral infection was observed at 2 weeks p.i., with a con
centration of viral RNA in follicular dendritic cells (FDC) in the ger
minal centres of the developing lymphoid follicles. This FDC-associate
d virus persisted at high levels for 2 months p.i. In the FIV model, t
he number of infected cells detected in LN was very low compared with
that found in the SIV model, and a similar role played by FDC was foun
d.