Infection with the human immunodeficiency virus type 1 (HIV-1) may result in persistent generalized lymphadenopathy (PGL). Lymph nodes in PGL most commonly show a florid follicular hyperplasia (FH) in which regressive changes, such as loss of mantle zones and fragmentation of the germinal centre (GC) can be observed.1,2 Fragmentation of the framework of follicular dendritic cells (FDC) has been demonstrated by immunohistochemistry.1,3 Intact HIV-1 virus particles are regularly found between the extensions of FDC within GCs of HIV-1 infected individuals.4,5 These observations have been associated with a cytopathic action of the virus on FDC.6,7 A proportion of FDC may be infected and produce virus.8 FDC function as accessory cells in GCs. Impairment of FDC function by cytopathic effects of the virus may influence GC microenvironment. The distinct types of B-cells can be distinguished and quantified at the ultrastructural level.9,10 Ultrastructural analysis of of the light and dark zones in tonsils shows that FDC subtypes can be recognized representing distinct differentiation stages of FDC (Rademakers and Schuurman, this issue). We applied this approach to GCs in lymph nodes of HIV-1 infected patients to analyze alterations in the GC microenvironment.KeywordsGerminal CentreFollicular Dendritic CellDark ZoneLight ZoneFollicular Hyperplasia