Signalling through CD30 differentially affects HIV-1 X4 and R5 replication in TH1/TH2 polarized Cord blood derived cells.
Int Conf AIDS 2000 Jul 9-14; 13:(abstract no. MoOrA174)
Biswas P, Panina-Bordignon P, Mantelli B, Sinigaglia F, Poli G, Lazzarin A, Delfanti F P. Biswas, Scientific Institute H S. Raffaele, Lab. of Clinical Immunology, Infectious Diseases Dept., Via Stamira d' Ancona 20, 20127 Milano, Italy, Tel.: +39 2 2643 79 35, Fax: +39 2 2643 79 89, E-mail: Priscilla.Biswas@hsr.it
We have previously shown that CD30 triggering induced HIV expression in a chronically HIV-infected T cell line. In the present study we have evaluated whether signalling through CD30 could modulate acute in vitro infection of TH1 and TH2 polarized cells with X4 (IIIB) and R5 (Bal) HIV-1 strains under different stimulatory conditions. No substantial effects by CD30 triggering were observed when infection was carried out with IL-2 alone. Strikingly, when TH1 and TH2 cells were infected and then cultured in the presence of phytohemagglutinin (PHA), replication of both X4 and R5 HIV-1 was abrogated. Of note, in this experimental condition, triggering of CD30 selectively rescued X4, but not Bal, HIV-1 replication only in TH2 cells, whereas proliferation of TH1 cells was irreversibly inhibited by the PHA treatment. On the other hand, when TH1 and TH2 cells were infected and then stimulated by CD3 triggering, CD30 costimulation had no substantial effect on IIIB, but enhanced Bal replication in both TH1 and TH2 cells. However, both PHA and CD3 stimulation resulted in the generation of a small percentage CD30+ cells in TH2 as well as in TH1 polarized cells. Therefore, CD30 and its ligand (CD30L) are involved in the complex mechanisms that regulate HIV-1 replication.
Keywords: AEGIS, Antigens, CD30, HIV-1, Virus Replication, Th2 Cells, Th1 Cells, HIV Infections, Antigens, CD3, Fetal Blood, HIV, HIV Envelope Protein gp120, HIV Core Protein p24, T-Lymphocytes, Membrane Glycoproteins, CD30L, In Vitro, immunology, virology 000709
MoOrA174
