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13th International AIDS ConferenceDurban, South Africa - July 9-July 14, 2000 |
Int Conf AIDS 2000 Jul 9-14; 13:(abstract no. WeOrB540)
Beretta A, Lazzarin A, Hasson H, Fumagalli L, Clerici M, Ferrante P, Saniabadi A, Adachi M
A. Beretta, S. Raffaele Scientific Institute, Infectious Disease Clinic, Via Stamira D'Ancona 20, 20127 Milano, Italy, Tel.: +39 022 643 79 39, Fax: +39 022 643 70 30, E-mail: giuliana.uslenghi@hsr.it
BACKGROUND: HIV infection results in immune alterations which are only partially reversed by current antiretroviral therapies (HAART).In addition, some HAART-treated patients never respond with a significant rise in CD4+ cell counts (immunological non responders). Some monocyte-derived cytokines, like TNFalpha play a major role in HIV pathogenesis. TNF alpha has a direct effect on HIV replication and it is associated with AIDS-related cachexia and lipodistrophy. In addition, monocytes are infectable by HIV and represent a potential viral reservoire. For these reasons we tested whether renewal of the pool of circulating monocytes by selective monocyte apheresis may improve the immune reconstitution which follows HAART treatment. For monocytes apheresis we used a novel, especially designed, device (G1 columns)
METHODS: 24 HIV-infected patients were selected and divided into three groups: group A immunologically non-responders (CD4 counts >200), group B virologically non-responders (HIV RNA > 50.000 copies/ml), group C immunogically and virologically non-responders (CD4 counts >200 and HIV RNA >50.000 copies/ml). Four individuals in each group were randomly assigned to receive G1 apheresis, the other four patients were used as controls. HAART was mantained in all patients. Each G1-treated patient received a total of 8 apheresis (one/week)
RESULTS: G1 apheresis was well tolerated, not accompanied by adverse responses and followed by clinical improvement. A profound suppression in TNF alpha production following G1 apheresis was observed in 3/4 group A and 3/4 group B G1 patients but none of the controls. There was a significant (p = 0.047) increase in CD4 cell counts in patients of all three groups compared to the control patients. The rise in CD4 cells was mantained for at least 8 weeks after the last apheresis. Two/4 group B patients and 1/4 group A patients but none of the control patients displayed a significant reduction (>2 log) of plasma HIV viraemia.
CONCLUSIONS: the results of this pilot study show that G1 apheresis was well tolerated and was followed by clinical and immunological and virological improvement. G1 apheresis may be considered in patients in whom HAART is only partially effective.
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