REGULATION AND CHARACTERIZATION OF THE INTERFERON-ALPHA PRESENT IN PATIENTS WITH ADVANCED HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DISEASE

Citation
S. Swindells et al., REGULATION AND CHARACTERIZATION OF THE INTERFERON-ALPHA PRESENT IN PATIENTS WITH ADVANCED HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DISEASE, Journal of interferon & cytokine research, 16(2), 1996, pp. 127-137
Citations number
60
Categorie Soggetti
Biology,Immunology
ISSN journal
10799907
Volume
16
Issue
2
Year of publication
1996
Pages
127 - 137
Database
ISI
SICI code
1079-9907(1996)16:2<127:RACOTI>2.0.ZU;2-G
Abstract
To examine a possible association between plasma viremia and interfero n-alpha (IFN-alpha) in patients with the acquired immunodeficiency syn drome (AIDS), we performed IFN plasma immunoadsorption by apheresis (I FN-alpha apheresis) in four volunteers with AIDS who had sustained lev els of endogenous plasma IFN-alpha. IFN-alpha apheresis with two plasm a volume exchanges was performed daily for 5 days, Clinical signs and symptoms and hematologic, virologic, and immunologic parameters were m onitored, Two subjects developed anemia from phlebotomy, and one had a catheter-associated bacteremia, The IFN-alpha apheresis was effective only in transiently removing IFN-alpha: depletion of IFN-alpha led on ly to its rapid reconstitution, Cell-associated HIV-1 was unchanged, b ut three of four subjects had a modest decrease in culturable plasma v irus burden following the procedures, The recovery of in vivo HIV-1-re lated IFN-alpha by apheresis allowed its biologic and biochemical char acterization. The HIV-1 IFN-alpha showed characteristics on ELISA, wes tern blot, and biologic assays similar to two subspecies of the natura l protein, The natural, recombinant, and HIV-1-induced IFN-alpha s dem onstrated nearly identical antiviral activities. The HIV-1 IFN-alpha e luted from the column was not acid labile, The inability of large amou nts of plasma IFN-alpha found in some patients with AIDS to affect vir al burden likely reflects properties of the virus or of host factors i ndependent of IFN-alpha.