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Cyclodextrin sulphates alpha (a) and beta (b) were found to be inhibitors of replication of human immunodeficiency virus (HIV-1) in phytohaemagglutinin (PHA)-stimulated human peripheral blood mononuclear cells (PBMC); the same cells were also stimulated to proliferate (Anand et al., 1990). B-Cyclodextrin sulphate was also found to stimulate another, more complex, cell proliferation-neovascularization process in rabbit cornea (Folkman et al., 1989). Since the process of neovascularization is generally associated with progression of tumour growth and other pathologies, it is obvious that its stimulation by an antiviral compound may be a serious side effect. Nevertheless endotoxin-induced neovascularization can be suppressed by simultaneous treatment with b-cyclodextrin sulphate and glucocorticoids (Folkman et al., 1989). The same co-treatment may possibly be used to improve antiviral action of cyclodextrin sulphates, but such a combination therapy may not be free of complications. Glucocorticoids also affect the stability of various cellular membranes. Treatment of cells in vitro by glucocorticoids is known to stabilize their lysozymes. Glucocorticoids affect both the proliferative capacity of the cells (Cristofalo, 1972) and cytopathic effects of rabies viral infection. Furthermore, it has been reported that the cytopathic effects of rabies and of yellow fever viruses were inhibited while those of the polio virus were only mildly affected (Hannoun et al., 1965). Consequently, in this work we evaluated effects of a glucocorticoid and of glucocorticoid-a-cyclodextrin sulphate combination on HIV-1 replication.

Alpha-Cyclodextrin Sulphate, an anti-HIV Agent, Retains its Antiviral Effect in the Presence of Hydrocortisol Phosphate