Comparative inhibitory effects of suramin and other selected compounds on the infectivity and replication of human T‐cell lymphotropic virus (HTLV‐III)/lymphadenopathy‐associated virus (LAV)

Abstract

Suramin and various other selected compounds were evaluated for their in vitro inhibitory effects on the infectivity and replication of human T‐cell lymphotropic virus (HTLV/III)/iymphadenopathy‐associated virus (LAV). As parameters for infectivity and replication, respectively, we followed the cytopathic effect of HTLV‐III/LAV on ATH 8 cells, a T‐cell clone with high susceptibility to HTLV‐III/LAV, and the expression of HTLV‐III/LAV p24 gag protein in H9 cells infected with HTLV‐III/LAV. As the most effective inhibitors of HTLV‐III/LAV the following substances emerged (in order of decreasing activity): Evans Blue ⋍ suramin > phosphonoformic acid > Direct Yellow 50. Several purine nucleoside analogues including vidarabine, tubercidin, neplanocin A, dihydroxypropyladenine, pyrazofurin and ribavirin were not inhibitory to HTLV‐III/LAV. In our test systems, involving a high multiplicity of infection, HPA‐23, previously reported to be effective against LAV reverse transcriptase, showed no inhibitory effect on HTLV‐III/LAV infectivity for ATH 8 cells and proved only weakly inhibitory to HTLV‐III/LAV replication in H9 cells. Thus, among the anionic dyes that are structurally related to suramin, compounds were found which were as active as suramin itself, if not more so.