Simian immunodeficiency virus from macaques (SIV) is closely related in its structure and biological activity to human immunodeficiency virus, and is the best animal model for the acquired immunodeficiency syndrome. We investigated the kinetics of membrane fusion between SIV and phospholipid vesicles and the effects of various parameters on this process. Purified SIV was labelled with octadecyl rhodamine B chloride, and fusion was continuously monitored as the dilution of the probe in target membranes. These studies show that SIV fusion is strongly dependent upon the liposome composition. Fusion with pure cardiolipin (CL) liposomes is significantly faster than with CL/dioleoylphosphatidylcholine (DOPC) (3:7), phosphatidylserine (PS) or disialoganglioside (G)/DOPC (1.5:8.5) vesicles. SIV does not fuse appreciably with pure DOPC liposomes. Reduction of pH from 7.5 to 4.5 greatly enhances the rate of SIV fusion with CL, CL/DOPC and PS membranes, but does not affect fusion with DOPC or G/DOPC membranes. Calcium stimulates viral fusion with CL liposomes, but not with CL/DOPC or DOPC liposomes. SIV fuses with human erythrocyte ghost membranes only slowly at reduced pH. Our results indicate that SIV can fuse with membranes lacking the known viral receptor, CD4. Although the mechanism of SIV fusion with model and biological membranes remains to be determined, the fusion activity of SIV shares similarities with other lipid-enveloped viruses such as Sendai and influenza viruses.


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