Chikungunya virus infectivity was markedly stabilized in the presence of washed suspensions of human platelets but rapidly disappeared in similar preparations of rabbit platelets. Supernatant fluids collected from human platelets had some stabilizing effect on chikungunya virus over a 6-day incubation period at 37 °C. Rabbit platelet supernatant fluid had no virus-stabilizing effect, nor did it demonstrate any capacity to inactivate virus as compared to whole rabbit platelet preparations. Thin-section electron microscopy demonstrated that chikungunya virus formed an association with human platelets by becoming entrapped in platelet aggregates; during this process some of the platelets appeared to have undergone degranulation and lysis. Rabbit platelets exposed to chikungunya virus for 24 h demonstrated a considerable amount of platelet degranulation and lysis but virus was not visualized eitherin association with platelet membranes or within phagocytic vacuoles in the platelet cytoplasm. Human platelets, which appear to be more stable under these incubation conditions, may protect chikungunya virus infectivity from heat inactivation by surrounding viruses with large platelet aggregates whereas rabbit platelets, which appear to be more fragile, do not afford this type of protection. Thus, chikungunya virus in the presence of rabbit platelets may become inactivated by heat or may become bound irreversibly to membranes in such a fashion that infectivity assay and electron microscopy techniques may prove to be too insensitive for detection of virus.