Several authors have suggested that this increased activation may be important in the pathogenesis of HIV-1 infection. The uncontrolled T cell destruction characteristic of HIV infection is not due to the direct cytopathic effects of the virus but is more likely the result of activation-induced cell death. Immune activation markers (namely HLA-DR, Ki-67 and CD38) have been shown to be more predictive of CD4 decline than plasma HIV-1 RNA viral load. Treatment of helminth infections can result in reversal of this activated immune state.