This can be explained by cross-recognition of the variant by the wild-type-specific cells that are highly effective against both wild-type and L268M viruses, express an anti-apoptotic phenotype and are long-lived.[34, 35] Although in this case the subject initiated ART through choice after 9 years of infection, viral load was well contained for much of this time at <2,000 copies/ml, and absolute CD4 counts were maintained at high levels of 500–700 cells/mm3 until ART intervention. The gene discussed is CD4; the disease is infection.