The immunological interplay between AD and MC warrants particular attention: MCV encodes a protein homologous to interleukin-18 (IL-18)-binding protein (13), while AD-driven Th1-cell responses produce interferon-gamma (IFN-γ) and IL-18, creating a proinflammatory microenvironment that may theoretically facilitate MC persistence (10, 14, 15). The gene discussed is IFNG; the disease is Alzheimer disease.