After a first, temporal wave of NF-κB activation that is elicited by, e.g., envelope and tegument proteins of virus particles during virus attachment to and entry in host cells, the NF-κB pathway is again activated later in infection in an aberrant and persistent manner consisting of the continued degradation of the NF-κB inhibitory protein IκBα and binding of NF-κB to DNA (10, 11, 20, 21). The gene discussed is NFKB1; the disease is infection.