While the loss of Tax and sense mRNA expression has been attributed to the negative selection pressure exerted by the host immune system (Tax-specific cytotoxic T lymphocytes (CTLs)) on virus-infected cells [41,42,43], the cellular senescence response triggered by Tax during productive infection in cell culture most likely also plays a role (discussed below) [54,55,56,57]. The gene discussed is CNTN2; the disease is infection.