To assess if the decline in BCA2 is a result of its own half-life or a consequence of viral infection, uninfected Jurkat CD4+ T cells and human PBMCs were seeded at the same concentrations as for the infectivity assays, and the endogenous levels of BCA2 were monitored at the selected time points by Western blotting. The gene discussed is RNF115; the disease is viral infectious disease.