During its infection, overexpression of Beclin 1 (the mammalian Atg6 ortholog) in neurons could inhibit the Sindbis virus spread, reduce cellular apoptosis, and protect against fatal Sindbis virus encephalitis (Liang et al., 1998), whereas Atg5 (an essential component for the formation of autophagosomes in mammalian cells) deficiency in Sindbis-infected neurons leads to delayed clearance of viral proteins, accumulation of the p62 (also known as SQSTM1) adaptor protein, and increased cell death in neurons (Mizushima et al., 2001). The gene discussed is BECN1; the disease is infection.