Furthermore, double KO neurons were largely protected from TeNT, as evidenced by the lack of cleavage of syb II; moreover, these neurons could be re-sensitized through infection with viruses that expressed SV2A or B. Using viruses that encode mutant forms of SV2, we found that glycosylation at any one of the three N-linked glycosylation sites was not required for TeNT to bind and enter neurons. The gene discussed is SV2A; the disease is infection.