This is similar to the case of Lassa virus infection, in which the impairment of virus glycoprotein mediated entry imposed by deletion of host receptor glycosylated α-dystroglycan can be overcome by using high titer virus (m.o.i > 0.5), resulting in virus entry through an alternate pathway involving heparin sulfate, lysosome-resident protein, and pH-dependent endocytosis [52]. The gene discussed is DAG1; the disease is lassa virus infectious disease.