ITIH4 and infection: These findings suggest a model for the development or progression of HIV-related CNS damage in which HIV-1 downregulates autophagy to facilitate viral replication during the permissive infection of susceptible cells; in contrast, different products of infection and cells that bind HIV-1 gp120 and that are nonpermissive to HIV-1 replication improve autophagy to eliminate toxic stress and maintain cell survival [215].