Moesin phosphorylation in response to HIV-1 Env/CD4 binding is required for cell fusion, and this is related to the capacity of phosphorylated moesin to anchor and redistribute F-actin to a pole of the cell, where CD4 and CXCR4 reorganize, aggregate, and interact, thereby representing enriched CD4/CXCR4 sites for T-cell/virus contact, entry, and infection [80]. This evidence concerns the gene ERVW-1 and infection.