Due to its ability to bind to cellular receptors, localize to the cytoplasmic membrane of an infected cell and transfer to an adjacent uninfected cell, Env can activate mitochondrial dysfunction and lymphocyte apoptosis without direct infection with virions, which is one of the explanations for the rapid decline in CD4 + T-lymphocytes at an early stage of infections [36]. This evidence concerns the gene ERVW-1 and infection.