The role of the host receptor’s genetic variation in viral diseases has been extensively studied in the HIV infection model; in particular, the CCR5 co-receptor Δ32 deletion can prevent HIV infection in homozygous individuals carrying such a genotype [22] and lead to the cure of HIV-1 infection in subjects who undergo conditioning and hematopoietic stem cell transplantation with a CCR5 Δ32 homozygous donor [23]. This evidence concerns the gene CCR5 and viral load.