[21]). In summary, in the case of CCR5, point mutations of negatively charged residues at the N-terminus showed their involvement in binding. In addition, insertion of CCR5 N-terminus (CCR5-Nt) into other chemokine receptors resulted in chimeric receptors capable of mediating viral infection, therefore demonstrating the involvement of the N-terminus in viral activity [21]. In the case of CXCR4, mutations of negatively charged residues at the N-terminus and ECL2, or the removal of a glycosylation site within the N-terminus, resulted in weaker interactions or inhibition of viral entry [21]. The gene discussed is CCR5; the disease is viral infectious disease.