Several approaches have been attempted in the past decade to minimize the viral infection-enhancing activity of semen amyloids for lowering the sexual transmission of HIV, some of which include (i) inhibiting the proteolytic cleavage of PAP to form PAP f39; (ii) inhibiting the conversion of PAP f39 monomers to infection-promoting amyloids; (iii) remodeling the existing fibrils to quantitatively reduce amyloid load; and (iv) neutralizing the charged surface of the fibrils and in turn disrupting the ability of the fibrils to mediate interaction between viruses and cells [4,9]. The gene discussed is ACP3; the disease is viral infectious disease.