These three proteins form a heterodimer of heterologous proteins, linked via disulfide bonds, that interacts with the CD163 protein to facilitate host cell entry, and in the absence of this heterologous protein trimer, the virus is unable recognize and interact with host cell receptors, indicating that the GP2-GP3-GP4 protein complex plays an essential role in host cell infection [87,88,89]. This evidence concerns the gene CD36 and infection.