Another possible mechanism for CoV entry may occur through antibodies. During the binding of the virus-antibody complex, simultaneous binding of viral proteins to antigen-binding fragment (Fab) regions of immunoglobulin G (IgG) and of the fragment crystallizable (Fc) portion of the antibody to Fc gamma receptors (FcγRs) that are expressed by immune cells occurs, promoting viral entry without the use of the ACE2 receptor (69, 70). However, the presence of viral RNA in the endosomes signals via the Toll-like 3 (TLR3), TLR7, or TLR8 receptor, activating the host cell to release pro-inflammatory cytokines that lead to exacerbated tissue damage, a phenomenon called antibody-dependent enhancement (ADE) (71).