Viral entry proteins and host-cell interfaces

Viral proteins and viral entry interfaces encompass the molecular machinery and interaction sites required for a virus to recognize, attach to, and penetrate a host cell (Marsh & Helenius, 2006, Cell). This target class includes viral surface glycoproteins, such as the SARS-CoV-2 Spike protein or HIV-1 gp120, and their corresponding host cell receptors or co-receptors, such as ACE2 or CCR5 (Wilen et al., 2012, Cold Spring Harb Perspect Med). The primary biological function of these interfaces is to mediate the binding of the virion to the cell surface and trigger the fusion of viral and cellular membranes or facilitate endocytic uptake (Harrison, 2008, Nature). In the context of infectious diseases, these interfaces are the first point of contact and are essential for the establishment of infection; blocking them can prevent the viral genome from entering the host cell entirely (NIH: StatPearls, 2023). Therapeutic strategies include monoclonal antibodies that neutralize viral proteins and small molecule antagonists that block host receptors (FDA, 2021). However, the high mutation rate of many viruses often leads to the emergence of escape mutants, and targeting host proteins carries the risk of interfering with normal physiological signaling (Science, 2020).

Other names

Viral attachment proteinsViral fusion proteinsViral entry receptorsHost-virus entry interfacesViral glycoproteins

Inhibition of viral attachment to host receptors, blockade of co-receptor binding, and prevention of viral-host membrane fusion (PubMed: 32718239, NIH: NBK541002).