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English: FIGURE 2. Host mechanism of HIV-1 infection and targets of anti-HIV-1 drugs. HIV infection of cells involves five processes: adsorption, invasion, decapitation, synthesis, and assembly. The viral glycoprotein spike gp120 binds to CD4 on the host cell surface. Under the mediation of CCR5 or CXCR4, the virus fuses with the host cell membrane. In this process, fostemsavir tromethamine (Wang et al., 2021) is active on gp120, enfuvirtide (Monteiro et al., 2021; Yeruva and Lee, 2022) and albuvirtide (Chong et al., 2012) act on gp41 6-HB, maraviroc, plerixafor, and salmeterol function on CCR5 or CXCR4 (Woollard and Kanmogne, 2015; Mirza et al., 2020; Wang et al., 2020), and ibalizumab (Bettiker et al., 2018) acts on CD4 receptor in host cells. All of these drugs’ act to prevent viral adsorption or invasion. When viral RNA is reverse-transcribed to form RNA-DNA and enters the host cell nucleus, integrase inhibitors such as cabotegravir sodium prevent its integration into host DNA. Even if viral genetic material is already successfully integrated, foscarnet sodium (Devianne-Garrigue et al., 1998) and resveratrol (Zhang et al., 2009) can prevent its transcription and translation to form viral proteins, respectively. Impressively, the capsid protein inhibitor lenacapavir and GSK878 are now available and efficiently blocks viral infection of host cells (Segal-Maurer et al., 2022). Created with BioRender.com.