There are several strategies used in antiviral drug design. Since viral life cycles include three main phases (attachment, genome replication and assembly) potential targets can be either viral proteins or cellular proteins. The second approach with targeted cellular proteins is characterized by a broader activity spectrum, less chance of resistance development but higher toxicity. Within all phases, host cell proteins and mechanisms play an important role in virus life. The first is cellular attachment and penetration. Attachment and penetration can occur through receptor-mediated endocytosis or through direct membrane fusion. Second, the viral genome is released for replication and protein expression. In this phase, the virus can rely on host enzymes to facilitate capsid uncoating or host machinery to replicate the viral genome. Finally, assembly and maturation yield newly constructed viral particles poised for release. In this stage, viral proteins can require post-translational modification by host factors, or intracellular transport systems for proper localization. 
 J. R. Taylor, J. G. Skeate, and W. Martin Kast, “Annexin A2 in virus infection,” Front. Microbiol., vol. 9, no. DEC, Dec. 2018, doi: 10.3389/fmicb.2018.02954.
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