Adeno-Associated Virus (AAV) belongs to the genus Dependovirus of the family Parvoviridae, and is a non-enveloped single-stranded linear DNA virus. First discovered in adenovirus-contaminated cell cultures in 1965, the virus is unique in that it requires helper viruses such as adenovirus and herpesvirus to complete its full replication cycle. AAV has high genetic stability, and more than 13 human serotypes and hundreds of variants have been identified so far. Different serotypes exhibit different tissue tropism due to differences in capsid proteins, but the core genome structure is highly conserved. Its genome is approximately 4.7kb in length, containing two core open reading frames (rep for replication-related and cap for capsid-related) and inverted terminal repeats (ITRs) at both ends. These structural characteristics make it a highly promising vector model in the field of gene therapy.

AAV viral particles exhibit a typical regular icosahedral symmetric structure with a diameter of only 20-26nm, making them one of the smallest known animal viruses, with no lipid envelope. The core of the virus is a single-stranded linear DNA genome, and the ITRs at both ends can fold to form a hairpin structure, which serves as the initiation signal and packaging signal for genome replication. The capsid is composed of three proteins (VP1, VP2, VP3) encoded by the cap gene in a ratio of 1:1:10, with a total of 60 capsomeres forming a complete capsid. Among them, VP3 is the major capsid protein, accounting for more than 80% of the total capsid protein, which determines the antigenicity and tissue tropism of the virus; VP1 and VP2 are mainly involved in the uncoating and nuclear localization of the virus after invading host cells, and the unique functional domains at their N-termini are crucial for viral replication. The amino acid sequence of the loop region on the capsid surface varies greatly, which is the key site for distinguishing different serotypes.

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