**1. Introduction**

Parvoviruses are among the smallest of eukaryotic viruses. They are subdivided into three major groups namely densoviruses, autonomous parvoviruses (APV), and dependoviruses [1]. Whereas densoviruses infect only insects, APV and dependoviruses infect vertebrate animals. APV replicate in proliferating target cells without the need of helper viruses but dependoviruses require helper virus functions for replication. Vector development has focused on three rodent APVs that can infect human cells, namely, LuIII, MVM, and H1. Dependovirus is also known as Adeno-associated virus (AAV) because dependovirus cannot replicate and form viral capsids in its host cell without the cell being coinfected by a helper virus such as an adenovirus, a herpesvirus, or a vaccinia virus [2–5]. AAVs of humans and of numerous other vertebrates are known. More than 90% of human adults have antibodies to AAV, which shows that the virus is common and widely distributed. AAV serotypes 2, 3 and 5 are endemic in humans; AAV-4 infects mainly nonhuman primates and the host for

serotypes 1, 6, 7 and 8 is unclear [2, 6–12]. It is noteworthy that APVs and AAVs do not cause disease in humans. Even though human exposure to AAV and H1 may lead to mild and harmless viraemia, B19 (of the Erythrovirus genus) is the only virus of the Parvovirinae subfamily known to cause pathogenicity in humans [13, 14].

In past few decades, parvoviruses have progressed from a biologically interesting observation into a crucial driver in human gene therapy. Its potential has been displayed in various preclinical and clinical research studies all around the world. Their small size, simple genetic composition and structure, and the high degree of flexibility and amenability of genome and capsid to genetic engineering are some of the key characteristics of these viruses with respect to their development and use as recombinant gene therapy vectors for DNA delivery.
