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Human adenovirus B (HAdV-B) is a species of non-enveloped, double-stranded DNA viruses belonging to the Adenoviridae family [1, 5]. It encompasses several serotypes, including HAdV-3, 7, 11, 14, 21, 34, and 35, which are responsible for a variety of clinical manifestations such as acute respiratory infections, pneumonia, conjunctivitis, and urinary tract infections [1, 5, 11]. The virus initiates infection by binding to host cell receptors, most notably CD46 and desmoglein-2 (DSG2), through its fiber protein, followed by integrin-mediated endocytosis [6, 17, 24]. Although no specific antiviral therapies are currently approved for HAdV-B, the viral DNA polymerase is a primary target for off-label treatments like cidofovir and brincidofovir [1, 5, 18]. Beyond its role as a pathogen, HAdV-B is a significant focus in biotechnology for the development of oncolytic viruses and gene therapy vectors, leveraging its broad tissue tropism and ability to evade certain host immune responses [10, 20, 21]. As a virus species rather than a single molecular target, HAdV-B represents a complex pathogen with multiple potential therapeutic targets within its genome and capsid structure [1, 5]. The replication cycle involves the expression of early genes that modulate the host cell environment and late genes that encode structural proteins for virion assembly [14, 21]. In immunocompromised individuals, HAdV-B can cause severe, disseminated disease with high mortality rates, necessitating the use of broad-spectrum antivirals [1, 7, 18].
Inhibition of viral DNA polymerase and interference with viral entry or endosomal escape [1, 5, 18].
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