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Aristolochic acids (AAs) have long been considered as a potent carcinogen due to its nephrotoxicity. Aristolochic acid I (AAI) reacts with DNA to form covalent aristolactam (AL)–DNA adducts, leading to subsequent A to T transversion mutation, commonly referred as AA mutational signature. Previous research inferred that AAs were widely implicated in liver cancer throughout Asia. In this study, we explored whether AAs exposure was the main cause of liver cancer in the context of HBV infection in mainland China. Totally 1256 liver cancer samples were randomly retrieved from 3 medical centers and a refined bioanalytical method was used to detect AAI–DNA adducts. 5.10% of these samples could be identified as AAI positive exposure. Whole genome sequencing suggested 8.41% of 107 liver cancer patients exhibited the dominant AA mutational signature, indicating a relatively low overall AAI exposure rate. In animal models, long-term administration of AAI barely increased liver tumorigenesis in adult mice, opposite from its tumor-inducing role when subjected to infant mice. Furthermore, AAI induced dose-dependent accumulation of AA–DNA adduct in target organs in adult mice, with the most detected in kidney instead of liver. Taken together, our data indicate that AA exposure was not the major threat of liver cancer in adulthood. [ABSTRACT FROM AUTHOR]

We present the first complete genome sequence of an aviadenovirus Oriolus adenovirus (OrAdV) sequenced from the cloaca of a Oriolus chinensis (a passerine bird widely distributed in Asia), which was collected from an island off the east coast of China. Thirty-one protein coding genes were predicted in this 40425-bp-long genome. OrAdV genome is highly divergent and has only 57% average protein identity compared with other aviadenovirus genomes. Comparative genomic analysis indicates that this passerine virus is a new species of aviadenovirus. One unique thymidylate kinase gene was discovered in OrAdV genome. This gene is absent in other adenovirus genomes and usually reported to occur in herpesvirus. Protein sequence alignment against all known proteins indicates that this gene may be originated from ancient horizontal gene transfer event between virus and parasitic eukaryote like protozoan. This new aviadenovirus genome enriches the genomic information of adenovirus and suggests that there is a large unknown space of adenovirus world. [ABSTRACT FROM AUTHOR]