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J Gen Virol ; 103(11)2022 11.
Artículo en Inglés | MEDLINE | ID: mdl-36382885

RESUMEN

The devil facial tumour disease (DFTD) has led to a massive decline in the wild Tasmanian devil (Sarcophilus harrisii) population. The disease is caused by two independent devil facial tumours (DFT1 and DFT2). These transmissible cancers have a mortality rate of nearly 100 %. An adenoviral vector-based vaccine has been proposed as a conservation strategy for the Tasmanian devil. This study aimed to determine if a human adenovirus serotype 5 could express functional transgenes in devil cells. As DFT1 cells do not constitutively express major histocompatibility complex class I (MHC-I), we developed a replication-deficient adenoviral vector that encodes devil interferon gamma (IFN-γ) fused to a fluorescent protein reporter. Our results show that adenoviral-expressed IFN-γ was able to stimulate upregulation of beta-2 microglobulin, a component of MHC-I, on DFT1, DFT2 and devil fibroblast cell lines. This work suggests that human adenoviruses can serve as a vaccine platform for devils and potentially other marsupials.


Asunto(s)
Infecciones por Adenoviridae , Adenovirus Humanos , Neoplasias Faciales , Marsupiales , Animales , Humanos , Adenovirus Humanos/genética , Interferón gamma , Adenoviridae/genética , Neoplasias Faciales/genética , Neoplasias Faciales/veterinaria , Antígenos de Histocompatibilidad Clase I/genética
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