Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, China Agricultural University, Beijing 100193, China.
College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Viruses. 2019 Jan 27;11(2):107. doi: 10.3390/v11020107.
Fowl adenovirus serotype 4 (FAdV-4) causes hepatitis-hydropericardium syndrome (HHS), leading to severe economic losses in the poultry industry. Although the pathogenesis of FAdV-4 infection has caused much attention, the underlying molecular mechanisms remain poorly understood. Here, we identified chaperonin containing TCP-1 subunit eta (CCT7) as an interacting partner of the FAdV-4 capsid protein hexon. We found that ectopic expression of CCT7 in leghorn male hepatocellular (LMH) cells enhanced hexon expression in pRK5-flag-hexon transfected cells. On the contrary, knockdown of cellular CCT7 by RNAi markedly reduced hexon expression in FAdV-4-infected cells and suppressed viral replication. These data suggest that CCT7 is required for FAdV-4 replication and may serve as a potential target for controlling FAdV-4 infection.
禽腺病毒血清型 4（FAdV-4）引起肝炎-心包积水综合征（HHS），给家禽业造成严重的经济损失。尽管 FAdV-4 感染的发病机制引起了广泛关注，但潜在的分子机制仍知之甚少。在这里，我们鉴定出包含 TCP-1 亚基 eta 的伴侣蛋白（CCT7）是 FAdV-4 衣壳蛋白六邻体的相互作用伙伴。我们发现，在蛋鸡原代肝细胞（LMH）细胞中外源表达 CCT7 可增强转染 pRK5-flag-hexon 的细胞中六邻体的表达。相反，通过 RNAi 敲低细胞 CCT7 可显著降低 FAdV-4 感染细胞中六邻体的表达并抑制病毒复制。这些数据表明 CCT7 是 FAdV-4 复制所必需的，可能成为控制 FAdV-4 感染的潜在靶标。
