Peripheral B Lymphocyte Serves as a Reservoir for the Persistently Covert Infection of Mandarin Fish Siniperca chuatsi Ranavirus

文献类型: 外文期刊

第一作者: Zhang, Wenfeng

作者: Zhang, Wenfeng;Sun, Qianqian;Fu, Yuting;Wu, Xiaosi;Weng, Shaoping;He, Jianguo;Dong, Chuanfu;Zhang, Wenfeng;Sun, Qianqian;Fu, Yuting;Wu, Xiaosi;Weng, Shaoping;He, Jianguo;Dong, Chuanfu;Zhang, Wenfeng;Sun, Qianqian;Fu, Yuting;Wu, Xiaosi;Weng, Shaoping;He, Jianguo;Dong, Chuanfu;Gong, Hui;Deng, Hengwei

作者机构:

关键词: mandarin fish ranavirus (MRV); persistent infection; B lymphocytes; reactivation; TLR

期刊名称:VIRUSES-BASEL ( 影响因子:3.5; 五年影响因子:3.7 )

ISSN:

年卷期: 2024 年 16 卷 12 期

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收录情况: SCI

摘要: Mandarin fish ranavirus (MRV) is a distinctive member among the genus Ranavirus of the family Iridoviridae. The persistently covert infection of MRV was previously observed in a natural outbreak of MRV, but the underlying mechanism remains unclear. Here, we show that mandarin fish peripheral B lymphocytes are implemented as viral reservoirs to maintain the persistent infection. When mandarin fish were infected with a sublethal dosage of MRV under a nonpermissive temperature (19 degrees C) and a permissive temperature (26 degrees C), all of the fish in the 19 degrees C group survived and entered the persistent phase of infection, characterized by a very low viral load in white blood cells, whereas some of the fish died of MRV infection in the 26 degrees C group, and the survival fish then initiated a persistent infection status. Raising the temperature, vaccination and dexamethasone treatment can reactivate the quiescent MRV to replicate and result in partial mortality. The viral reservoir investigation showed that IgM+-labeled B lymphocytes, but not CD3 Delta+-labeled T lymphocytes and MRC-1+-labeled macrophages, are target cells for the persistent infection of MRV. Moreover, the reactivation of the quiescent MRV was confirmed through a non-TLR5 signal pathway manner. Collectively, we demonstrate the presence of the B cell-dependent persistent infection of ranavirus, and provide a new clue for better understanding the complex infection mechanism of vertebrate iridovirus.

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