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
作者： Zhang, Wenfeng 1 ; Gong, Hui 4 ; Sun, Qianqian 1 ; Fu, Yuting 1 ; Wu, Xiaosi 1 ; Deng, Hengwei 5 ; Weng, Shaoping 1 ; He, Jianguo 1 ; Dong, Chuanfu 1 ;
作者机构： 1.Sun Yat Sen Univ, Sch Life Sci, State Key Lab Biocontrol, Guangzhou 510275, Peoples R China
2.Southern Marine Sci & Engn Guangdong Lab Zhuhai, Zhuhai 519000, Peoples R China
3.Sun Yat Sen Univ, Inst Aquat Econ Anim, Guangdong Prov Key Lab Aquat Econ Anim, Guangzhou 510275, Peoples R China
4.Fujian Acad Agr Sci, Inst Biotechnol, Fish Dis Unit, Fuzhou 350003, Peoples R China
5.Hainan Univ, Sch Marine Biol & Fisheries, Haikou 570228, Peoples R China
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
页码：
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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