4.5 Article

Channel catfish virus entry into host cells via clathrin-mediated endocytosis

Journal

VIRUS RESEARCH
Volume 315, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.virusres.2022.198794

Keywords

Channel catfish virus; Virus entry; Endocytosis; Antiviral target

Categories

Funding

  1. Key Research and Development Plan of Jiangsu Province [BE2021369]
  2. Earmarked Fund for Jiangsu Agricultural Industry Technology System [JATS (2021) 519]
  3. National Natural Science Foundation of China [32002433]
  4. Natural Science Foundation of Jiangsu Province [BK20200522, BK20190484]

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The study found that channel catfish virus (CCV) invades host cells via a low-pH-dependent endocytic pathway, mediated by clathrin. Inhibiting endosomal acidification and clathrin-mediated endocytosis can effectively block CCV infection in host cells.
Channel catfish virus (CCV), an important member of the family Alloherpesviridae, causes a lethal infection in channel catfish. As with most animal viruses, the initial step of infection by CCV is entry into host cells, which is also a promising antiviral target for CCV disease. This study investigated the mechanism of host cell invasion by CCV using a series of biochemical inhibitor assays in channel catfish cells. CCV infection in host cells was doesdependently inhibited when cells were treated with endosomal acidification inhibitors (5 mu M chloroquine, 50 nM bafilomycin A1, and 1 mM ammonium chloride) and hypertonic medium (50 mM sucrose) , which suggests that CCV invades host cells in a manner dependent on low-pH and the endocytic pathway. Moreover, when the cells were pretreated with inhibitors of clathrin-mediated endocytosis, including chlorpromazine (2 mu M) and dynasore (50 mu M), the CCV infection in the host cells was strongly inhibited. In contrast, the destruction of cellular cholesterol by methyl-beta-cyclodextrin and nystatin and inhibition of macropinocytosis had no effect on viral entry. Altogether, these findings indicate that CCV infects host cells via clathrin-mediated endocytosis in a low-pHdependent manner, suggesting that this CCV entry pathway offers an antiviral target against CCV disease.

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