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Article summary:
1. African swine fever virus (ASFV) enters host cells through both clathrin-mediated endocytosis and macropinocytosis.
2. Once inside the cell, ASFV particles move to late, multivesicular endosomes where they become uncoated through a pH-driven loss of the two outermost layers.
3. The fusion of the inner viral envelope with the limiting endosomal membrane delivers naked cores into the cytosol, and this process is dependent on virus protein pE248R.
Article analysis:
The article provides a detailed analysis of the entry and uncoating pathway used by African swine fever virus (ASFV) to infect swine macrophages, its primary target cell. The authors use a combination of flow cytometry, fluorescence and electron microscopy approaches to dissect the internalization pathway of extracellular ASFV in swine macrophages. They find that ASFV enters via both constitutive macropinocytosis and clathrin-mediated endocytosis, moves to late endosomes, where it undergoes a pH-driven loss of the two outermost layers, and finally fuses with the limiting endosomal membrane to deliver naked cores into the cytosol.
The article is well-written and provides valuable insights into the mechanism of ASFV entry. However, there are some potential biases and limitations that need to be considered. Firstly, the study was conducted in vitro using purified virions and may not fully reflect the complexity of ASFV infection in vivo. Secondly, while the authors provide evidence for both macropinocytosis and clathrin-mediated endocytosis as entry mechanisms for ASFV, they do not explore potential interactions or crosstalk between these pathways. Thirdly, while the authors identify pE248R as a key viral protein involved in virus fusion with endosomal membranes, they do not provide any information on how this protein interacts with host cell factors or how it triggers membrane fusion.
Overall, this article provides valuable insights into the mechanism of ASFV entry but further studies are needed to fully understand the complexity of this process in vivo and to identify potential targets for antiviral strategies against ASFV.