Abstract
African Swine Fever Virus (ASFV) causes a serious swine disease that is endemic in Africa and Sardinia and presently spreading in Russia and neighboring countries, including Poland and recently, the Czech Republic. This uncontrolled dissemination is a world-wide threat, as no specific protection or vaccine is available. ASFV is a very complex icosahedral, enveloped virus about 200 nm in diameter, which infects several members of pigs. The virus enters host cells by receptor-mediated endocytosis that depends on energy, vacuolar pH and temperature. The specific receptor(s) and attachment factor(s) involved in viral entry are still unknown, although macropinocytosis and clathrin-dependent mechanisms have been proposed. After internalization, ASFV traffics through the endolysosomal system. The capsid and inner envelope are found in early endosomes or macropinosomes early after infection, colocalizing with EEA1 and Rab5, while at later times they co-localize with markers of late endosomes and lysosomes, such as Rab7 or Lamp 1. A direct relationship has been established between the maturity of the endosomal pathway and the progression of infection in the cell. Finally, ASFV uncoating first involves the loss of the outer capsid layers, and later fusion of the inner membrane with endosomes, releasing the nude core into the cytosol.
Highlights
African Swine Fever Virus (ASFV) causes a serious swine disease that is endemic in Africa and Sardinia and presently spreading in Russia and neighboring countries, including Poland and recently, the Czech Republic
African Swine Fever Virus (ASFV) is one such virus that enters the host cell by endocytosis, a process first observed in transmission electron microscopy (TEM) studies that showed viral particles internalizing in cytoplasmic vesicles from the cell membrane; besides, the infection was inhibited in the presence of lysosomotropic drugs that increase vacuolar pH [1,2,3]
The cellular and viral factors involved in this process as well as the different endocytosis mechanisms used by ASFV to enter host cells are discussed in the present review
Summary
Endocytosis, or internalization through endosomes, is an efficient mechanism used by many viruses to overcome the physical barrier of the cellular plasma membrane, entering the cell to initiate productive infection. African Swine Fever Virus (ASFV) is one such virus that enters the host cell by endocytosis, a process first observed in transmission electron microscopy (TEM) studies that showed viral particles internalizing in cytoplasmic vesicles from the cell membrane; besides, the infection was inhibited in the presence of lysosomotropic drugs that increase vacuolar pH [1,2,3]. The cellular and viral factors involved in this process as well as the different endocytosis mechanisms used by ASFV to enter host cells are discussed in the present review
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