Abstract

Abstract The endoplasmic reticulum (ER) is crucial for the production, processing and transport of proteins. Infection with pathogens activates Unfolded Protein Response (UPR), which can lead to their survival/replication or elimination from the body. Although little is known about the role of the ER stress response in the pathogenesis of viral infections, the regulation of ER stress may be important in intractable infectious diseases. We conducted a comparative analysis of the expression of genes involved in ER stress response in peripheral blood mononuclear cells (PBMCs) from animals immunized with an attenuated strain of ASFV strain Congo-a (KK262) and then stimulated in vitro by two serologically different virulent strains Congo-v (K49) or Mozambique-v (M78), to expand our understanding of the early determinants of response to homologous and heterologous infection. We found up-regulation of genes of all three sensory molecules (PERK, ATF6 and IRE1) of UPR pathway in cells infected with only a homologous strain. For the first time, a number of up-regulated genes of the ER-associated degradation pathway (ERAD), which destroys misfolded proteins, were also detected. By understanding how viruses modify elements of cellular response to stress, we learn more about the pathogenesis, as well as how we can use it to prevent viral diseases.

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