“…In summary, the genes up-regulated in their expression encode the pro-inflammatory cytokine IL-6, which can be induced by the presence of viruses, MX1 (MX dynamin-like GTPase 1), MX2 (MX dynamin-like GTPase 2), IFI6 (interferon alpha inducible protein 6) and ISG15 (interferon-stimulated gene 15), which inhibit viral replication, OAS2 (2’-5’-oligoadenylate synthetase 2) and OAS3 (2’-5’-oligoadenylate synthetase 3), which synthesize secondary messengers that serve to activate RNase L, which degrades viral and cellular RNA, and ISG20 (interferon stimulated exonuclease gene 20 kDa), which is an endoribonuclease that supports the degradation of viral RNA (Tanaka et al, 2014), (Sun et al, 2012; Haller et al, 2015; Zhu et al, 2015; Sajid et al, 2021; Deymier et al, 2022). In addition, the genes BST2 (bone marrow stroma cell antigen 2), IFI27 (interferon alpha-inducible protein 27), DDIT4 (DNA-damage-inducible transcript 4), GBP4 (guanylate binding protein 4), DDX60 (DEAD-box helicase 60), which are also involved in the antiviral immune response, are up-regulated (Miyashita et al, 2011; Tretina et al, 2019; Busse et al, 2020; Ullah et al, 2021; Zhao et al, 2022). It was shown that a type I interferon (IFN) response occurs during P. berghei replication in the liver.…”