The article discusses the interferon (IFN)-mediated antiviral response, focusing on key effector pathways and proteins involved in viral defense. Four main pathways have been identified: the Mx GTPase pathway, the 2',5'-oligoadenylate-synthetase-directed ribonuclease L (RNaseL) pathway, the protein kinase R (PKR) pathway, and the ISG15 ubiquitin-like pathway. These pathways collectively block viral transcription, degrade viral RNA, inhibit translation, and modify protein function to control all steps of viral replication. Ongoing research continues to uncover additional activities of these effector proteins and has revealed unanticipated functions of the antiviral response. Type I IFNs are crucial for the innate immune response against viral infections and are essential for mounting a robust host response. They induce over 300 IFN-stimulated genes (ISGs), many of which encode pattern-recognition receptors (PRRs) that detect viral molecules and modulate signaling pathways, or transcription factors that form an amplification loop to increase IFN production and protect against virus spread. Some ISGs encode proteins with direct antiviral activity, including those that catalyze cytoskeletal remodelling, induce apoptosis, regulate post-transcriptional events, and are involved in post-translational modification. ISG15, a ubiquitin-like protein, is one of the most highly induced ISGs and modulates numerous cellular activities when coupled to protein substrates. It is involved in the ubiquitin-like process called ISGylation, which is reversible and involves enzymes such as UBE1L, UBCH6, UBCH8, HERC5, and TRIM25. ISG15 has been shown to prevent virus-mediated degradation of IFN-regulatory factor 3 (IRF3), thereby increasing the induction of IFNβ expression. ISG15 is also secreted and acts as a cytokine to modulate immune responses. The Mx GTPases, including MxA and MxB in humans and Mx1 and Mx2 in mice, are antiviral proteins that target viruses replicating in either the nucleus or cytoplasm. They are induced by type I and III IFNs and play a role in blocking viral gene transcription. The OAS and RNaseL pathway involves the synthesis of 2',5'-oligoadenylates, which activate RNaseL to mediate RNA degradation. This pathway functions as an antiviral RNA decay pathway and also acts as a double-stranded RNA (dsRNA)-specific PRR to trigger the antiviral response. PKR is a protein kinase that is constitutively expressed and upregulated by type I and III IFNs. It is activated by viral RNA and phosphorylates EIF2α, halting translation and allowing the cell to reconfigure gene expression. PKR also playsThe article discusses the interferon (IFN)-mediated antiviral response, focusing on key effector pathways and proteins involved in viral defense. Four main pathways have been identified: the Mx GTPase pathway, the 2',5'-oligoadenylate-synthetase-directed ribonuclease L (RNaseL) pathway, the protein kinase R (PKR) pathway, and the ISG15 ubiquitin-like pathway. These pathways collectively block viral transcription, degrade viral RNA, inhibit translation, and modify protein function to control all steps of viral replication. Ongoing research continues to uncover additional activities of these effector proteins and has revealed unanticipated functions of the antiviral response. Type I IFNs are crucial for the innate immune response against viral infections and are essential for mounting a robust host response. They induce over 300 IFN-stimulated genes (ISGs), many of which encode pattern-recognition receptors (PRRs) that detect viral molecules and modulate signaling pathways, or transcription factors that form an amplification loop to increase IFN production and protect against virus spread. Some ISGs encode proteins with direct antiviral activity, including those that catalyze cytoskeletal remodelling, induce apoptosis, regulate post-transcriptional events, and are involved in post-translational modification. ISG15, a ubiquitin-like protein, is one of the most highly induced ISGs and modulates numerous cellular activities when coupled to protein substrates. It is involved in the ubiquitin-like process called ISGylation, which is reversible and involves enzymes such as UBE1L, UBCH6, UBCH8, HERC5, and TRIM25. ISG15 has been shown to prevent virus-mediated degradation of IFN-regulatory factor 3 (IRF3), thereby increasing the induction of IFNβ expression. ISG15 is also secreted and acts as a cytokine to modulate immune responses. The Mx GTPases, including MxA and MxB in humans and Mx1 and Mx2 in mice, are antiviral proteins that target viruses replicating in either the nucleus or cytoplasm. They are induced by type I and III IFNs and play a role in blocking viral gene transcription. The OAS and RNaseL pathway involves the synthesis of 2',5'-oligoadenylates, which activate RNaseL to mediate RNA degradation. This pathway functions as an antiviral RNA decay pathway and also acts as a double-stranded RNA (dsRNA)-specific PRR to trigger the antiviral response. PKR is a protein kinase that is constitutively expressed and upregulated by type I and III IFNs. It is activated by viral RNA and phosphorylates EIF2α, halting translation and allowing the cell to reconfigure gene expression. PKR also plays