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. 2023 Mar 2;11(2):e04438-22. doi: 10.1128/spectrum.04438-22

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FIG 7 — Hypothetical mechanism of HERV-K102 upregulation and the phenotypic effect. Step 1: IFN-γ binds to and activates IFN-γRs, resulting in STAT1 homodimer formation and translocation into the nucleus. Step 2: STAT1 homodimers bind to the GAS site in IRF1 gene to induce rapid and strong transcription. Following translation, IRF1 translocates into the nucleus. Step 3: IRF1 (and potentially STAT1) bind to LTR12F to induce HERV-K102 upregulation. Step 4: HML-2 transcripts (including HERV-K102) accumulate in the cytoplasm. The RLRs (retinoic acid-inducible gene I-like receptors), RIG-I and MDA-5 (melanoma differentiation-associated gene 5), can respond to increases in HERV RNA, leading to MAVS signaling and subsequently, IRFs 3/7 activation and translocation into the nucleus. Step 5: IRFs 3/7 induce the expression of IFN-I and various ISRE-containing genes to enhance autocrine and paracrine pro-inflammatory signaling.