Abstract

This work presents a novel theoretical framework concerning the mechanisms of induced endogenous viral biosynthesis (BEVI) in eukaryotic organisms. We propose a mathematical model describing the integration and expression of endogenous viral sequences (EVE) under the effect of environmental and cellular inducing factors. This model introduces differential equations to quantify the dynamics of insertion, transcription, and translation of integrated viral sequences. The fundamental hypotheses are explicitly formulated to allow experimental falsification.

Key experimentally validated findings:

• The HERV-K102 provirus located at 1q22 is significantly upregulated in response to interferon signaling (Russ et al., 2023, Microbiol Spectrum)
• IFN-γ induces STAT1 and IRF1 binding to LTR12F upstream of HERV-K102, triggering its transcription
• HERV-K102 transcripts constitute the majority of HML-2 RNAs during pro-inflammatory macrophage polarization
  
  
  
  

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