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Conserved viral genomic sequences in hemorrhagic fever viruses refer to highly stable and essential segments of the viral genome, typically RNA, that are shared across different strains or species of viruses causing hemorrhagic fevers, such as Filoviridae (Ebola, Marburg) and Arenaviridae (Lassa) (Source: PubMed, PMID: 20729952). These sequences often reside in the 5' or 3' untranslated regions (UTRs) or within critical genes like the L-polymerase, where they serve as promoters or signals for replication, transcription, and packaging (Source: UniProt, Viral Genome Organization). Because these regions are vital for the viral life cycle, they are less prone to mutation, making them ideal targets for broad-spectrum or pan-viral therapeutic interventions. Drugs targeting these sequences, such as antisense oligonucleotides (ASOs) like AVI-6002 and small interfering RNAs (siRNAs) like TKM-Ebola, work by binding to the viral genome to trigger degradation or physically block the machinery required for protein synthesis and genome copying (Source: Nature Medicine, doi:10.1038/nm.2202). This approach aims to provide a high barrier to resistance and potentially treat multiple related viral threats with a single platform, though challenges remain regarding delivery and potential off-target effects on host RNA (Source: NIH, Viral Hemorrhagic Fevers Research).
Sequence-specific hybridization to viral RNA leading to enzymatic degradation (via RNase H or RISC) or steric blockade of viral replication and translation machinery.
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