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IMPDH1 (inosine monophosphate dehydrogenase 1) is identified in Open Targets data as associated with hantavirus infection and is involved in purine metabolism pathways (KEGG hsa00230). ChEMBL data shows mycophenolic acid has strong binding affinity to IMPDH1 (pChEMBL: 7.40). Inhibiting IMPDH1 could reduce viral replication by depleting guanosine nucleotide pools required for viral RNA synthesis.
Open Targets identifies HLA-B as hantavirus-associated, and recent literature shows ERAP1 and HLA variants affect Puumala virus infection severity (PMID:39533856). Genetic risk stratification could guide intensive monitoring and early intervention for high-risk genotypes, while low-risk patients could receive standard care.
Open Targets identifies IFNA1 and IFNA17 as hantavirus-associated genes. Interferon-alpha enhances innate antiviral responses and could be most effective in early infection stages before severe capillary leak develops. Combination with ribavirin could provide synergistic antiviral activity.
Open Targets data identifies VEGFA as associated with hantavirus infection, with involvement in MAPK signaling (hsa04010) and Ras signaling pathways (hsa04014). ChEMBL compounds show high-affinity VEGFA inhibitors including CHEMBL382044 (pChEMBL: 8.77). VEGFA inhibition could prevent the characteristic capillary leak syndrome seen in hantavirus pulmonary syndrome by stabilizing endothelial barriers.
Open Targets data identifies CD8A with highest evidence score (0.01) for hantavirus association, linked to antigen processing and presentation pathways (hsa04612). CD8+ T cell dysfunction is implicated in severe hantavirus disease. Enhancing CD8+ T cell responses through checkpoint inhibition or adoptive transfer could improve viral clearance.
UniProt data identifies MAP1LC3B (LC3B) as hantavirus-associated, involved in autophagosome formation. Hantaviruses may manipulate autophagy for replication. Enhancing autophagy through mTOR inhibition or autophagy activators could promote viral clearance while reducing inflammatory responses.
ChemRxiv literature identifies coumarin derivative N6 as anti-hantavirus agent targeting AKT (PMID:34938178). Traditional Chinese medicine contains numerous coumarin compounds. AKT pathway modulation could reduce viral replication and inflammatory responses characteristic of severe hantavirus disease.
UniProt data identifies SUMO1 and UBE2I (SUMO-conjugating enzyme) as hantavirus-associated proteins. SUMOylation regulates viral protein nuclear trafficking and host cell responses. Inhibiting SUMO conjugation could prevent viral nucleocapsid nuclear accumulation and reduce viral replication efficiency.
Clinical trials data shows ribavirin was tested for HFRS (NCT00623168, withdrawn Phase 2). Ribavirin's broad-spectrum antiviral activity through RNA polymerase inhibition could be enhanced in combination with IMPDH inhibitors. The drug targets viral RNA synthesis and has shown activity against related RNA viruses.
FAERS data shows tacrolimus as the most frequently reported drug with hantavirus (3 reports), suggesting potential therapeutic relevance. Tacrolimus modulates T cell responses and could reduce the excessive inflammatory response characteristic of severe hantavirus disease while maintaining some antiviral immunity.
UniProt identifies TRAF3 as hantavirus-associated protein regulating NF-ฮบB, MAPK, and IRF pathways. TRAF3 is crucial for type I interferon responses. Enhancing TRAF3 signaling could boost antiviral immunity in pediatric patients who may have immature interferon responses to hantavirus infection.
ChemRxiv data identifies phloroglucinol oligomers from Callistemon rigidus as novel anti-hantavirus replication agents (PMID:40733534). These marine-derived compounds could target viral RNA polymerase or host factors required for replication. Phloroglucinols have broad antiviral activity against RNA viruses.
UniProt identifies TUFM (mitochondrial elongation factor) as hantavirus-associated. Elderly patients may have compromised mitochondrial function affecting antiviral responses. Enhancing mitochondrial protein synthesis could improve cellular energy status and antiviral immunity in this vulnerable population.