Suppressor of cytokine signaling (SOCS) proteins in human retroviral infections
Farjami Z., Akbarin MM., Álvarez HR.
Narrative Review, published in Mol Biol Rep (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Mol Biol Rep (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41642494
- PMCID
- PMC12876071
- DOI
- 10.1007/s11033-026-11513-7
Abstract (original English)
Retroviruses such as human immunodeficiency virus type 1 (HIV-1) and human T-cell leukemia virus type 1 (HTLV-1) have evolved sophisticated mechanisms to establish persistent infection by manipulating host immune signaling networks. A central target of this viral interference is the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, which governs cytokine-, interferon-, and growth factor–mediated immune responses. Tight control of this pathway is mediated by the suppressor of cytokine signaling (SOCS) protein family, comprising eight members (SOCS1–SOCS7 and cytokine-inducible SH2-containing protein, CIS) that function as inducible negative feedback regulators of JAK activity and cytokine receptor signaling. Accumulating evidence indicates that HIV-1 and HTLV-1 exploit SOCS proteins most prominently SOCS1 and SOCS3 to dampen antiviral interferon signaling, inhibit STAT activation, impair antigen presentation, and promote viral persistence. In HTLV-1 infection, dysregulation of SOCS expression further contributes to the survival, proliferation, and immune evasion of infected T cells, implicating SOCS pathways in the pathogenesis of adult T-cell leukemia/lymphoma. Despite these insights, the majority of studies have focused narrowly on SOCS1 and SOCS3, leaving the roles of other SOCS family members largely unexplored. This mini-review summarizes cur
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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