Year: 2026
Type: article
Abstract: 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 current knowledge on SOCS-mediated modulation of JAK/STAT signaling in HIV-1 and HTLV-1 infections, identifies critical gaps in our understanding of SOCS family diversity in retroviral immune evasion, and discusses the therapeutic potential of targeting SOCS pathways to restore antiviral immunity and limit retrovirus-associated disease.
Source: Molecular Biology Reports
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,290
OpenAlex ID: W7127970552