Stress granules (SGs) are dynamic cytoplasmic ribonucleoprotein aggregates that form in response to cellular stress and function as key regulators of mRNA translation, stability, and antiviral defense. Increasing evidence demonstrates that retroviruses, including HIV-1, HTLV-1, and other oncogenic retroviruses, interact extensively with stress granule pathways to promote viral replication, persistence, and immune evasion. This review summarizes current knowledge of the molecular mechanisms governing stress granule assembly and highlights how retroviruses manipulate SG components, such as G3BP1, TIA-1, TIAR, and eIF2α signaling, to control host translational arrest and innate immune responses. In HIV-1 infection, viral proteins, including Gag, Tat, and Vpr, interfere with SG formation to support viral RNA translation and replication. Similarly, HTLV-1 modulates stress-response pathways to favor viral persistence and transformation. We also discuss the dual role of stress granules as both antiviral platforms and viral replication facilitators, depending on the stage of infection and cellular context. Importantly, emerging data suggest that dysregulated stress granule dynamics may contribute to chronic inflammation, neurodegeneration, and virus-associated malignancies. Understanding the interplay between retroviruses and stress granule biology provides insight into host-virus coevolution and identifies potential therapeutic targets to restore antiviral stress responses. Targeting SG-associated pathways may represent a novel strategy to limit retroviral replication and virus-induced pathogenesis.
Akbarin et al. (2026) studied this question.