The Multifaceted Role of Th17 Cells in Viral Infections: From Protective Immunity to Immunopathology

T helper 17 (Th17) cells have emerged as a critical yet enigmatic subset of CD4⁺ T lymphocytes in the context of viral infections. Initially recognized for their protective functions at mucosal barriers against bacterial and fungal pathogens, Th17 cells and their signature cytokine, interleukin-17 (IL-17), play a complex, virus-specific role in antiviral immunity. This review synthesizes recent advances from 2025–2026, revealing a paradigm where Th17 responses are neither uniformly protective nor purely detrimental. Instead, the outcome is dictated by the viral pathogen, the tissue microenvironment, and the interplay with other T-cell subsets. We explore the novel concept of Th17 plasticity in viral diseases, where these cells can transdifferentiate into other phenotypes, thereby shifting the immune balance. Key findings include: (i) a newly appreciated flexibility in T-cell immunity against influenza, where protection can occur independently of classical Th1 or Th17 master regulators; (ii) the detrimental role of IL-17 in severe COVID-19 and RSV pathology, driving neutrophilic inflammation; (iii) the selective depletion of gut Th17 cells by HIV as a central mechanism driving chronic inflammation and microbial translocation; (iv) the divergent Th17 polarization patterns in HBV versus HCV infection; and (v) the involvement of Th17 cells in neuroinflammation and demyelination in HSV, EBV, and HTLV-1 infections. Furthermore, we highlight the emerging role of immunometabolism as a regulator of Th17/Treg balance and the potential of therapeutic interventions targeting metabolic pathways. By providing a comprehensive overview of recent discoveries, this review aims to inform future diagnostic and therapeutic strategies that modulate Th17 responses in viral diseases.