The study investigates the role of interleukin-10 (IL-10) in viral persistence and T-cell dysfunction. In mice infected with the lymphocytic choriomeningitis virus (LCMV) variant Clone 13 (CI 13), which causes persistent infection, IL-10 production by antigen-presenting cells (APCs) is significantly upregulated, leading to impaired T-cell responses. Genetic deletion of *Il10* resulted in robust effector T-cell responses, rapid virus elimination, and the development of antiviral memory T-cell responses. Therapeutic administration of an IL-10 receptor-blocking antibody restored T-cell function and eliminated viral infection. The findings suggest that IL-10 is a key molecule that induces immunosuppression and promotes viral persistence, and that neutralizing IL-10 can prevent or treat persistent infections.The study investigates the role of interleukin-10 (IL-10) in viral persistence and T-cell dysfunction. In mice infected with the lymphocytic choriomeningitis virus (LCMV) variant Clone 13 (CI 13), which causes persistent infection, IL-10 production by antigen-presenting cells (APCs) is significantly upregulated, leading to impaired T-cell responses. Genetic deletion of *Il10* resulted in robust effector T-cell responses, rapid virus elimination, and the development of antiviral memory T-cell responses. Therapeutic administration of an IL-10 receptor-blocking antibody restored T-cell function and eliminated viral infection. The findings suggest that IL-10 is a key molecule that induces immunosuppression and promotes viral persistence, and that neutralizing IL-10 can prevent or treat persistent infections.