Immune responses against viral infections are crucial for eliminating the infection. However, these robust antiviral immune responses, when excessive, can lead to lung damage and respiratory failure. Foxp3+ regulatory T (Tregs) cells are instrumental in limiting intense inflammation and can promote tissue repair. Here, we explore the potential use of Tregs in treating viral infections. Using the transgenic and adeno-associated vectors (AAV) expression systems, we demonstrate a self-contained local expression of IL-2 resulting in the expansion of Tregs (CD4+, Foxp3+) in the lungs without affecting the lymphocyte population in other organs, including the draining lymph nodes of the lung. The expanded Tregs had increased expression of CD69 (tissue homing marker), CD44, ICOS, FoxP3 and CD25 (activation markers). Lung-specific Tregs are promising for alleviating pathologies due to viral injury, and hence an AAV-mediated expansion of this population is a promising therapeutic modality to limit inflammatory damage during a respiratory infection. This therapeutic has, in particular, high potential for future epidemics and pandemics, including novel strains of influenza and coronavirus, as by targeting the immune system, the therapeutic is virus-agnostic.