Even though lack of CD69 in EC did not impair viral replication or acute viral infection symptoms (O2 saturation and weight loss), hypothetically because of the low percentage of lung ECs expressing CD69, AAV-induced expression of CD69 in lung ECs showed less S1PR1 and claudin-5 levels, suggesting junctional dysfunction and enhanced vascular leak. This evidence concerns the gene S1PR1 and viral infectious disease.