Type I IFNs produced in response to viral infection affected the expression levels of factors related to T cell migration from the LN to pulmonary infection sites, such as CXCL9 and CXCL10, eventually delaying the Mtb-specific Th1 cell response in the lung and thereby inducing exacerbation of pulmonary pathology with uncontrolled bacterial growth. This evidence concerns the gene CXCL10 and viral infectious disease.