Conversely, our study raises questions about how intra-host viral diversity, frequency of episodic bursts, and virus shedding would be altered in the setting of immunocompromised mice, such as CD4 or CD8 T cell deficiency (e.g., mirroring clinical application of alemtuzumab, natalizumab or idiopathic CD4 lymphopenia) and absolute/relative decline in antiviral antibodies (mirroring anti-CD20 therapy). This evidence concerns the gene CD8A and congenital T-cell immunodeficiency.