CD8α Dendritic Cells Drive Establishment of HSV-1 Latency

It is generally accepted that CD8 T cells play the key role to maintain HSV-1 latency in trigeminal ganglia of ocularly infected mice. Yet, comparably little is known about the role of innate immunity in establishment of viral latency. In the current study, we investigated whether CD8 alpha DCs impact HSV-1 latency by examining latency in the trigeminal ganglia (TG) of wildtype (WT) C57BL/6 versus CD8 alpha(-/-) (lack functional CD8 T cells and CD8 alpha(+) DCs), CD8 beta(-/-) (have functional CD8 alpha(+) T cells and CD8 alpha(+) DCs), and beta 2m(-/-) (lack functional CD8 T cells but have CD8 alpha(+) DCs) mice as well as BXH2 (have functional CD8 T cells but lack CD8 alpha(+) DCs) versus WT C3H (have functional CD8 alpha T cells and CD8 alpha(+) DCs) mice. We also determined whether the phenotype of CD8 alpha(-/-) and BXH2 mice could be restored to that of WT mice by adoptive transfer of WT CD8(+) T cells or bone marrow (BM) derived CD8 alpha(+) DCs. Our results clearly demonstrate that CD8 alpha DCs, rather than CD8 T cells, are responsible for enhanced viral latency and recurrences.