| First Author | Mott KR | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 4 | Pages | e93444 |
| PubMed ID | 24695322 | Mgi Jnum | J:215038 |
| Mgi Id | MGI:5604568 | Doi | 10.1371/journal.pone.0093444 |
| Citation | Mott KR, et al. (2014) CD8alpha dendritic cells drive establishment of HSV-1 latency. PLoS One 9(4):e93444 |
| abstractText | 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 CD8alpha DCs impact HSV-1 latency by examining latency in the trigeminal ganglia (TG) of wild-type (WT) C57BL/6 versus CD8alpha-/- (lack functional CD8 T cells and CD8alpha+ DCs), CD8beta-/- (have functional CD8alpha+ T cells and CD8alpha+ DCs), and beta2m-/- (lack functional CD8 T cells but have CD8alpha+ DCs) mice as well as BXH2 (have functional CD8 T cells but lack CD8alpha+ DCs) versus WT C3H (have functional CD8alpha T cells and CD8alpha+ DCs) mice. We also determined whether the phenotype of CD8alpha-/- and BXH2 mice could be restored to that of WT mice by adoptive transfer of WT CD8+ T cells or bone marrow (BM) derived CD8alpha+ DCs. Our results clearly demonstrate that CD8alpha DCs, rather than CD8 T cells, are responsible for enhanced viral latency and recurrences. |
