MHC class Ib-restricted CD8⁺ T cells have been shown to participate in the immune response towards a number of intracellular bacterial pathogens.  In contrast, the role of non-classical CD8⁺ T cells during viral infections is largely unknown.  We sought to investigate their contributions using murine cytomegalovirus (MCMV) infection, a well-established model for human CMV.  By utilizing K^bD^b-/- mice, which lack MHC class Ia molecules, we are able to circumvent the role of classical CD8⁺ T cells.  Following MCMV challenge, we find that a subset of non-classical CD8⁺ T cells undergoes robust expansion and acquires an effector phenotype.  Importantly, this response is not due to MCMV induced inflammation.  We also demonstrate that while this population is β₂m-restricted, CD1d is dispensable.  Interestingly, despite the absence of classical CD8⁺ T cells, these mice are relatively resistant to infection.  However, there is a prolonged inflammatory phenotype not present in B6 wild-type animals, which control MCMV infection.  Additionally, non-classical CD8⁺ T cells from long-term infected mice are also capable of robust proliferation in response to secondary MCMV infection, indicating these T cells exhibit a memory-like phenotype. Taken together, these data support an important role for MHC class 1b-restricted CD8⁺ T cells during viral infection.