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Viral infections can be broadly divided into infections that are cleared fromthe host (acute) and those that persist (chronic). Why some viruses establishchronic infections while other do not is poorly understood. One possibility isthat the host's immune response is impaired during chronic infections and isunable to clear the virus from the host. In this report we use a recentlyproposed framework to estimate the per capita killing efficacy of CD8$^+$ Tcells, specific for the MT389 epitope of polyoma virus (PyV), which establishesa chronic infection in mice. Surprisingly, the estimated per cell killingefficacy of MT389-specific effector CD8$^+$ T cells during the acute phase ofthe infection was very similar to the previously estimated efficacy of effectorCD8$^+$ T cells specific to lymphocytic choriomeningitis virus(LCMV-Armstrong), which is cleared from the host. We also find that during thechronic phase of the infection the killing efficacy of PyV-specific CD8$^+$ Tcells was only half of that of cells in the acute phase. This decrease in thekilling efficacy is again surprisingly similar to the change in the killingefficacy of LCMV-specific CD8$^+$ T cells from the peak of the response to thememory phase. Interestingly, we also find that PyV-specific CD8$^+$ T cells inthe chronic phase of the infection require lower doses of antigen to kill atarget cell. In summary, we find little support for the hypothesis thatpersistence of infections is caused by inability of the host to mount anefficient immune response, and that even in the presence of an efficientCD8$^+$ T cell response, some viruses can still establish a persistentinfection.

Similar in vivo killing efficacy of polyoma virus-specific CD8 T cells during acute and chronic phases of the infection