Increased Frequency of CD56(Bright) NK-Cells, CD3(-)CD16(+)CD56(-) NK-Cells and Activated CD4(+)T-Cells or B-Cells in Parallel With CD4(+)CDC25(High) T-Cells Control Potentially Viremia in Blood Donors With HCV

A detailed phenotypic analysis of major and minor circulating lymphocyte subsets is described in potential blood donors with markers of hepatitis C virus (HCV), including non-viremic and viremic groups. Although there were no changes in the hematological profile of either group, increased the levels of pre-NK cells (CD3(-)CD16(+)CD56(-)) and a lower frequency of mature NK cells (CD3(-)CD16(+)CD56(+)) characterized innate immunity in the non-viremic group. Both non-viremic and viremic groups displayed significantly increased levels of CD56(Bright) NK cells. Furthermore, this subset was significantly elevated in the viremic subgroup with a low viral load. In addition, an increase in the NKT2 subset was observed only in this subgroup. An enhanced frequency of activated CD4(+) T-cells (CD4(+)HLA-DR+) was a characteristic feature of the non-viremic group, whereas elevated CD19(+) B-cells and CD19(+)CD86(+) cell populations were the major phenotypic features of the viremic group, particularly in individuals with a low viral load. Although CD4(+)CD25(High) T-cells were significantly elevated in both the viremic and nonviremic groups, it was particularly evident in the viremic low viral load subgroup. A parallel increase in CD4(+)CD25(High) T-cells, pre-NK, and activated CD4(+) T-cells was observed in the nonviremic group, whereas a parallel increase in CD4(+)CD25(High) T-cells and CD19+ B-cells was characteristic of the low viral load subgroup. These findings suggest that CD56(Bright) NK cells, together with pre-NK cells and activated CD4(+) T-cells in combination with CD4(+)CD25(High) T-cells, might play an important role in controlling viremia. Elevated CD56(Bright) NK cells, B-cell responses and a T-regulated immunological profile appeared to be associated with a low viral load. J. Med. Virol. 81:49-59, 2009. (c) 2008 Wiley-Liss, Inc.