CD8 LYMPHOCYTOSIS IN PRIMARY CYTOMEGALOVIRUS (CMV) INFECTION OF ALLOGRAFT RECIPIENTS - EXPANSION OF AN UNCOMMON CD8(-) SUBSET AND ITS PROGRESSIVE REPLACEMENT BY CD8(+) CD57(+) T-CELLS() CD57()

Allograft recipients undergoing cytomegalovirus infection present incr eased proportions of circulating CD8(+) lymphocytes. A longitudinal st udy of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction reveale d selective imbalances of peripheral blood CD8(+) T cell subsets. Init ially, CMV viraemia is associated with elevated CD8(+bright) T cell nu mbers and T cell activation. Activation markers fall to normal when vi ral cultures become negative (before the end of the first month). Duri ng the second to sixth month, most (12/16) patients keep up high CD8() T cell counts (1050-2900 CD8(+) cells/mm(3)), comprising an uncommon CD8(+) T cell subset, as 45-73% of CD8(+bright) lymphocytes were CD3( +) and TCR alpha beta(+), but were not stained by anti-CD28, CD11b, CD 16, CD56, and CD57 antibody. Unexpectedly, CD8(+)CD57(+) T cells, a ha llmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively th ereafter. They become the predominant CD8(+) T cell subset after 6 mon ths of infection and their persistence for several (up to 4) years is strongly correlated (r = 0.87) with expansion of CD8(+) cells. By anal ysis with MoAbs, there was no bias towards the use of particular TCR-V beta gene families at any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8(+)CD57(-) subset and its progressive replacement b y CD8(+)CD57(+) T cells that are chronically elicited by CMV.