A. Webster et al., CYTOMEGALOVIRUS (CMV) INFECTION, CD4-1-INFECTED HEMOPHILIAC PATIENTS(LYMPHOCYTE COUNTS AND THE DEVELOPMENT OF AIDS IN HIV), Clinical and experimental immunology, 88(1), 1992, pp. 6-9
After a maximum of 11 years (median 8.3 years) from the time of HIV se
roconversion, 25 out of 59 (42%) of CMV-seropositive haemophiliacs had
progressed to AIDS, as opposed to eight out of 50 (16%) CMV seronegat
ives. The age-adjusted relative risk for AIDS among CMV seropositives
was 2.4 (P = 0.03). In order to determine how this adverse effect is m
ediated, the mean rate of decline in serial CD4+ lymphocyte counts was
studied. CD4+ lymphocyte counts tended to decline more rapidly in CMV
seropositives than in seronegatives (-0.087 x 10(9)/l per annum versu
s -0.082 x 10(9)/l per annum), but this difference did not reach stati
stical significance. The average CD4+ lymphocyte count at the time of
HIV seroconversion was estimated to be similar in CMV seropositives an
d negatives, because in HIV-l-negative haemophiliacs the CD4+ counts w
ere virtually identical, after adjustment for age (0.94 x 10(9)/l and
0.97 x 10(9)/l, respectively). The median CD4+ cell count at which AID
S developed was higher in the CMV-seropositive group (0.07 x 10(9)/l)
than in the seronegative group (0.04 x 10(9)/l), but this difference d
id not reach statistical significance. We conclude from these findings
that the adverse effect of CMV is not wholly mediated via a more rapi
d loss of CD4+ cells. We discuss other processes that may be mediated
by CMV, such as a functional deficiency of residual CD4+ cells, or dis
semination of HIV in other organs, which may be important in determini
ng the earlier onset of AIDS among CMV-seropositive subjects.