Comparative analysis of host responses related to immunosuppression between measles patients and vaccine recipients with live attenuated measles vaccines
H. Okada et al., Comparative analysis of host responses related to immunosuppression between measles patients and vaccine recipients with live attenuated measles vaccines, ARCH VIROL, 146(5), 2001, pp. 859-874
Measles virus infection induces a profound immunosuppression. We analyzed i
n a time-dependent manner peripheral bloods of one to two-year-old children
immunized with live attenuated measles vaccines, compared with age-matched
measles patients, for immunosuppression. In contrast to transient severe l
ymphopenia with measles patients, primarily due to extensive apoptosis of a
broad spectrum of uninfected lymphocytes, neither apoptosis nor lymphopeni
a occurred with measles vaccine recipients. Increase in number and activati
on of NK cells, which might compensate for the lymphopenia in measles patie
nts, were not found with the vaccinees. While cell surface expression of ap
optosis-related molecules such as TNF-related apoptosis-inducing ligand (TR
AIL), TRAIL-receptors, CD95(Fas) and Fas-ligand, and plasma interferon-gamm
a were increased for measles patients, they remained unchanged after vaccin
ation. Plasma interleukin (IL)-18, which is responsible for inducing apopto
sis in several infectious diseases, was increased predominantly with measle
s patients, whereas the increase remained marginal with the vaccinees. IL-1
0 was elevated transiently in both measles patients and vaccinees. Decrease
in plasma IL-12, which is often correlated with T cell suppression, was no
t found for both cases. Serum IgM and IgG antibodies to measles virus were
induced at lower titers in the vaccinees than measles patients. These resul
ts indicate that in contrast to wild-type measles virus, live measles vacci
nes hardly provoked host cytokine responses that lead to apoptotic cytolysi
s of uninfected lymphocytes, lymphopenia and immunosuppression, and thereby
induced weaker immune responses to the virus.