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Intravenous Immunoglobulin (IVIG) Treatment for
Modulation of Immune Activation in Human Immunodeficiency Virus Type 1
Infected Therapy-Naive Individuals.
AIDS Res Hum Retroviruses. 2007 Nov;23(11):1348-53.
Vermeulen JN, Prins JM, Bunnik E, Hack CE, Jurriaans S, Miedema F, Lange JM, Schuitemaker H.
IATEC,
Amsterdam, the Netherlands., Center for Poverty-related Communicable
diseases, Department of Internal Medicine, Center for Infection and
Immunity Amsterdam, Academic Medical Center, University of Amsterdam,
Amsterdam, the Netherlands.
We evaluated the ability of
intravenous immunoglobuline (IVIG) to diminish immune hyperactivation,
which is considered a major cause of CD4(+) T cell loss during chronic
HIV-1 infection and whether this affected CD4(+) T cell counts and
plasma HIV-1 RNA (pVL).
Therefore, we treated six chronically
HIV-1-infected, antiretroviral-therapy-naive patients with IVIG (0.4
g/kg) at weeks 0 and 4, with a follow-up of 12 weeks after the second
dosage during which pVL, T cell numbers, and T cell activation were
measured. At baseline median CD4(+) T cell counts were 300 (range
200-460) x 10(6)/liter and median pVL was 5.0 (range 3.2-5.2)
log(10)copies/ml. IgG plasma levels peaked during the first days after
administration. We observed a decrease in the percentage of activated
(CD38(+) HLA-DR(+)) CD4(+) and CD8(+) T cells [3.5% (range 1-7%) and 5%
(1-10%), respectively (p = 0.027)], but no effect on the fraction of
proliferating CD4(+) or CD8(+) T cells as measured by Ki67 expression.
CD4(+) T cell counts were significantly increased on day 4 (median +55
cells, range 0-150, p = 0.043). pVL was significantly increased on day
1 after IVIG infusion (median +0.13 log(10), range 0.01-0.55, p =
0.028). All these parameters returned to baseline levels within 1 week
after infusion. In conclusion, administration of IVIG caused a
temporary decrease in T cell activation and an increase in CD4(+) T
cell counts, despite an increase in pVL. Our results support the
hypothesis that T cell activation, rather than direct HIV-1 infection,
mediates the loss of CD4(+) T cells and suggest that immunomodulating
therapy in HIV-1 infection could indeed be effective.
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