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Temporarily controlled HIV-1 replication after intravenous immunoglobulin treatment of Guillain-Barre syndrome

Journal article
Authors Magnus Gisslén
Pam Fredman
Dietmar Fuchs
Annika Lekman
Lars Rosengren
Published in Scand J Infect Dis
Volume 37
Issue 11-12
Pages 877-81
ISSN 0036-5548 (Print)
Publication year 2005
Published at Institute of Internal Medicine, Dept of Infectious Diseases
Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Pages 877-81
Language en
Keywords Adult, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes/immunology/virology, Guillain-Barre Syndrome/cerebrospinal fluid/*complications/*therapy, HIV Infections/*complications/immunology/*therapy/virology, *HIV-1/physiology, Humans, Immunoglobulins, Intravenous/*therapeutic use, Lymphocyte Activation, Male, RNA, Viral/blood/cerebrospinal fluid, Sulfoglycosphingolipids/cerebrospinal fluid, Virus Replication
Subject categories Neurochemistry, Microbiology in the medical area


HIV establishes a latent infection in resting CD4(+) T-lymphocytes. A possible strategy to eliminate cellular reservoirs in long-lived, HIV-1-infected quiescent CD4(+) T-lymphocytes might be to add T-cell-activating agents to potent antiretroviral therapy. In this report we describe a patient with Guillain-Barre syndrome treated with high dose intravenous immunoglobulin (IVIG) in addition to antiretroviral therapy. A transiently increased viral load and immunoactivation during the IVIG treatment suggest activation of latently infected cells and increased turnover rate of the latent viral reservoir. HIV replication was controlled with plasma viral load <20 copies/ml, for at least 3 months after antiretroviral treatment interruption. CSF neural markers reflecting degenerative processes in the brain during the symptomatic period and follow-up were also analysed. Very high CSF sulfatide concentrations were found indicating that the pathology involves severe demyelination.We hypothesize that IVIG in this case contributed to an activation of latently infected cells, which led to a transient increase in plasma HIV-1 RNA during the IVIG treatment and a long period of undetectable viral load after antiretroviral treatment interruption. Further, this is the first time, to our knowledge, that detailed CSF findings are described in HIV-1 associated GBS.

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