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

Artikel i vetenskaplig tidskrift
Författare Magnus Gisslén
Pam Fredman
Dietmar Fuchs
Annika Lekman
Lars Rosengren
Publicerad i Scand J Infect Dis
Volym 37
Nummer/häfte 11-12
Sidor 877-81
ISSN 0036-5548 (Print)
Publiceringsår 2005
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för infektionssjukdomar
Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap
Sidor 877-81
Språk en
Länkar dx.doi.org/10.1080/0036554050027722...
Ämnesord 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
Ämneskategorier Neurokemi, Mikrobiologi inom det medicinska området

Sammanfattning

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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