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

Gisslén, Magnus, 1962 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för infektionssjukdomar,Institute of Internal Medicine, Dept of Infectious Diseases
Fredman, Pam, 1950 (author)
Gothenburg University,Göteborgs universitet,Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap,Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Fuchs, Dietmar (author)
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Lekman, Annika, 1949 (author)
Gothenburg University,Göteborgs universitet,Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap,Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Rosengren, Lars, 1954 (author)
Gothenburg University,Göteborgs universitet,Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap,Institute of Clinical Neurosciences, Section of Experimental Neuroscience
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 (creator_code:org_t)
2009-07-08
2005
English.
In: Scand J Infect Dis. - : Informa UK Limited. - 0036-5548. ; 37:11-12, s. 877-81
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)

Keyword

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

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