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Viral load determines the B-cell response in the cerebrospinal fluid during human immunodeficiency virus infection
Sabine Cepok1, Gloria von Geldern, Thorsten Nolting
1Department of Neurology, Heinrich Heine-University, Düsseldorf, Germany.
Insights
Human immunodeficiency virus (HIV) central nervous system (CNS) infection triggers an early B-cell response in cerebrospinal fluid (CSF). Plasmablasts, a key B-cell subset, correlate with HIV load in the CSF, especially in early, untreated infection.
Area of Science:
- Neuroimmunology
- Virology
- Immunology
Background:
- HIV infection of the central nervous system (CNS) often involves increased immunoglobulin synthesis and cerebrospinal fluid (CSF) pleocytosis.
- The specific B-cell response within the CNS during HIV infection remains poorly understood.
Purpose of the Study:
- To investigate the relationship between HIV viral load and the frequency/phenotype of B cells in the CSF of HIV-infected individuals.
- To characterize the B-cell response in the CNS during HIV infection.
Main Methods:
- Flow cytometry was used to analyze T cells, B cells, plasmablasts, and plasma cells in CSF and peripheral blood from 33 HIV-infected patients and 12 controls.
- HIV RNA levels in CSF and serum were quantified using kinetic polymerase chain reaction.
Main Results:
- B-cell and plasmablast levels were elevated in the CSF of HIV-infected patients compared to controls.
- CSF plasmablasts were more frequent in early HIV infection and correlated strongly with intrathecal IgG synthesis and CSF HIV RNA levels.
- Antiviral treatment significantly reduced HIV RNA and CSF plasmablasts in previously untreated patients.
Conclusions:
- HIV CNS infection elicits a significant early B-cell response.
- Plasmablasts are the predominant virus-related B-cell subset in the CSF during HIV infection.
Objective:
Human immunodeficiency virus (HIV) infection of the central nervous system (CNS) is frequently associated with intrathecal immunoglobulin synthesis and cerebrospinal fluid (CSF) pleocytosis, but little is known about the B-cell response in the CSF of these patients. In this study, we investigated the relation between virus load and the frequency and phenotype of B cells in the CSF of HIV-infected patients.
Methods:
The distribution of T cells, B cells, short-lived plasmablasts, and long-lived plasma cells was analyzed by flow cytometry in CSF and peripheral blood of 33 patients with HIV infection compared with 12 patients with noninfectious CNS diseases. HIV RNA copy number in CSF and serum was quantified by kinetic polymerase chain reaction.
Results:
B-cell and plasmablast levels were increased in the CSF of HIV-infected patients compared with patients with noninfectious CNS diseases. Whereas CSF B cells were found at similar frequency during early and late stages of HIV infection, plasmablasts were more prevalent in the CSF during early infection. Plasmablasts in the CSF correlated with intrathecal IgG synthesis and even stronger with HIV RNA copy numbers in CSF, in particular, in untreated, early HIV-infected individuals. Initiation of antiviral treatment in therapy-naive patients strongly decreased HIV copy numbers and plasmablasts in CSF.
Interpretation:
Our findings demonstrate that HIV infection of the CNS triggers an early profound B-cell response, with plasmablasts serving as the main virus-related B-cell subset in the CSF.
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