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Alterations of the B-Cell Response by HIV-1 Replication

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An Erratum to this article was published on 29 January 2011

Abstract

While the hallmark of HIV-1 infection is the progressive depletion of CD4+ T cells, extensive B-cell dysfunction ensues that impairs the quality of the humoral response. HIV-1 infection causes hypergammaglobulinemia, polyclonal activation, loss of memory B-cell subsets, B-cell exhaustion, aberrant B-cell surface markers, and impaired humoral responses against infections and vaccinations. The totality of the mechanisms that contribute to B-cell dysfunction in vivo is unknown, although roles for HIV proteins (Env, Tat, and Nef) and virions binding to CD21 on B cells have been identified. Recent studies suggest that early antiretroviral therapy, that minimizes virus replication, can profoundly preserve the early B-cell response to HIV-1. Thus, it is clear that there is an intricate interplay between HIV replication and stimulation of the host B-cell response to infection. A better understanding of how HIV-1 subverts a productive B-cell response is needed to inform vaccine strategies that aim to elicit long-lived plasma cells and memory B-cell responses that can act quickly upon antigen stimulation.

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Acknowledgments

G.D.T is supported by the Bill and Melinda Gates Foundation (38619), National Institutes of Health (NIH/NIAID) grants: RO1AI052779, AI068618 (HIV Vaccine Trials Network), U19AI067854 (Center for HIV/AIDS Vaccine Immunology), and AI64518 (Duke Center for AIDS Research).

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No potential conflicts of interest relevant to this article were reported.

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Correspondence to Georgia D. Tomaras.

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An erratum to this article can be found at http://dx.doi.org/10.1007/s11904-011-0072-x

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Shen, X., Tomaras, G.D. Alterations of the B-Cell Response by HIV-1 Replication. Curr HIV/AIDS Rep 8, 23–30 (2011). https://doi.org/10.1007/s11904-010-0064-2

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