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Basic Characteristics of Mutations
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Mutation Site
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F195A |
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Mutation Site Sentence
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To gain insight into the molecular mechanism by which NEF impairs CD4 T‐cell help, we analyzed the activity of a series of mutant NEF proteins in the adoptive transfer model (Fig 3A). This included NEF F195A which lacks the ability to associate with the cellular p21‐activated kinase 2 (PAK2) to negatively modulate host cell actin dynamics and motility (O'Neill et al, 2006; Stolp et al, 2009; Stolp et al, 2012), a NEF variant with disrupted di‐leucine motif (NEF LLAA) that lacks the ability to internalize cell surface receptors such as CD4 (Craig et al, 1998; Greenberg et al, 1998), NEF AxxA in which an SH3 domain‐binding PxxP motif is disrupted and fails, e.g., to relocalize the TCR proximal kinase Lck from the plasma membrane to intracellular compartments (Saksela et al, 1995; Pan et al, 2012), as well as NEF variants carrying a deletion of an N‐terminal protein interaction platform (NEF ∆12‐39) or a mutation in an interaction motif within residues 12‐39 (NEF A32‐39) required for CD4 downregulation and SERINC5 antagonism (Ananth et al, 2019). |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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Nef |
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Standardized Encoding Gene
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Nef
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Genotype/Subtype
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HIV-1 |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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HIV Infections
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Immune
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Y |
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
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- |
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Location
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- |
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Literature Information
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PMID
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33146906
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Title
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HIV-1 infection of CD4 T cells impairs antigen-specific B cell function
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Author
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Kaw S,Ananth S,Tsopoulidis N,Morath K,Coban BM,Hohenberger R,Bulut OC,Klein F,Stolp B,Fackler OT
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Journal
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The EMBO journal
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Journal Info
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2020 Dec 15;39(24):e105594
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Abstract
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Failures to produce neutralizing antibodies upon HIV-1 infection result in part from B-cell dysfunction due to unspecific B-cell activation. How HIV-1 affects antigen-specific B-cell functions remains elusive. Using an adoptive transfer mouse model and ex vivo HIV infection of human tonsil tissue, we found that expression of the HIV-1 pathogenesis factor NEF in CD4 T cells undermines their helper function and impairs cognate B-cell functions including mounting of efficient specific IgG responses. NEF interfered with T cell help via a specific protein interaction motif that prevents polarized cytokine secretion at the T-cell-B-cell immune synapse. This interference reduced B-cell activation and proliferation and thus disrupted germinal center formation and affinity maturation. These results identify NEF as a key component for HIV-mediated dysfunction of antigen-specific B cells. Therapeutic targeting of the identified molecular surface in NEF will facilitate host control of HIV infection.
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Sequence Data
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-
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