Involvement of FcγR I (CD64) in the Mechanism of HIV-1 Inhibition by Polyclonal IgG Purified from Infected Patients in Cultured Monocyte-Derived Macrophages

Holl, Vincent; Hemmerter, Stéphane; Burrer, Renaud; Schmidt, Sylvie; Bohbot, Alain; Aubertin, Anne-Marie; Moog, Christiane

doi:10.4049/jimmunol.173.10.6274

Cited by 70 publications

(81 citation statements)

References 51 publications

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“…The coordinates were deposited with the Research Collaboratory for Structural Bioinformatics (RCSB) PDB with ID code 4R61. The HIV-1 inhibitory activity of the covNHR constructs was studied using neutralizing assays on TZM-bL cells infected with HIV-1 SF-162 pseudoviruses and PBMCs using HIV-1 primary isolates from various subtypes sensitive to neutralization (34,35). Comprehensive experimental details are given in SI Appendix.…”

Section: Methodsmentioning

confidence: 99%

Single-chain protein mimetics of the N-terminal heptad-repeat region of gp41 with potential as anti–HIV-1 drugs

Crespillo

Cámara-Artigas

Casares

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance The envelope subunit gp41 is an attractive target for therapeutic intervention against HIV-1. Interfering with the interaction between the heptad-repeat regions of gp41 is a promising approach to inhibit HIV-1 fusion to the host cell membrane. Here, we present an alternative rational design and protein-engineering approach to produce highly stable single-chain proteins that accurately mimic the trimeric coiled-coil surface of the gp41 N-terminal heptad repeat. This approach has a strong potential for development to HIV-1 drugs, vaccines, or microbicides and could be extendable to the design of proteins interfering with other types of coiled-coil interactions.

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Section: Methodsmentioning

confidence: 99%

Single-chain protein mimetics of the N-terminal heptad-repeat region of gp41 with potential as anti–HIV-1 drugs

Crespillo

Cámara-Artigas

Casares

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…These cells play important roles in HIV infection because they are susceptible to infection and they are potentially components of anti-HIV immunity or pathogenesis (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). The Fc␥Rs found on these cells include Fc␥RI (CD64), Fc␥RIIa and IIb (CD32), and Fc␥RIIIa (CD16) (18).…”

Section: H Uman Immunodeficiency Virus (Hiv) Infection Is Char-mentioning

confidence: 99%

FcγRIIa Genotype Predicts Progression of HIV Infection

Forthal

Landucci

Bream

et al. 2007

The Journal of Immunology

119

129

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Polymorphisms in FcγR genes are associated with susceptibility to or severity of a number of autoimmune and infectious diseases. We found that HIV-infected men in the Multicenter AIDS Cohort Study with the FcγRIIa RR genotype progressed to a CD4+ cell count of <200/mm3 at a faster rate than individuals with the RH or HH genotypes (relative hazard = 1.6; p = 0.0001). However, progression to AIDS (using the broad definition of either a CD4+ cell count <200/mm3 or development of an AIDS-defining illness) was less impacted by FcγRIIa genotype, largely because HH homozygotes had an increased risk of Pneumocystis jiroveci pneumonia as an AIDS-defining illness. We also showed that chronically infected subjects develop a substantial anti-gp120-specific IgG2 response. Moreover, HIV-1 immune complexes are more efficiently internalized by monocytes from HH subjects compared with RR subjects, likely because of the presence of IgG2 in the complexes. Finally, the FcγRIIIa F/V gene polymorphism was not associated with progression of HIV infection, but, as demonstrated previously, did predict the risk of Kaposi’s sarcoma. These results demonstrate the importance of FcγRs in AIDS pathogenesis and point toward a critical role for interactions between FcγRs and immune complexes in disease progression.

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“…Ces anticorps possèdent des fonctions inhibitrices dépendantes de leur région Fc et de l'expression des RFc [19,20]. Chez les patients infectés, des anticorps inhibiteurs sont fréquemment détectés très tôt après la phase aiguë de l'infection ( Figure 1, courbe rouge) [21,22]. De manière intéressante, une activité inhibitrice dépendante des RFc est détectée de manière significativement plus élevée dans une cohorte de patient dits « contrôleurs » ou « élites » (patients ayant une virémie indétectable pendant plusieurs années en absence de tout traitement) par rapport aux patients virémiques [23].…”

Section: Les Anticorps Non Neutralisants Inhibiteurs In Vivounclassified