Aggregate complexes of HIV-1 induced by multimeric antibodies

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• 作者：Daniel J Stieh (1) (2)
  Deborah F King (3)
  Katja Klein (3)
  Pinghuang Liu (4) (9)
  Xiaoying Shen (4)
  Kwan Ki Hwang (4)
  Guido Ferrari (4)
  David C Montefiori (4)
  Barton Haynes (4)
  Punnee Pitisuttithum (5)
  Jaranit Kaewkungwal (5)
  Sorachai Nitayaphan (6)
  Supachai Rerks-Ngarm (7)
  Nelson L Michael (8)
  Merlin L Robb (8)
  Jerome H Kim (8)
  Thomas N Denny (4)
  Georgia D Tomaras (4)
  Robin J Shattock (3)
  
  1. Center for Infection ; Department of Cellular and Molecular Medicine ; St George鈥檚 ; University of London ; London ; SW17 0RE ; UK
  2. Current address ; Department of Cellular and Molecular Biology ; Northwestern University ; Feinberg School of Medicine ; Chicago ; IL ; 60611 ; USA
  3. Mucosal Infection & Immunity Group ; Section of Infectious Diseases ; Imperial College London ; St Mary鈥檚 Campus ; London ; W2 1PG ; UK
  4. Duke Human Vaccine Center ; Duke University Medical Center ; Durham ; NC ; 27710 ; USA
  9. Current address ; Division of Swine Infectious Diseases ; Harbin Veterinary Research Institute ; Chinese Academy of Agricultural Sciences ; Harbin ; 150001 ; China
  5. Faculty of Tropical Medicine ; Mahidol ; Thailand
  6. Armed Forces Research Institute of Medical Sciences ; Bangkok ; Thailand
  7. Ministry of Public Health ; Bangkok ; Thailand
  8. Military HIV Research Program ; Walter Reed Army Institute of Research ; Silver Spring ; Maryland ; United States of America
  
• 关键词：HIV ; 1 ; Mucosal immunity ; Immunoglobulin A ; Aggregation
• 刊名：Retrovirology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：11
• 期：1
• 全文大小：1,128 KB
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• 刊物主题：Virology; Infectious Diseases; Cancer Research;
• 出版者：BioMed Central
• ISSN：1742-4690

文摘

Background Antibody mediated viral aggregation may impede viral transfer across mucosal surfaces by hindering viral movement in mucus, preventing transcytosis, or reducing inter-cellular penetration of epithelia thereby limiting access to susceptible mucosal CD4 T cells and dendritic cells. These functions may work together to provide effective immune exclusion of virus from mucosal tissue; however little is known about the antibody characteristics required to induce HIV aggregation. Such knowledge may be critical to the design of successful immunization strategies to facilitate viral immune exclusion at the mucosal portals of entry. Results The potential of neutralizing and non-neutralizing IgG and IgA monoclonals (mAbs) to induce HIV-1 aggregation was assessed by Dynamic light scattering (DLS). Although neutralizing and non-neutralizing IgG mAbs and polyclonal HIV-Ig efficiently aggregated soluble Env trimers, they were not capable of forming viral aggregates. In contrast, dimeric (but not monomeric) IgA mAbs induced stable viral aggregate populations that could be separated from uncomplexed virions. Epitope specificity influenced both the degree of aggregation and formation of higher order complexes by dIgA. IgA purified from serum of uninfected RV144 vaccine trial responders were able to efficiently opsonize viral particles in the absence of significant aggregation, reflective of monomeric IgA. Conclusions These results collectively demonstrate that dIgA is capable of forming stable viral aggregates providing a plausible basis for testing the effectiveness of aggregation as a potential protection mechanism at the mucosal portals of viral entry.