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Esadze, A.

Publications and source records attributed to Esadze, A..

2 recordsLinked to original sources

Structure-Based Design of a Highly Immunogenic, Conformationally Stabilized FimH Antigen for a Urinary Tract Infection Vaccine

Adhesion of E. coli to the urinary tract epithelium is a critical step in establishing urinary tract infections. FimH is an adhesin positioned on the fimbrial tip which binds to mannosylated proteins on the urinary tract epithelium via its lectin domain (FimHLD). FimH is of interest as a target of vaccines to prevent urinary tract infections (UTI). Previously, difficulties in obtaining purified recombinant FimH from E. coli along with the poor inherent immunogenicity of FimH have hindered the development of effective FimH vaccine candidates. To overcome these challenges, we have devised a novel production method using mammalian cells to produce high yields of homogeneous FimH protein with comparable biochemical and immunogenic properties to FimH produced in E. coli. Next, to optimize conformational stability and immunogenicity of FimH, we used a computational approach to design improved FimH mutants and evaluated their biophysical and biochemical properties, and murine immunogenicity. This approach identified a highly immunogenic FimH variant (FimH-DSG TM) that is produced at high yields in mammalian cells. By x-ray crystallography, we confirmed that the stabilized structure of the FimHLD in FimH-DSG TM is similar to native FimH on the fimbrial tip. Characterization of monoclonal antibodies elicited by FimH-DSG TM that can block bacterial binding to mannosylated surfaces identified 4 non-overlapping binding sites whose epitopes were mapped via a combinatorial cryogenic electron microscopy approach. Novel inhibitory epitopes in the lectin binding FimH were identified, revealing diverse functional mechanisms of FimH-directed antibodies with relevance to FimH-targeted UTI vaccines. Author summaryEscherichia coli is the primary cause of urinary tract infections. Adherence to uroepithelial surfaces is mediated by the pilus adhesin protein FimH, which is of interest as a vaccine candidate. We developed a method for producing recombinant FimH at bioprocess scale, previously a barrier to commercial development. Structure-based design and screening was used to identify a novel FimH vaccine candidate with improved stability and immunogenicity in mice. Structure of this full-length protein was determined by X-ray crystallography and shown to closely resemble the pilus adhesin present in its native form on the bacterial surface. Binding sites of biologically active FimH monoclonal antibodies were determined by X-ray crystallography or by cryo-electron microscopy, providing insights into mechanisms by which antibodies block binding of the bacteria to urinary tract receptors. One sentence summaryStructure-based design of a conformationally stabilized E. coli FimH vaccine candidate capable of eliciting antibodies to diverse epitopes with the ability to block bacterial binding to bladder epithelial cells.

microbiology↗

Deficient uracil base excision repair leads to persistent dUMP in HIV proviruses during infection of monocytes and macrophages

Non-dividing cells of the myeloid lineage such as monocytes and macrophages are target cells of HIV that have low dNTP pool concentrations and elevated levels of dUTP, which leads to frequent incorporation of dUMP opposite to A during reverse transcription ("uracilation"). One factor determining the fate of dUMP in proviral DNA is the host cell uracil base excision repair (UBER) system. Here we explore the relative UBER capacity of monocytes (MC) and monocyte-derived macrophages (MDM) and the fate of integrated uracilated viruses in both cell types to understand the implications of viral dUMP on HIV diversification and infectivity. We find that monocytes are almost completely devoid of functional UBER, while macrophages are mainly deficient in the initial enzyme uracil DNA glycosylase (hUNG2). Accordingly, dUMP persists in viral DNA during the lifetime of a MC and can only be removed after differentiation of MC into MDM. Overexpression of human uracil DNA glycosylase in MDM prior to infection resulted in rapid removal of dUMP from HIV cDNA and near complete depletion of dUMP-containing viral copies. This finding establishes that the low hUNG2 expression level in these cells limits UBER but that hUNG2 is restrictive against uracilated viruses. In contrast, overexpression of hUNG2 after viral integration did not accelerate the excision of uracils, suggesting that they may poorly accessible in the context of chromatin. We found that viral DNA molecules with incorporated dUMP contained unique (+) strand transversion mutations that were not observed when dUMP was absent (G[->]T, T[->]A, T[->]G, A[->]C). These observations and other considerations suggest that dUMP introduces errors predominantly during (-) strand synthesis when the template is RNA. These mutations may arise from the increased mispairing and duplex destabilizing effects of dUMP relative to dTMP during reverse transcription. Overall, the likelihood of producing a functional virus from in vitro infection of MC is about 50-fold and 300-fold reduced as compared to MDM and activated T cells. The results implicate viral dUMP incorporation in MC and MDM as a potential viral diversification and restriction pathway during human HIV infection.

microbiology↗