Structural Approaches to HIV-1 Immunogen Design and BNAb Analysis

NIH Pandemic-Era Grants

Pandemic Era Grants

2019

Document text

Principal Investigator: ELLIS L REINHERZ
Organization: DANA-FARBER CANCER INST
Fiscal Year: 2019
Award: $1,289,810
Funding agency: National Institute of Allergy and Infectious Diseases

ABSTRACT 
 There are only a handful of sites on the HIV-1 envelope protein that represent regions of vulnerability for 
elicitation of broadly neutralizing antibody (BNAbs). Four are associated with the gp120 subunit while one of 
the sites resides in the membrane proximal external region (MPER) of gp41. We previously showed that the 
MPER is a conserved structural element consisting of two helices separated by a hinge with tandem joints that 
facilitates viral hemifusion and fusion. MPER-specific BNAbs exert their anti-viral effect by disturbing gp41 
conformational change required for viral entry into host cells. These BNAbs manifest extraordinary HIV-1 strain 
and clade neutralization breadth as exemplified by the mAb 10E8. Until recently, it was not known how to elicit 
anti-MPER specific Abs. The MPER is poorly immunogenic either as a component of the intact gp160 trimeric 
spike or in the context of an isolated gp41 subunit immunogen. Hence, anti-MPER Abs are not the most 
frequent specificity elicited during natural infections. This subdominance is not surprising given the fact that the 
MPER is lipid immersed to a significant degree. However, very recently, stealth liposomes arraying the isolated 
MPER and cargoing conjoint CD4 T cell epitope and TLR ligands were found to effectively foster MPER- 
specific bone marrow (BM) plasma cell development in the mouse, including those producing Abs with somatic 
hypermutation and lengthy CDRH3 as shown by microengraving and single-cell PCR analysis. Immunogenicity 
of this segment is dominated by residue accessibility and modulated by stereochemistry. The consequence of 
the latter is that unwanted specificities can be engendered during fabricated insertion of the MPER segment 
into a lipid membrane. Here, by appending transmembrane (TM) segments with relevant membrane tilt angles 
guided by computational predictions and structural/biophysical verification as well as removal of exposed 
misguiding chemical adducts, we shall program the desired nanovaccine immunogenicity for B cell memory 
and plasma cell development. In Aim I, we shall use native HIV-1 or variant TM sequences to insert the MPER 
into nanodiscs and liposomes. Orientation and depth of MPER residues will be assessed by NMR and EPR 
methods and iteratively adjusted and refined in conjunction with molecular electron microscopy and X-ray 
crystallographic studies using anti-MPER Abs. In Aim II, using conventional mice as well as the KyMouse with 
complete humanization of the mouse Ig loci, we shall establish both immunogens and vaccine schedules to 
engender BNAb elicitation, comparing them with those arising from natural HIV-1 infection. Existing liposome 
formulations, novel nanodiscs and evolving biomaterial arrays will be used for immunization and then MPER 
residue specificity, extraction activity, native spike binding and HIV-1 neutralizing activity of elicited antibodies 
will be assessed by examining bulk IgG and single BM plasma cell Abs. Optimization of several MPER 
sequences for induction of highly potent BNAbs against M subgroup clades will be performed in preparation for 
future clinical nanovaccine trials.

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