ADE-VA may be of concern for other pathogens, especially rapidly mutating RNA viruses susceptible to neutralization escape. Vaccine development will need to consider potential enhancement of host susceptibility to infection due to ADE [47,48]. We propose that our strategy – passive immunization with purified polyclonal IgG isolated from previously infected/vaccinated individuals, combined with in-vivo end-point virus titration to assess the amount of virus needed to achieve infection of naïve versus passively immunized animals, can play an important role in assessing the potential for ADE-VA.
Acknowledgements
We thank F. Villinger and S. Gong (UL Lafayette/NIRC) for critical reading of the manuscript; A. Gray and E. Plake (Texas Biomed) for assistance with in vitro assays, J. Hoxie (University of Pennsylvania) for providing the SupT1.R5 cell line, C. Ochsenbauer (University of Alabama, Birmingham) for plasmid pNL-LucR.T2A. We thank K. Brasky and P. Frost for coordinating the primate studies and S. Joubran for assistance with the preparation of the manuscript. The following reagents were obtained through the NIH HIV Reagent Program, Division of AIDS, NIAID, NIH: HIV-1MN gp41 recombinant protein made in E. coli, ARP-12027 (contributed by DAIDS/NIAID; produced by ImmunoDX, LLC); recombinant HIV-1 CN54 gp140 from CHO cells, ARP-12064 (contributed by DAIDS/NIAID; produced by Polymun Scientific, Inc.).
Funding: This work was supported by NIH grants R01 DE023049 and U19 AI142636 to R.M.R.
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