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Updated: May 29, 2026
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Generation of Escape Variants of Neutralizing Influenza Virus Monoclonal Antibodies
Published on: August 29, 2017
HCMV grabs a mechanism to escape neutralization
Roselyn J Eisenberg1, Tina M Cairns, Gary H Cohen
1School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA. roselyn@dental.upenn.edu
Cell Host & Microbe
|September 20, 2011
Summary
Monoclonal antibody MSL-109 failed to prevent human cytomegalovirus (HCMV) disease. Researchers discovered MSL-109 rapidly induces antibody resistance through a nongenetic mechanism, impacting antibody interactions within cells and virions.
Area of Science:
- Immunology
- Virology
- Microbiology
Background:
- Human cytomegalovirus (HCMV) is a significant pathogen causing disease, particularly in immunocompromised individuals.
- Monoclonal antibodies are explored as therapeutic agents against viral infections.
- The neutralizing antibody MSL-109 was investigated for its efficacy against HCMV.
Purpose of the Study:
- To investigate the mechanism behind the clinical failure of the HCMV-neutralizing monoclonal antibody MSL-109.
- To understand how HCMV develops resistance to antibody-mediated therapies.
- To elucidate the interactions of antibodies with HCMV targets both extracellularly and intracellularly.
Main Methods:
- The study involved analyzing the interaction of MSL-109 with HCMV.
- Experiments were designed to identify the mechanism of antibody resistance.
- Methods likely included cell-based assays and potentially virion-based analyses.
Main Results:
- MSL-109 failed to prevent HCMV-induced disease in clinical trials.
- The antibody MSL-109 was found to rapidly induce antibody resistance in HCMV.
- This resistance was mediated by a nongenetic mechanism, suggesting rapid adaptation by the virus.
Conclusions:
- Antibody resistance can develop rapidly in HCMV through nongenetic mechanisms.
- Understanding these resistance pathways is crucial for developing effective antiviral therapies.
- Antibodies may interact with viral targets in complex ways, both inside and outside host cells and virions.
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