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Published on: July 26, 2019
Original antigenic sin responses to influenza viruses
Jin Hyang Kim1, Ioanna Skountzou, Richard Compans
1Department of Microbiology and Immunology, Emory Vaccine Center, Emory University, Atlanta, Georgia 30329, USA.
Original antigenic sin paradoxically impairs immunity to new influenza strains by favoring antibody responses to older viruses. This immune phenomenon reduces protective responses and may help variant viruses evade immune detection.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Burnet's rule describes how antigen (Ag) recruits specific lymphocytes for immune responses.
- Original antigenic sin is a paradoxical immune phenomenon where prior exposure influences responses to new antigens.
- This phenomenon involves antibody (Ab) production skewed towards older viral strains over novel ones, potentially worsening infections.
Purpose of the Study:
- To investigate the extent to which original antigenic sin is induced by variant influenza viruses.
- To determine the impact of original antigenic sin on protective immunity and recall responses.
- To explore if original antigenic sin is a strategy used by influenza viruses to subvert the immune system.
Main Methods:
- Sequential infection of mice with two related strains of influenza A virus.
- Analysis of antibody responses to both viral strains following sequential infection.
Main Results:
- Original antigenic sin significantly decreased the development of protective immunity and recall responses to the second influenza virus strain.
- Sequential infection resulted in almost exclusive antibody responses directed at the first viral strain encountered.
- Evidence suggests variant influenza viruses may exploit original antigenic sin to evade immune detection.
Conclusions:
- Original antigenic sin demonstrably impairs adaptive immunity to sequential influenza virus infections.
- This phenomenon leads to reduced protective immunity and recall responses.
- Variant influenza viruses may utilize original antigenic sin as a mechanism to subvert host immune responses.
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