Abstract
The emergence of a novel influenza A virus strain into humans poses a continuous public health threat. Vaccination is the most effective means of protection against influenza. The generation of memory B cells and long-lived plasma cells that can maintain protective levels of influenza-specific antibodies for protracted periods of time is the foundation for the success of such vaccines. Influenza vaccines elicit an antibody response that is primarily targeting viral surface glycoproteins. However, frequent amino acid mutations within the immunodominant epitopes allow the virus to efficiently escape neutralization by pre-existing antibodies and consequently cause annual epidemics and occasional pandemics. Recently, monoclonal antibodies (mAbs) that target subdominant influenza epitopes have been extensively characterized. These epitopes are immunogenic, can mediate virus neutralization, and most importantly are conserved among different influenza strains. It remains puzzling, however, that despite being repeatedly exposed to such conserved domains of influenza hemagglutinin (HA) either in the form of vaccination or natural infection, most humans do not develop immunological memory that can provide broad protection against emerging virus strains. Here we will discuss the conditions that may be required for engaging such cross-reactive memory B cells in the immune response to influenza infection and vaccination in humans.
Highlights
Since the isolation of the first human influenza virus in 1933, controlling infections mediated by this respiratory pathogen has represented a formidable challenge (Webby and Webster, 2003)
Using the 2005/2006 and 2006/2007 seasonal vaccine formulations, we demonstrated that, at least in adults, the influenza-specific antibody-secreting cells (ASCs) response to seasonal vaccines peaks around 1 week post-immunization, and is characterized by several features that are reminiscent of memory B cell responses such as the enhanced kinetics of the ASCs generation, the predominance of isotype switched, highly mutated IgG secreting cells among responding ASCs (Wrammert et al, 2008)
Using an ex vivo ELISPOT assay in which memory B cells are polyclonally activated, we have shown that Influenza-specific IgG memory B cells are transiently boosted after immunization
Summary
Since the isolation of the first human influenza virus in 1933, controlling infections mediated by this respiratory pathogen has represented a formidable challenge (Webby and Webster, 2003). Two B cell populations are responsible for sustaining the humoral immune memory: the long-lived plasma cells (PCs) and memory B cells (Slifka and Ahmed, 1998; Yoshida et al, 2010). Long-lived PCs secrete antigen-specific antibodies for protracted periods of time (Slifka and Ahmed, 1998; Manz et al, 2002; Yoshida et al, 2010). Protective vaccines against influenza viruses have been introduced several decades ago, a thorough understanding of the role of memory B cells in mediating protection against influenza virus challenge remains poorly defined. We will discuss recent advances, and yet to be answered questions, regarding the role of cross-reactive memory B cell responses elicited by either infection or vaccination in protection against influenza
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