Measles and ‘Immune Amnesia’

Posted on 2019-11-11

How the Immune System Forgets to Fight

Designed by kjpargeter / Freepik

Measles is a highly contagious infectious disease, caused by the measles virus (MV). Though it is infamous for its virulence and previously devastating death count, it is perhaps more recently well-known for the impressive global vaccination efforts against it. Unfortunately, this hopeful path towards the elimination, and potential eradication, of the disease is darkened by the increased reduction in vaccinations. Measles cases have increased>30% from 2017 to 2018 worldwide; a sobering reality that the virus remains a global threat.

Immunosuppression following infection has long been associated with measles, yet the precise mechanisms that underpin this have, until recently, remained poorly understood. Through the detailed analysis of antibody(Ab) repertoires, before and after MV infection, two modes of immune restructuring have been identified: (i) the incomplete reconstitution of naïveB cell pools, resulting in immunological immaturity, and (ii) compromised immune memory to previously encountered pathogens, due to a depletion in B memory clones.

Naïve B cells are immune cells, continuously maintained by a pool of bone marrow progenitors, which have not yet been exposed to an antigen. Upon antigen exposure, they are destined to differentiate into memory B or plasma cells, eliciting an antigen-specific Ab response. The clonal expansion of memory B cells then generates immunological memory, mediated through antigen-specific B cell receptors (BCRs).

The recognition of new antigens is dependent on the pool ofnaïve B cells. Following MV infection, it has been identified that the naïveBCR repertoires have a restricted use of IGHV (Immunoglobulin Heavy Variable) genes, which inevitably disrupts their ability to respond to novel pathogens. Additionally, the ability of memory B cells to recognise previously encountered pathogens is replaced by a generation of measles-specific B cell clones. Not only does this result in ‘immune amnesia’, leaving the immune system vulnerable to pathogens it was previously armed against, but a depletion in naïve B cells makes it more difficult to generate an effective response to future pathogens.

Although this is a bleak revelation on the damage that MVincurs on naïve and memory B cell diversity, and the subsequent role that this plays in mortality and secondary infections, this research is perhaps the push needed to reignite vaccination efforts. It clearly highlights the importance of vaccination and herd immunity, to protect against not only MV, but the loss of immunity for other pathogens. Additionally, there is now a strong foundation for future research into the bone marrow effects of MV, and this is a firm reminder that the complex interactions between host, virus and the immune system, should not be underestimated.

Further reading:

Incomplete genetic reconstitution of B cell pools contributes to prolonged immunosuppression after measles

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