Inflammation Prompts Unsustainable Immune Response to Chronic Viral Infection
A new study suggests a new mechanism explaining the inadequate immune defence against chronic viral infection, which according to the researchers, could open avenues to vaccine development.
Scientists at the University of Basel found that in the course of an infection, specialised cells of our immune system called B cells produce antibodies that bind viruses and inactivate them. In the context of chronic viral infections such as HIV or hepatitis C virus, however, antibody production by B cells is quantitatively inadequate and starts too late.
The researchers found that inadequate antibody response to chronic viral diseases is due to the strong inflammatory reaction upon infection. While most pronounced at the onset of an infection, inflammation can persist for decades, especially in HIV/AIDS.
When triggered by inflammation, B cells produce as many antibodies as they possibly can. However, this hasty response occurs at the expense of sustainability. B cells that turn on antibody production too quickly lose their potential to proliferate and die shortly thereafter. As a consequence, the immune response takes an impetuous start but subsides rapidly.
Unsustainable Response
The scientists theorise that this panic reaction of B cells reflects a mechanism ensuring an optimised response to acute life threatening infections. In the context of chronic infections, however, the battle is not decided within a matter of days, but rather only after months or years. Under these circumstances, the hasty reaction of our body seems inappropriate and may actually favour the virus.
The researchers hope that this fundamental mechanism may provide a basis to improve vaccination strategies against chronic viral diseases.
The findings were published in the journal Science Immunology.
Source of this article:
Interferon-driven deletion of antiviral B cells at the onset of chronic infection
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