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Age-associated B cells are long-lasting effectors that restrain reactivation of latent γHV68

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Abstract Age-associated B cells (ABCs; CD19 + CD11c + T-bet + ) are a unique population that are increased in an array of viral infections, though their role during latent infection is largely unexplored. Here, we use murine gammaherpesvirus 68 (γHV68) to demonstrate that ABCs remain elevated long-term during latent infection and express IFNγ and TNF. Using a strain of γHV68 that is cleared following acute infection, we show that ABCs persist in the absence of latent virus, though their expression of IFNγ and TNF is decreased. With a fluorescent virus we demonstrate that ABCs are infected with γHV68 at similar rates to other previously activated B cells. We find that mice without ABCs display defects in anti-viral IgG2a/c antibodies and are more susceptible to γHV68 reactivation when challenged with heterologous infection. Together, these results indicate that ABCs are a persistent effector subset during latent viral infection that restrains γHV68 reactivation.
Title: Age-associated B cells are long-lasting effectors that restrain reactivation of latent γHV68
Description:
Abstract Age-associated B cells (ABCs; CD19 + CD11c + T-bet + ) are a unique population that are increased in an array of viral infections, though their role during latent infection is largely unexplored.
Here, we use murine gammaherpesvirus 68 (γHV68) to demonstrate that ABCs remain elevated long-term during latent infection and express IFNγ and TNF.
Using a strain of γHV68 that is cleared following acute infection, we show that ABCs persist in the absence of latent virus, though their expression of IFNγ and TNF is decreased.
With a fluorescent virus we demonstrate that ABCs are infected with γHV68 at similar rates to other previously activated B cells.
We find that mice without ABCs display defects in anti-viral IgG2a/c antibodies and are more susceptible to γHV68 reactivation when challenged with heterologous infection.
Together, these results indicate that ABCs are a persistent effector subset during latent viral infection that restrains γHV68 reactivation.

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