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Antiviral Tfh response by “tolerant” congenitally infected virus carriers drives antibody-mediated viral load control [scRNA-Seq]

ABSTRACT: Congenital infection can result in viral persistence as commonly observed for hepatitis B virus in humans. The accompanying “neonatal tolerance” state remains immunologically ill-defined and treatment options are unsatisfactory. Studying congenital lymphocytic choriomeningitis virus infection, the prototypic mouse model of neonatal antiviral tolerance, we observe antibody-mediated suppression of viral replication. These responses are driven by canonical antiviral CD4 Tfh responses, whereas CD8 T cells are irrelevant for viral load control. Viral epitope-specific CD4 T cells of congenitally infected animals are less abundant than in adult infection. They exhibit reduced clonal diversity and distinct differences in gene expression patterns. Importantly, exogenous supplementation of T help augments antiviral germinal center B responses of congenitally infected mice. These findings reveal that humoral immune defense is partially exempt from neonatal tolerance and remains effective against congenital infection. Imperfect virus control by limited CD4 Tfh responses may offer opportunities for a functional cure by immunotherapy.

ORGANISM(S): Mus musculus

PROVIDER: GSE272558 | GEO | 2026/03/30

REPOSITORIES: GEO

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Project description:Wodarz2007 - HIV/CD4 T-cell interaction A deterministic model illustrating how CD4 T-cells can influence HIV infection. This model is described in the article: Infection dynamics in HIV-specific CD4 T cells: does a CD4 T cell boost benefit the host or the virus? Wodarz D, Hamer DH. Math Biosci 2007 Sep; 209(1): 14-29 Abstract: Recent experimental data have shown that HIV-specific CD4 T cells provide a very important target for HIV replication. We use mathematical models to explore the effect of specific CD4 T cell infection on the dynamics of virus spread and immune responses. Infected CD4 T cells can provide antigen for their own stimulation. We show that such autocatalytic cell division can significantly enhance virus spread, and can also provide an additional reservoir for virus persistence during anti-viral drug therapy. In addition, the initial number of HIV-specific CD4 T cells is an important determinant of acute infection dynamics. A high initial number of HIV-specific CD4 T cells can lead to a sudden and fast drop of the population of HIV-specific CD4 T cells which results quickly in their extinction. On the other hand, a low initial number of HIV-specific CD4 T cells can lead to a prolonged persistence of HIV-specific CD4 T cell help at higher levels. The model suggests that boosting the population of HIV-specific CD4 T cells can increase the amount of virus-induced immune impairment, lead to less efficient anti-viral effector responses, and thus speed up disease progression, especially if effector responses such as CTL have not been sufficiently boosted at the same time. This model is hosted on BioModels Database and identified by: BIOMD0000000663. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Antiviral Tfh response by “tolerant” congenitally infected virus carriers drives antibody-mediated viral load control [scRNA-Seq]

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