
Vaccines, Journal Year: 2024, Volume and Issue: 12(12), P. 1372 - 1372
Published: Dec. 5, 2024
HIV causes intense polyclonal activation of B cells, resulting in increased numbers spontaneously antibody-secreting cells the circulation and hypergammaglobulinemia. It is accompanied by significant perturbations various cell subsets, such as frequencies immature/transitional activated memory atypical short-lived plasmablasts regulatory well decreased resting naïve cells. Furthermore, both antigen-inexperienced show exhausted immune-senescent phenotypes. also drives expansion functional impairment CD4+ T follicular helper which provide help to crucial for generation germinal center reactions production long-lived plasma By suppressing viral replication, anti-retroviral therapy reverses virus-induced defects, albeit inadequately. Due HIV’s lingering impact on immune senescence residual chronic inflammation, people with (PWH), especially non-responders, are immunocompromised mount suboptimal antibody responses vaccination SARS-CoV-2. Here, we review how functionally phenotypically distinct subsets induced response a vaccine an infection (ART) them. We role played HIV-induced defects induction humoral currently used anti-SARS-CoV-2 vaccines PWH ART. outline different strategies that could potentially enhance vaccine-induced PWH. The will guidance impetus further research improve immunogenicity these this human population.
Language: Английский