Effect of XBB.1.5-adapted booster vaccination on the imprinting of SARS-CoV-2 immunity.

In the present study, Pušnik et al. investigated whether the XBB.1.

Vaccination impairs de novo immune response to omicron breakthrough infection, a precondition for the original antigenic sin.

Several studies have suggested the imprinting of SARS-CoV-2 immunity by original immune challenge without addressing the formation of the de novo response to successive antigen exposures. As this is crucial for the development of the original antigenic sin, we assessed the immune response against the mutated epitopes of omicron SARS-CoV-2 after vaccine breakthrough. Our data demonstrate a robust humoral response in thrice-vaccinated individuals following omicron breakthrough which is a recall of vaccine-induced memory.

Persistent Maintenance of Intermediate Memory B Cells Following SARS-CoV-2 Infection and Vaccination Recall Response.

Robust population-wide immunity will help to curb the SARS-CoV-2 pandemics. To maintain the immunity at protective levels, the quality and persistence of the immune response elicited by infection or vaccination must be determined. We analyzed the dynamics of B cell response during 12 months following SARS-CoV-2 infection on an individual level.

Memory B cells targeting SARS-CoV-2 spike protein and their dependence on CD4 T cell help.

Memory B cells seem to be more durable than antibodies and thus crucial for the long-term immunity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Here we investigate SARS-CoV-2 spike-specific memory B cells and their dependence on CD4 T cell help in different settings of coronavirus disease 2019 (COVID-19). Compared with severely ill individuals, those who recovered from mild COVID-19 develop fewer but functionally superior spike-specific memory B cells.

Production of HIV-1 Env-specific antibodies mediating innate immune functions depends on cognate IL-21- secreting CD4+ T cells.

Antibodies with a functional Fc region were previously associated with protection from HIV-1 acquisition and spontaneous suppression of viral replication. Unlike broadly neutralizing antibodies, they are not restricted to neutralizing epitopes and do not require unconventional structural traits to exert their antiviral activity. They, therefore, develop earlier after infection and can be detected in the majority of cases.

Expansion of Stem Cell-Like CD4 Memory T Cells during Acute HIV-1 Infection Is Linked to Rapid Disease Progression.

Acute HIV-1 infection is characterized by high viremia and massive depletion of CD4 T cells throughout all tissue compartments. During this time the latent viral reservoir is established but the dynamics of memory CD4 T cell subset development, their infectability and influence on disease progression during acute HIV-1 infection has not been carefully described. We therefore investigated the dynamics of CD4 T cell memory populations in the RV217 (ECHO) cohort during the acute phase of infection.