Mapping CMV-related immune signatures in blood, aorta and perivascular mediastinal adipose tissue

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Cytomegalovirus (CMV) establishes lifelong latency and is linked to immunosenescence in older and immunocompromised individuals. We hypothesize that CMV drives systemic and tissue-specific immune changes that may contribute to cardiovascular disease (CVD). Thoracic aorta, blood and perivascular mediastinal adipose tissue from cardiac surgery patients ( n = 11) were processed within 30-60 min of excision. CMV IgG titres were quantified through ELISA to determine CMV status: CMV(-) ( n = 4) and CMV(+) ( n = 7). Immune profiling was performed using flow cytometry and single-cell RNA sequencing. Analyses included MiloR and differential gene expression. Participants (mean age 69.7 ± 8.4 years) were 80% male and 70% Caucasian. CMV(-) and CMV(+) participants had mean IgG titres of 0.038 and 13.55 IU ml -1 , respectively. CD8 + T-cells expressing CD57 + , GPR56 + and CX3CR1 + (CGC) were increased in the blood of CMV(+) participants. In the aorta of CMV(+) participants, CD8 + T cells and CD4 + T cells had decreased HLA-C expression and suppressed interferon-α pathways. In contrast, the TNF-α signalling pathway was increased. CMV infection shapes immune responses and in this pilot, we observed suppression of interferon-α signalling and increased TNF-α-associated pathways in the aorta. Larger studies are needed to define how CMV-driven immune remodelling contributes to CVD.This article is

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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