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Updated: Jul 27, 2025
Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
Published on: September 28, 2022
Epstein-Barr virus downregulates the α7 nicotinic acetylcholine receptor of CD8
Lvyan Tao1, Tiesong Zhang1, Yuantao Zhou1
1Yunnan Medical Center for Pediatric Diseases, Yunnan Institute of Pediatrics, Kunming Children's Hospital, Kunming 650228, Yunnan, China; Kunming Key Laboratory of Children Infection and Immunity, Yunnan Key Laboratory of Children's Major Disease Research, Yunnan Province Clinical Research Center for Children's Health and Disease, Kunming 650228, Yunnan, China.
Insights
Epstein-Barr virus (EBV) infection status impacts coronary artery lesions (CALs) in Kawasaki disease (KD). Acute EBV infection without detectable DNA showed higher CALs than acute EBV infection with DNA, with latent EBV infection showing the highest CALs.
Area of Science:
- Pediatrics
- Immunology
- Infectious Diseases
Background:
- Kawasaki disease (KD) is a critical pediatric vasculitis linked to immune dysregulation and pathogens like Epstein-Barr virus (EBV).
- Coronary artery lesions (CALs) in KD can lead to severe cardiac complications, but the interplay between pathogens, immune responses, and CALs remains unclear, especially with EBV co-infection.
Purpose of the Study:
- To investigate the relationship between EBV infection status and the incidence of CALs in pediatric KD patients.
- To analyze immunological differences and regulatory mechanisms associated with varying EBV infection states in KD.
Main Methods:
- Studied pathogen carriage and clinical data in 281 KD patients.
- Analyzed immunological profiles (IL-6, B cells, CD8+ T cells, α7nAChR, PI3K/AKT/mTOR, NF-κB) in relation to CALs and EBV infection status (acute EBV-DNA positive, acute EBV-DNA negative, latent EBV).
Main Results:
- EBV was the most prevalent pathogen in KD patients.
- CAL incidence was 0% in acute EBV-DNA (+) group, 27.27% in acute EBV-DNA (-) group, and 41.67% in latent EBV group.
- Patients with acute EBV-DNA (-) and latent EBV infections were younger, had higher IL-6 and B cells, lower CD8+ T cells, downregulated α7nAChR and PI3K/AKT/mTOR, and activated NF-κB compared to the acute EBV-DNA (+) group.
Conclusions:
- Different EBV infection statuses correlate with varying CAL incidence in KD.
- Downregulation of α7nAChR and PI3K/AKT/mTOR, alongside NF-κB and IL-6 activation, may contribute to CAL development in EBV-infected KD patients.
Objectives:
Kawasaki disease (KD) is a systemic vasculitis that is caused by immunological dysregulation in children exposed to pathogens like Epstein-Barr virus (EBV). Myocardial ischemia or infarction due to coronary artery lesions (CALs) might be lethal. However, it is unclear how pathogens, immunomodulation, and CALs interact, particularly in KD patients co-infected with the most widespread virus, EBV.
Methods:
We investigated pathogen carriage and fundamental clinical data in 281 KD patients. Immunological differences between CALs and non-CALs in KD patients under different conditions were analyzed. Then, the effect of infection by different pathogens on the immune response was excluded, and most EBV co-infected KD patients were included to assess the incidence of CALs, the level of immune modulation, and regulatory mechanisms in different EBV infection states.
Results:
Our results showed multiple pathogenic infections occur in KD patients, with EBV being the most prevalent. The incidence of CALs in the EBV-DNA (+) acute infection group, EBV-DNA (-) acute infection group, and EBV latent infection group was 0 (0/6), 27.27% (3/11) and 41.67% (10/24), respectively. The two groups were younger and had increased IL-6 levels and B cells, decreasing CD8+ T cells than the EBV-DNA (+) acute infection group. Interestingly, the increased B cells were not associated with immunoglobulin release. Additionally, these patients down-regulated α7 nicotinic acetylcholine receptor (α7nAChR) and downstream molecule PI3K/AKT/mTOR while activating the NF-κB.
Conclusion:
Patients with different EBV infection statuses exhibit different incidences of CALs. In acute EBV-DNA (-) infected and latent EBV-infected patients, the number of CD8+ T cells decreased and downregulated CD8+ T cells' α7nAChR and PI3K/AKT/mTOR, which may associate with CALs, while the expression of NF-κB and the pro-inflammatory factor IL-6 was upregulated by inhibiting the anti-inflammatory molecule α7nAChR.
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