EBV Infection Alters NK Cell Phenotype Distinctly From hCMV

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F25%3A00143843" target="_blank" >RIV/00216224:14740/25:00143843 - isvavai.cz</a>

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.70620?getft_integrator=clarivate&src=getftr&utm_source=clarivate" target="_blank" >https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.70620?getft_integrator=clarivate&src=getftr&utm_source=clarivate</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/jmv.70620" target="_blank" >10.1002/jmv.70620</a>

Jazyk výsledku

angličtina

Název v původním jazyce

EBV Infection Alters NK Cell Phenotype Distinctly From hCMV

Popis výsledku v původním jazyce

Natural killer (NK) cells are vital in the antiviral response regulated by inhibitory and activating receptors, including NKG2 and KIR families, which bind HLA-I. While the adaptive features of NK cells in response to human cytomegalovirus (hCMV) have been well described, their behavior during Epstein-Barr virus (EBV) infection and the influence of KIR-HLA combinations in healthy carriers of these viruses remains unclear. We performed high-resolution HLA genotyping, phenotypic profiling of NK cell subsets, and serological testing for hCMV and EBV-specific IgG in 85 healthy adult donors. hCMV-seropositive individuals exhibited significant expansions of NKG2C+ and HLA-DR+ NK cell subsets, with the proportion of NKG2C+ cells strongly correlating with hCMV-IgG titers. In contrast, EBV infection was associated with increased frequencies of terminally differentiated CD56dim, NKG2A-, CD57+ NK cells and elevated expression of inhibitory KIRs, but not NKG2C or HLA-DR. EBV-IgG titers correlated with CD57 and KIR2DS4 levels. Among KIR2DS4-expressing donors, carriage of at least one HLA-C2 allele was associated with elevated EBV-IgGs. The precise analysis of KIR2DL2/DL3, KIR2DS4, and KIR2DL1 revealed dependencies on EBV-IgG titers, with no associations with hCMV. These findings highlight the differential impacts of hCMV and EBV on NK cells and underscore the relevance of HLA-KIR landscapes in shaping antiviral immunity.

Název v anglickém jazyce

EBV Infection Alters NK Cell Phenotype Distinctly From hCMV

Popis výsledku anglicky

Natural killer (NK) cells are vital in the antiviral response regulated by inhibitory and activating receptors, including NKG2 and KIR families, which bind HLA-I. While the adaptive features of NK cells in response to human cytomegalovirus (hCMV) have been well described, their behavior during Epstein-Barr virus (EBV) infection and the influence of KIR-HLA combinations in healthy carriers of these viruses remains unclear. We performed high-resolution HLA genotyping, phenotypic profiling of NK cell subsets, and serological testing for hCMV and EBV-specific IgG in 85 healthy adult donors. hCMV-seropositive individuals exhibited significant expansions of NKG2C+ and HLA-DR+ NK cell subsets, with the proportion of NKG2C+ cells strongly correlating with hCMV-IgG titers. In contrast, EBV infection was associated with increased frequencies of terminally differentiated CD56dim, NKG2A-, CD57+ NK cells and elevated expression of inhibitory KIRs, but not NKG2C or HLA-DR. EBV-IgG titers correlated with CD57 and KIR2DS4 levels. Among KIR2DS4-expressing donors, carriage of at least one HLA-C2 allele was associated with elevated EBV-IgGs. The precise analysis of KIR2DL2/DL3, KIR2DS4, and KIR2DL1 revealed dependencies on EBV-IgG titers, with no associations with hCMV. These findings highlight the differential impacts of hCMV and EBV on NK cells and underscore the relevance of HLA-KIR landscapes in shaping antiviral immunity.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10607 - Virology

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Medical Virology

ISSN

0146-6615

e-ISSN

—

Svazek periodika

97

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

1-13

Kód UT WoS článku

001580767200001

EID výsledku v databázi Scopus

2-s2.0-105017028824