Characterization of EBV infection and NK subpopulations at the site of viral entry and reactivation in pediatric patients

FERRESSINI N; VISTAROP A; COHEN, M; CALDIROLA MS; GALLIARD MI; PRECIADO MV; PAOLA ANDREA CHABAY

Madison

Congreso; The International Symposium on EBV and KSHV; 2018

EBV association

Our aim wasto characterize EBV infectionin relation to NK cell subsets at the tonsils,site of viral entry and reactivation in children from Argentina.We analyzed 50patients (2-15 years,median 5) undergoing tonsillectomy. EBV primary infection, reactivation or carrier status was defined by serology. Viral load(VL) was measured by qPCR.Viral antigen expression was assessed by Immunohistochemistry (IHC) for LMP1, EBNA2 and BMRF1, and EBERS in situ Hybridization (ISH). CD56, CD16and IFNg IHC (positive cells/mm2) was performed tocharacterize NK cells. CD3,CD56,CD16, NKG2A and NKG2DNK subsets were identifiedin 34patients by Flow Cytometry (FC). Eighteen primary infected patients (PI),25 healthy carriers (HC),7 patients with viral reactivation (RP)and none EBV-seronegative patients were described. No significant differencesregarding age andVL among groups were demonstrated(p> 0.05). In primary infected patients, there was a negative correlation between age and viral load (r=-0.5, p=0.0335). No specific latent or lytic pattern was observed in PI, given that latency III pattern was observed exclusively in HC (p=0.0466, X2 test). CD56+ and IFN+ cells by IHC displayed a positive correlation between them in the whole series (r=0.4012, p=0,0047) and specifically in PI (r=0.7, p=0.002). FC analysis demonstrate a negative correlation between CD56+ and VL in all patients (r=-0,6623, p=0.005) and particularly in PI (r=-0,6623, p=0.005). In PI we observed correlation between age and NKG2A+NKG2D+ NK cells (r=0,6685, p=0.0245)Low viral inoculum, restricted expression of EBV latent and lytic proteins was found in PI, maybe related to the lack of symptoms. Lower viral load together with increased CD56+ cell numbers may reflect a recruitment of NK cells to control viral infection, in particular in older children, in which NKG2A+NKG2D+ NK cells prevail. IFN- producing NK cells may be involved the control of viral infection.