Patricia Araujo
Federal São Paulo University,Brazil
Title: HLA pattern contributes to the protection or susceptibility to HBV infection in Brazilian blood donors
Biography
Biography: Patricia Araujo
Abstract
In a previous study, we observed that killer cell immunoglobulin-like receptors (KIR)/ Human leukocyte antigen (HLA) interactions contributed to protection or susceptibility to hepatitis B virus (HBV) infection, among blood donors with occult HBV infection (OBI) and spontaneous HBV clearance (SHC). In this context, to investigate the HLA pattern in OBI and SHC in blood donors with reactivity isolated to anti-HBc were analyzed 20 OBI cases and 40 SHC and both immune response. All samples were tested for HBsAg and anti-HBc using Chemiluminescence Immunoassay (Abbott). The immune response was previously available by NK activity, HBcAg-T-cell response, cytokine production, Treg and PD-1 expression in both groups (OBI and SHC). HLA-A, B, C, DP, DQ and DR genotyping was performed using a Luminex Multi-analyte profiling system (One Lambda, Inc., Canoga Park, CA) with the LABType SSO OneLambda typing kit (One Lambda, Inc., Canoga Park, CA).Susceptibility to HBV infection (OBI) was associated with A33(P =0.001, odds ratio [OR] = 2.42); B7(P < .001, OR = 3.97) and B15(P < .0001, OR = 2.97); DRB1*03(P < .001, OR = 3.47) and *07(P < .0001, OR = 2.34); DPB1*0901(P < .001, OR = 5.75) and HLA-C2(P < .0001, OR = 2.56). HLA-A33, B15, DRB1*07 and HLA-C1 was associated with weak immune response (P<0.0001) observed in OBI. Protection to HBV (SHC) was associated with A*0301(P <.001, OR = 4.38); B*13 0101(P <.001, OR = 4.35), DR1(P <.001, OR = 4.18); DR4(P <.001, OR = 3.67) and DR13(P <.001, OR = 3.17); DPB1*0201(P <.0001, OR = 2.36); DQA1*0301(P <.0001, OR = 2.54) and HLA-C2(P < .0001, OR = 2,14). DPB1*0201, DQA1*0301and HLA-C1 was associated with strong immune response (P<0.0001) observed in SHC. The present findings will serve as a base for subsequent functional studies into HLA molecules and viral factors in order to understand the pathogenesis of HBV infection and the relation with protection or susceptibility in hepatitis B virus (HBV) infection