Phenotypic analysis of monocytes and CD4 + T cells in hepatitis E patients with or without pregnancy.

High mortality in pregnant women is a characteristic of hepatitis E virus (HEV) infection. Role of monocytes/T cells in HEV infection during pregnancy is still unclear. We compared CD14 ⁺ monocytes and CD4 ⁺ T cells by flow-cytometry in hepatitis-E patients including 13 pregnant (Antenatal care, ANC), 25 non-ANC patients and respective controls (12 and 20). Non-ANC-patients showed significantly higher frequency of monocytes with increased expression of CD80, CD86 and HLA-DR than control individuals (p < 0.001). Healthy pregnancy was associated with increased frequency of monocytes with higher CD80 expression and lower levels of HLA-DR (p < 0.05) compared to non-ANC controls. ANC-patients exhibited elevated levels of monocytes (p < 0.01) with higher expression of CD80 (p < 0.001) and reduced levels of HLA-DR and CD86 (p < 0.05) when compared with non-ANC patients. TLR2 and TLR4 surface expression on monocytes was higher in non-ANC-patients (p < 0.00) and lower in the ANC-patients (p < 0.01). Healthy-ANCs exhibited lower TLR4 expression on monocytes (p < 0.05). HEV infection did not change the frequency of CD4 ⁺ and CD4 ⁺ CD28 ⁺ T cells in patients' group (p > 0.05). Compared to respective controls, CD137 ⁺ and CD152 ⁺ CD4 ⁺ T cells were higher (p < 0.05) in both patients' categories. Higher levels of CD152 ⁺ CD4 ⁺ T cells (p < 0.001) was noted in healthy pregnant women. Among patients' groups, the CD4 ⁺ T cells and their subpopulation were not different (p > 0.05). We found higher and reduced levels of circulating inflammatory cytokines (IL12, TNFα, IL6 and IL8; miliplex-assay) in non-ANC and ANC-patients respectively. In conclusion, on contrary to the classical activation of CD14 ⁺ monocytes in the non-ANC-patients, impaired response was evident in the ANC-patients while the CD4 ⁺ T cell populations were similar in the patient groups.
(Copyright © 2019 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.)