Natural Killer Cell Subsets Distribution in Spontaneously Resolved and Chronic Persistent Hepatitis C Virus InfectionLaila M Al Kady1, Marwa A Mansour1*, Samaa T Gobran1 and Ebtesam I Ahmad2
- *Corresponding Author:
- Marwa Abd El Azim Mansour
Associate Professor of Medical Microbiology and Immunology
Faculty of Medicine, Zagazig University, Egypt
E-mail: [email protected]
Received date: March 29, 2017; Accepted date: May 09, 2017; Published date: May 22, 2017
Citation: Kady LMA, Mansour MA, Gobran ST, Ahmad EI (2017) Natural Killer Cell Subsets Distribution in Spontaneously Resolved and Chronic Persistent Hepatitis C Virus Infection. J Clin Cell Immunol 8:504. doi: 10.4172/2155-9899.1000504
Copyright: © 2017 Kady LMA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Altered natural killer cell subsets frequency and distribution have been reported in Hepatitis C Virus (HCV) infection. Aim of the work was to study the frequency of the NK cells and distribution of their subsets in spontaneously resolved (SR) and chronic persistent Hepatitis C Virus (CHC) infection. In addition, to study the frequency of inhibitory receptor CD158b in these clinical outcomes and to correlate its frequency with certain clinical and diagnostic parameters. This study was conducted on 48 patients divided into 3 groups. Group I; 16 chronic persistent HCV patients, Group II; 16 SR individuals and Group III; 16 healthy controls. Chronic persistent HCV patients and SR individual’s data were reported from patients' reports. Healthy controls serum antibodies against HCV were measured using ELISA technique. The three studied group’s fresh peripheral blood samples were analyzed by flow cytometry to determine total NK cells, CD56+dim CD16+, CD56+bright CD16- NK cell percentages and CD158b frequency. Total NK cells and CD56+dim CD16+ NK cells were decreased significantly in chronic persistent HCV patients and SR individuals in comparison to healthy controls (P<0.001). CD56+bright CD16- NK cells were significantly expanded in CHC patients in comparison with healthy controls (P<0.001), while their significant reduction was noticed in SR individuals in comparison with healthy controls (P<0.001). Significant elevation of CD158b inhibitory receptor frequency in CHC patients in comparison with healthy controls (P<0.001), while no significant elevation was noticed in SR individuals (P>0.05). Positive correlation between CD158b frequency and cirrhosis, unresponsiveness to IFN, WBCs and lymphocytes counts and AST and ALT levels in CHC patients was observed. However, there was negative correlation between it and total protein. Moreover, no correlation between CD158b frequency and viral load was detected in CHC patients. In conclusion, during the chronic HCV infection stage, the antiviral activity of NK cells is significantly depressed. The NK cell function was impaired and conferred inhibitory signals. There were total NK cells and CD56+dim CD16+ NK cells reduction, CD56+bright CD16- NK cells expansion and elevated CD158b inhibitory receptor representing this impairment. On the other hand, in SR individuals, total NK cells were significantly decreased. Also, CD56+dim CD16+ NK cells and CD56+bright CD16- NK cells percentages were significantly decreased (P<0.001) although preserving nearly the same ratio of healthy controls. Also, there was no significant elevation in CD158b frequency (P>0.05).