J Clin Lab Anal. 2019 Mar 29:e22886. doi: 10.1002/jcla.22886. [Epub ahead of print]
Toll-like receptors, long non-coding RNA NEAT1, and RIG-I expression are associated with HBeAg-positive chronic hepatitis B patients in the active phase.
Zeng Y1,2, Wu W1,2, Fu Y1,2, Chen S1,2, Chen T1,2, Yang B1,2, Ou Q1,2.
Author information
1
Department of Laboratory Medicine, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
2
Department of Gene Diagnosis, Fujian Medical University, Fuzhou, China.
Abstract
BACKGROUND:
Innate immunity plays a crucial role in host-virus interactions and greatly influences viral replication including HBV infection. However, few studies have investigated the possible antiviral immune roles played by TLRs, RIG-I, and long no-coding RNA NEAT1 in chronic HBV infection (CHB) patients in clinical samples and their relationships among immune responses. In this study, we sought to investigate the mRNA expression levels of TLR1-10, RIG-I, and NEAT1 expression in HBeAg-positive CHB treatment-naïve patients with the active phase.
METHODS:
The expression levels of TLR1-10, RIG-I, and NEAT1 of CHB patients with the active phase and healthy controls were measured by qPCR. Serum HBV DNA and routine liver biochemistry including ALT, etc were also measured to evaluate the impaired physiological function of the liver affected by CHB.
RESULTS:
The expression levels of TLR1 and TLR6 in CHB with active phase were remarkably lower than that in healthy controls. The levels of TLR3 in CHB patients with active phase were remarkably higher than that in healthy controls. The total NEAT1 expression was abnormally decreased in CHB patients as compared with healthy controls. The levels of RIG-I were significantly decreased in CHB patients in the active phase when compared to healthy controls. The expression of TLR6 and RIG-I was closely correlated with NEAT1 expression. TLR6 level was positively correlated with RIG-I level.
CONCLUSION:
Chronic HBV infection can alter the innate immune response by downregulating functional expression of TLR1, TLR6, NEAT1.