Cytokine, Genotype, and Viral Load Profile in the Acute and Chronic Hepatitis B

Abstract

Several hepatitis B virus (HBV) factors, including viral load, genotype, genome mutations, and cytokine production, have been reported to be associated with different risks of progression of liver disease. The aim of this study was to verify if there is an association among the levels of cytokines (interleukin [IL]-35, IL-6, IL-17A, interferon [IFN]-c) in the plasma, viral load, and the different genotypes of HBV in patients with acute or chronic hepatitis B. Methods: 49 serum samples, 20 from acute and 29 from chronic cases, were submitted to a real-time and nested-polymerase chain reaction to quantify, detect, and genotype HBV DNA. The cytokines IL-35, IL-6, IL-17A, and IFN-c were detected by an enzyme-linked immunosorbent assay (ELISA). The median viral load was 3.15 log 10 IU DNA/mL and 2.90 log 10 IU DNA/mL for acute and chronic patients, respectively. Genotype A, D, E, and F were identified in chronic carriers of HBV infection, while only genotype A and F were identified in individuals with acute infection. IFN-c (p = 0.024) and IL-17A (p = 0.046) levels were significantly increased in chronic patients and IL-6 and IL-35 were higher in patients with acute infection, however, without statistical difference. IL-17A and IFN-c can be modulating proinflammatory effects and inducing hepatocellular damage, in chronic patients, and IL-6 and IL-35 may be involved in viral elimination and protection against chronicity during the acute phase of infection. These results can contribute to understanding of the complex regulatory mechanisms of the host antiviral response related to cytokine production during acute and chronic HBV infection.

Expression patterns of immune checkpoint proteins and Plasmodium falciparum‐induced cytokines in chronic hepatitis B virus‐infected and uninfected individuals: A cross‐sectional study

“… 31 However, the pathophysiology of HBV has been linked to cytokines, providing evidence that immune‐modulating treatment can be effective. 12 , 14 Interleukin 1β (IL‐1β) enhances IFN‐α treatment response. In hepatic cell lines, IL‐4 suppressed the replication and expression of HBV.…”

“… 8 , 13 Proinflammatory cytokines such as IL‐1β, IL‐6, IL‐17, IL‐22, IFN‐α/β, and tumor necrosis factor‐α (TNF‐α) are believed to contribute to the development of liver cirrhosis and cancer in CHB individuals. 12 , 14 , 15 …”

Plasma interleukin-7 correlation with human immunodeficiency virus RNA and CD4+ T cell counts, and interleukin-5 with circulating hepatitis B virus DNA may have implications in viral control

“…With over two billion people infected with HBV world-wide, ∼350 million are chronically infected, with considerable odds for developing cirrhosis and hepatocellular carcinoma (HCC) ( 5 – 7 ). The hallmark of chronic HBV infection is the failure to mount a coordinated adaptive immune responses to clear the virus.…”

“…Cytokines are a diverse group of molecules that play a critical role in host immune responses. T helper 1 (Th1) responses marked by interleukin-2 (IL-2), gamma interferon (IFN-γ); Th2 responses heralded by signature cytokines IL-4, IL-5, IL-13, and IL-31, and Th17 cytokines (e.g., IL-17, IL-22, IL-23), are essential in mediating inflammation and antiviral surveillance ( 5 , 11 ). Cytokines play significant roles in the defense against viral infections by binding to their cognate receptors expressed on target cells and initiating downstream signaling pathways ( 12 ).…”

Hepatitis B Virus Genotypes and Pre-core and Core Genes Mutations in a Sample of Iraqi Patients with Chronic Hepatitis B Infection

“…Blood or other bodily fluids from an infected individual can spread the virus, making it extremely infectious. For a Hussain et al, HBV Genotypes and Pre-core and Core Genes Mutations minimum of seven days, HBV can survive outside of the body (2,3) . HBV genomes have been classified into genotypes ranging from A to J based on their genetic variability (>8% for the entire genome) (4)(5)(6) .…”