See the published version of this preprint at Virology Journal.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Research
José J. Barros
Oswaldo Cruz Foundation
Corresponding Author
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Background: The hepatitis B virus (HBV) is one of the leading causes of acute, chronic and occult hepatitis (OBI) representing a serious public health threat. Cytokines are known to be important chemical mediators that regulate the differentiation, proliferation and function of immune cells. Accumulating evidence indicate that the inadequate immune responses are responsible for HBV persistency. The aim of this study were to investigate the cytokines IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10 and IL-17A in patients with OBI and verify if there is an association between the levels of these cytokines with the determination of clinical courses during HBV occult infection.
Methods: 114 patients with chronic hepatitis C were investigated through serological and molecular tests, the OBI coinfected patients were subjected to the test for cytokines using the commercial human CBA kit. As controls, ten healthy donors with no history of liver disease and 10 chronic HBV monoinfected patients of similar age to OBI patients were selected.
Results: Among 114 HCV patients investigated, 11 individuals had occult hepatitis B. The levels of cytokines were heterogeneous between the groups, most of the cytokines showed higher levels of production detection among OBI/HCV individuals when compared to control group and HBV monoinfected patients. We found a high level of IL-17A in the HBV monoinfected group, high levels of TNF-α, IL-10, IL-6, IL-4 and IL-2 in OBI/HCV patients.
Conclusion: These cytokines could be involved in the persistence of HBV DNA in hepatocytes triggers a constant immune response, inducing continuous liver inflammation, which can accelerate liver damage and favor the development of liver cirrhosis in other chronic liver diseases.
Keywords
Occult hepatitis B infection, cytokines, HBV/HCV co-infection
Figure 1
This is a list of supplementary files associated with this preprint. Click to download.
- Supplementarytable1.xlsx
Supplementary table 1. Data file of clinical and epidemiological information of patients with occult hepatitis B and HCV enrolled in this study. SAH (Subarachnoid hemorrhage); HCC (Hepatocellular carcinoma); IFN-Peg (Pegylated interferon); HBV (Hepatitis B virus); HCV (Hepatitis C virus); HAV (Hepatitis A virus); HIV (human immunodeficiency virus); IgG (Immunoglobulin G); HBsAg (Hepatitis B virus surface antigen); HBc (Antigen “c” or core of the hepatitis B virus); AST (alanine aminotransferase); ALT (alkaline phosphatase); GGT (gamma-glutamyl transferase); TGO (oxalacetic glutamic transaminase); TGP (glutamic-pyruvic transaminase); ALB (albumin); AFP (alpha-fetoprotein); LDL (Low Density Lipoproteins); HDL (High Density Lipoproteins); HGB (Hemoglobin); A.T (After treatment).
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CURRENT STATUS: Published
View the published article at Virology Journal.
Version 3
Posted 07 Jan, 2021
No community comments so far
Editorial decision: Accept
On 27 Dec, 2020
Editor assigned
On 19 Dec, 2020
Submission checks complete
On 19 Dec, 2020
Editor invited
On 19 Dec, 2020
No comments provided
Reviewer #1 agreed
On 21 Oct, 2020
Review #1 received
Received 21 Oct, 2020
Reviewers invited
Invitations sent on 16 Oct, 2020
Editor assigned
On 15 Oct, 2020
Submission checks complete
On 14 Oct, 2020
Editor invited
On 14 Oct, 2020
No comments provided
Editorial decision: Major revision
On 13 Aug, 2020
Review #3 received
Received 28 Jul, 2020
Review #2 received
Received 27 Jul, 2020
Review #1 received
Received 24 Jul, 2020
Reviewer #3 agreed
On 14 Jul, 2020
Reviewer #2 agreed
On 10 Jul, 2020
Reviewer #1 agreed
On 09 Jul, 2020
Reviewers invited
Invitations sent on 08 Jul, 2020
Editor assigned
On 01 Jul, 2020
Submission checks complete
On 30 Jun, 2020
Editor invited
On 30 Jun, 2020
First submitted
On 23 Jun, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Virology
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See the published version of this preprint at Virology Journal.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
José J. Barros
Oswaldo Cruz Foundation
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Virology Journal.
Version 3
Posted 07 Jan, 2021
No community comments so far
Editorial decision: Accept
On 27 Dec, 2020
Editor assigned
On 19 Dec, 2020
Submission checks complete
On 19 Dec, 2020
Editor invited
On 19 Dec, 2020
No comments provided
Reviewer #1 agreed
On 21 Oct, 2020
Review #1 received
Received 21 Oct, 2020
Reviewers invited
Invitations sent on 16 Oct, 2020
Editor assigned
On 15 Oct, 2020
Submission checks complete
On 14 Oct, 2020
Editor invited
On 14 Oct, 2020
No comments provided
Editorial decision: Major revision
On 13 Aug, 2020
Review #3 received
Received 28 Jul, 2020
Review #2 received
Received 27 Jul, 2020
Review #1 received
Received 24 Jul, 2020
Reviewer #3 agreed
On 14 Jul, 2020
Reviewer #2 agreed
On 10 Jul, 2020
Reviewer #1 agreed
On 09 Jul, 2020
Reviewers invited
Invitations sent on 08 Jul, 2020
Editor assigned
On 01 Jul, 2020
Submission checks complete
On 30 Jun, 2020
Editor invited
On 30 Jun, 2020
First submitted
On 23 Jun, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Virology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Virology Journal.
Background: The hepatitis B virus (HBV) is one of the leading causes of acute, chronic and occult hepatitis (OBI) representing a serious public health threat. Cytokines are known to be important chemical mediators that regulate the differentiation, proliferation and function of immune cells. Accumulating evidence indicate that the inadequate immune responses are responsible for HBV persistency. The aim of this study were to investigate the cytokines IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10 and IL-17A in patients with OBI and verify if there is an association between the levels of these cytokines with the determination of clinical courses during HBV occult infection.
Methods: 114 patients with chronic hepatitis C were investigated through serological and molecular tests, the OBI coinfected patients were subjected to the test for cytokines using the commercial human CBA kit. As controls, ten healthy donors with no history of liver disease and 10 chronic HBV monoinfected patients of similar age to OBI patients were selected.
Results: Among 114 HCV patients investigated, 11 individuals had occult hepatitis B. The levels of cytokines were heterogeneous between the groups, most of the cytokines showed higher levels of production detection among OBI/HCV individuals when compared to control group and HBV monoinfected patients. We found a high level of IL-17A in the HBV monoinfected group, high levels of TNF-α, IL-10, IL-6, IL-4 and IL-2 in OBI/HCV patients.
Conclusion: These cytokines could be involved in the persistence of HBV DNA in hepatocytes triggers a constant immune response, inducing continuous liver inflammation, which can accelerate liver damage and favor the development of liver cirrhosis in other chronic liver diseases.
Figure 1
This is a list of supplementary files associated with this preprint. Click to download.
- Supplementarytable1.xlsx
Supplementary table 1. Data file of clinical and epidemiological information of patients with occult hepatitis B and HCV enrolled in this study. SAH (Subarachnoid hemorrhage); HCC (Hepatocellular carcinoma); IFN-Peg (Pegylated interferon); HBV (Hepatitis B virus); HCV (Hepatitis C virus); HAV (Hepatitis A virus); HIV (human immunodeficiency virus); IgG (Immunoglobulin G); HBsAg (Hepatitis B virus surface antigen); HBc (Antigen “c” or core of the hepatitis B virus); AST (alanine aminotransferase); ALT (alkaline phosphatase); GGT (gamma-glutamyl transferase); TGO (oxalacetic glutamic transaminase); TGP (glutamic-pyruvic transaminase); ALB (albumin); AFP (alpha-fetoprotein); LDL (Low Density Lipoproteins); HDL (High Density Lipoproteins); HGB (Hemoglobin); A.T (After treatment).
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