Effect of Hepatitis B Virus (HBV) Infection on Lipid Profile in
Ghanaian Patients

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Abstract

Background:

Worldwide, approximately 257 million people have chronic hepatitis B virus (HBV) infection, with the highest infection rates recorded in Africa and Asia. Although HBV infection has been associated with dyslipidemia, which may lead to death via liver related complications, the effect of the virus on the lipid profile of patients remain unclear. This study was designed to evaluate the effect of chronic hepatitis B virus infection on lipid profile of sero-positive individuals from Ghana.

Methods:

Blood samples were collected from chronic HBV infected patients who were recruited from the Korle-Bu Teaching Hospital, Accra, and HBV sero-negative healthy volunteers who were used as controls. Demographic and clinical data were obtained using a structured questionnaire. Blood pressure and body mass index were determined, and HBV profile markers and lipid profiles of the patients were determined using a commercially available kit and a chemistry analyzer, respectively.

Results:

Triglycerides, low density lipoproteins (LDL), high density lipoproteins (HDL), very low density lipoproteins (VLDL), and total cholesterol were used as indices of lipid metabolism disorder. Body mass index and diastolic blood pressures were significantly elevated in patients compared to healthy volunteers.

Conclusion:

The observed high total cholesterol and LDL, with a significantly lower HDL levels compared to healthy controls suggest an increased cardiovascular disease risk index in the patients. There is therefore the need to regularly monitor HBV infected patients for signs of cardiovascular diseases.

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Most cited references 16

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Immunology of hepatitis B virus and hepatitis C virus infection.

Barbara Rehermann, Michelina Nascimbeni (2005)

More than 500 million people worldwide are persistently infected with the hepatitis B virus (HBV) and/or hepatitis C virus (HCV) and are at risk of developing chronic liver disease, cirrhosis and hepatocellular carcinoma. Despite many common features in the pathogenesis of HBV- and HCV-related liver disease, these viruses markedly differ in their virological properties and in their immune escape and survival strategies. This review assesses recent advances in our understanding of viral hepatitis, contrasts mechanisms of virus-host interaction in acute hepatitis B and hepatitis C, and outlines areas for future studies.

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Increased risk of cardiovascular disease in non-alcoholic fatty liver disease: causal effect or epiphenomenon?

F. Marra, G Marchesini, G Targher (2008)

Non-alcoholic fatty liver disease (NAFLD), comprising a spectrum of conditions ranging from pure steatosis to steatohepatitis and cirrhosis, has reached epidemic proportions and represents the most common cause of chronic liver disease in the community. The prevalence of NAFLD has been estimated to be between 20% and 30% in the general population, but this value is much higher ( approximately 70-80%) in type 2 diabetic patients, who are also at higher risk of developing advanced fibrosis and cirrhosis. Increasing recognition of the importance of NAFLD and its strong relationship with the metabolic syndrome has stimulated an interest in the possible role of NAFLD in the development of cardiovascular disease (CVD). Several epidemiological studies indicate that NAFLD, especially in its more severe forms, is linked to an increased risk of CVD, independently of underlying cardiometabolic risk factors. This suggests that NAFLD is not merely a marker of CVD, but may also be actively involved in its pathogenesis. The possible molecular mediators linking NAFLD and CVD include the release of pro-atherogenic factors from the liver (C-reactive protein, fibrinogen, plasminogen activator inhibitor-1 and other inflammatory cytokines) as well as the contribution of NAFLD per se to whole-body insulin resistance and atherogenic dyslipidemia, in turn favouring CVD progression. The clinical impact of NAFLD on CVD risk deserves particular attention in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD.

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Circulating and liver resident CD4+CD25+ regulatory T cells actively influence the antiviral immune response and disease progression in patients with hepatitis B.

Zhengsheng Zou, Xin Fu, Xilai Ding … (2006)

CD4+CD25+ regulatory T cells (Treg) have been shown to maintain immune tolerance against self and foreign Ags, but their role in persistent viral infection has not been well-defined. In this study, we investigated whether and where CD4+CD25+ Treg contribute to the development of chronic hepatitis B (CHB). One hundred twenty-one patients were enrolled, including 16 patients with acute hepatitis B, 76 with CHB, and 29 with chronic severe hepatitis B. We demonstrated that in chronic severe hepatitis B patients, the frequencies of CD4+CD25+ Treg in both PBMC and liver-infiltrating lymphocytes were significantly increased and there was a dramatic increase of FoxP3(+)-cell and inflammatory cell infiltration in the liver compared with healthy controls. In CHB patients, circulating CD4+CD25+ Treg frequency significantly correlates with serum viral load. In acute hepatitis B patients, circulating CD4+CD25+ Treg frequency was initially low and with time, the profile reversed to exhibit an increased number of circulating Treg in the convalescent phase and restored to normal levels upon resolution. In PBMC taken from infected patients, depletion of CD4+CD25+ Treg led to an increase of IFN-gamma production by HBV-Ag-stimulated PBMC. In addition, CD4+CD25+ Treg were capable of suppressing proliferation of autologous PBMC mediated by HBV Ags, which probably reflects the generation of HBV-Ag-specific Treg in circulation and in the liver of HBV-infected patients. Together, our findings suggest that CD4+CD25+ Treg play an active role not only in modulating effectors of immune response to HBV infection, but also in influencing the disease prognosis in patients with hepatitis B.

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Author and article information

Journal

Journal ID (nlm-ta): Virology (Auckl)

Journal ID (iso-abbrev): Virology (Auckl)

Journal ID (publisher-id): VRT

Journal ID (hwp): spvrt

Title: Virology : Research and Treatment

Publisher: SAGE Publications (Sage UK: London, England )

ISSN (Electronic): 1178-122X

Publication date (Electronic): 18 February 2019

Publication date Collection: 2019

Volume: 10

Electronic Location Identifier: 1178122X19827606

Affiliations

[1 ]Department of Biochemistry, Cell and Molecular Biology, University of Ghana, Legon, Ghana

[2 ]West African Centre for Cell Biology of Infectious Pathogens, University of Ghana, Legon, Ghana

Author notes

[*]Osbourne Quaye, Department of Biochemistry, Cell and Molecular Biology, University of Ghana, Volta Road, P.O Box LG 54, Legon, Accra, 00233 Ghana. Email: OQuaye@ 123456ug.edu.gh

Article

Publisher ID: 10.1177_1178122X19827606

DOI: 10.1177/1178122X19827606

PMC ID: 6379792

SO-VID: 48f7beff-2dbd-4c08-8c7a-d590de71187c

License:

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

History

Date received : 3 December 2018

Date accepted : 10 January 2019

Custom metadata

cover-date January-December 2018

Keywords: lipid metabolism,lipoproteins,cholesterol,triglycerides,hepatitis b virus (hbv)

Data availability:

Keywords: lipid metabolism, lipoproteins, cholesterol, triglycerides, hepatitis b virus (hbv)

Effect of Hepatitis B Virus (HBV) Infection on Lipid Profile in Ghanaian Patients

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Abstract

Background:

Methods:

Results:

Conclusion:

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Point-Of-Care Testing for Hepatitis

Most cited references 16

Immunology of hepatitis B virus and hepatitis C virus infection.

Increased risk of cardiovascular disease in non-alcoholic fatty liver disease: causal effect or epiphenomenon?

Circulating and liver resident CD4+CD25+ regulatory T cells actively influence the antiviral immune response and disease progression in patients with hepatitis B.

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