QUANTITATIVE DETERMINATION OF HBsAg IN BLOOD SERA AND HEPATITIS B VIRUS COVALENTLY CLOSED CIRCULAR DNA IN LIVER TISSUE AS MARKERS OF CHRONIC VIRAL HEPATITIS B ACTIVITY


Cite item

Full Text

Abstract

Im. Quantitative evaluation of HBV covalently closed circular DNA (cccDNA) content in liver tissue of patients with moderately active CHBV course compared with inactive HBsAg carriers as well as establishment of a possible link between HBV cccDNA in liver cells and HBsAg level in blood sera in these groups of patients. Materials and methods. Patients (n=34) with CHBV diagnosis were examined for levels of ALT, HBsAg (qualitatively and quantitatively), anti-HBcor IgG, anti-HBe IgG, anti-HCV IgG+IgM, anti-HDV IgG+IgM, HBV DNA in qualitative and quantitative variant. Liver biopsy was carried out in all the patients. HBV DNA was determined in liver tissue by Pollicino Т. et al. (2004). Results. Based on HBV DNA PCR, the patients were allocated to a group of inactive HBsAg carriers (n=16) and CHBV (n=18) of moderate activity. Viral load in CHBV patients had a mean of 540+230 IU/ml. ALT level in carriers was comparatively lower than in patients with CHBV. HBsAg level in blood of inactive carriers was significantly lower, 940+259 IU/ml against 2559+982 IU/ml in patients with CHBV (p<0.05). The quantity of cccDNA per 1 cell in inactive HBsAg carriers - 0.15+0.14, and in patients group of CHBV with moderate activity - 1.71 + 1.32 (p=0.034). Conclusion. The method of quantitative determination of HBV cccDNA in liver tissue of patients was worked out. Differences in quantitative content of HBsAg in blood sera of inactive carriers and CHBV patients with moderate activity reflect changes in the extent of hepatocyte infection by HBV.

About the authors

A. V Semenov

Pasteur Research Institute of Epidemiology and Microbiology, St. Petersburg, Russia

I. A Vlasova

City Virological Consultative-Diagnostic Centre, St. Petersburg, Russia

Yu. V Ostankova

Pasteur Research Institute of Epidemiology and Microbiology, St. Petersburg, Russia

A. Totolyan Areg

Pasteur Research Institute of Epidemiology and Microbiology, St. Petersburg, Russia

References

  1. Мукомолов С.Л. Эпидемиологическая и клинико-лабораторная характеристика хронических носителей HBsAg в зависимости от выраженности патологического процесса. Автореф. дисс. канд. мед. наук. Л., 1984.
  2. Семенов А. В., Гончарова Л. Б. Вирусологические исследования. Молекулярнобиологические методы. В: Клиническая лабораторная диагностика: национальное руководство. В.В. Долгов, В. В. Меньшиков (ред.). М., ГЭОТАР-Медиа, 2012.
  3. Семенов А. В. Интерпретация результатов лабораторного выявления маркеров гепатита В. Справочник заведующего КДЛ. 2012, 11: 14-21.
  4. Шахгильдян И. В., Михайлов М. И., Онищенко Г. Г. Парентеральные вирусные гепатиты (эпидемиология, диагностика, профилактика). М., ГОУ ВУНМЦ МЗ РФ, 2003.
  5. EASL clinical practice guidelines: management of chronic hepatitis B. J. Hepatol. 2009, 50 (2): 227-242.
  6. Kim E.S., Seo Y.S., Keum et al. A threshold HBV DNA level for discriminating patients with hepatitis b e antigen-negative chronic hepatitis b from inactive carriers. Hep. Monthly. 2011, 5 (11): 351-357.
  7. Levrero M., Pollicino T., Petersen J. et al. Control of cccDNA function in hepatitis B virus infection. J. Hepatol. 2009, 51: 581-592.
  8. Moucari R., Makiewich L., Lada O. et al. Early serum HBsAg drop: a strong predictor of sustained virological response to pegylated interferon alfa-2a in HBeAg-negative patients. Hepatology. 2009, 49: 1151-1157.
  9. Menghini G. One-second needle biopsy of the liver. Gastroenterology. 1958, 35: 190.
  10. Malmstrnm S., Larsson S. B., Lindh M. Hepatitis B viral DNA decline at loss of HBeAg is mainly explained by reduced cccDNA load - down-regulated transcription of pgRNA has limited impact. PLoS One. 2012, 7 (7): e36349.
  11. Pollicino T., Squadrito G., Cerenzia G. et al. Hepatitis B virus maintains its pro-oncogenic properties in the case of occult HBV infection. Gastroenterology. 2004, 126 (1): 102-110.
  12. Sorrell M.F., Belongia E.A., Costa J. et al. National Institutes of Health consensus development conference statement: management of hepatitis B. Hepatology. 2009, 49 (5): 4-12.
  13. Yuki N., Nagaoka T., Yamashiro M. et al. Long-term histologic and virologic outcomes of acute self-limited hepatitis B. Hepatology. 2003, 37: 1172-1179.
  14. Zerbini A., Pilli M., Boni C. et al. The characteristics of the cell-mediated immune response identify different profiles of occult hepatitis B virus infection. Gastroenterology. 2008, 134: 1470-1481.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2014 Semenov A.V., Vlasova I.A., Ostankova Y.V., Areg A.T.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: ПИ № ФС77-75442 от 01.04.2019 г.


This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies