Zimbabwe is highly endemic for hepatitis B virus (HBV) and also has high human immunodeficiency virus (HIV) prevalence rates which may result in HIV/HBV coinfection, and as HIV/HBV coinfection may affect the classical HBV serology patterns and cause interpretation challenges, we assessed the seroprevalence of HBV in HIV positive patients and determined their serology profiles. This was a cross-sectional study on 957 HIV positive specimens from treatment naive patients. HBV serology tests were done using enzyme immunoassays for the detection of HBV markers in human serum or plasma. Hepatitis B surface antigen (HBsAg) prevalence was 17.1% (males 19.0%, females 15.8%). Previous and/or current HBV exposure was evident in 59.8% of the patients and hepatitis B e antigen markers were present in 103 (10.8%) specimens. There was high prevalence of unusual HBV patterns with 14.1% of total specimens showing an anti-HBc alone profile and an additional 4.3% HBsAg positive specimens that were anti-HBc negative. 1. Introduction Hepatitis B virus (HBV) can cause both acute and chronic disease and is the leading cause of viral hepatitis worldwide [1]. An estimated two billion people have been infected with HBV and more than 350 million have chronic HBV liver infections resulting in about 600?000 deaths every year [2]. It was previously reported that Zimbabwe has an overall HBV surface antigen (HBsAg) seroprevalence rate of 15.4% in the general population [3] and is classified as a high HBV endemic area. Zimbabwe also has high HIV prevalence rates of around 15% in the general population [4], but there is little or no data on HBV and HIV coinfection. The prevalence of HIV infected Zimbabweans carrying HBV serological markers is not known. Although some studies in sub-Saharan Africa have shown no major increase of HBV prevalence in HIV patients [5] other studies have reported higher HBV prevalence in HIV patients [6, 7]. This piece of information will be important as the clinical impact of HBV infection in HIV positive patients has progressively grown since the introduction of highly active antiretroviral therapy (HAART) given the increase in survival rates experienced by these patients who now experience the effect of other chronic infections such as HBV. Chronic HBV infection is defined as persistent detection of HBV surface antigen (HBsAg) for more than 6 months [8, 9]. HIV/HBV coinfections may have negative implications on chronic HBV patients including increased rates of chronic HBsAg positivity, high HBV DNA levels, and lower rates of anti-hepatitis B virus e antigen
References
[1]
C. J. Hoffmann and C. L. Thio, “Clinical implications of HIV and hepatitis B co-infection in Asia and Africa,” The Lancet Infectious Diseases, vol. 7, no. 6, pp. 402–409, 2007.
[2]
World Health Organisation Fact sheet no. 204, July 2012, http://www.who.int/mediacentre/factsheets/fs204/en/index.html.
[3]
S. Tswana, C. Chetsanga, L. Nystr?m, S. Moyo, M. Nzara, and L. Chieza, “A sero-epidemiological cross-sectional study of hepatitis B virus in Zimbabwe,” South African Medical Journal, vol. 86, no. 1, pp. 72–75, 1996.
[4]
UNAIDS Global AIDS response progress report 2012, http://www.unaids.org/en/dataanalysis/knowyourresponse/countryprogressreports/2012countries/ce_ZW_Narrative_Report.pdf.
[5]
R. J. Burnett, G. Francois, M. C. Kew, et al., “Hepatitis B virus and human immunodeficiency virus co-infection in sub-Saharan Africa: a call for further investigation,” Liver International, vol. 25, no. 2, pp. 201–213, 2005.
[6]
S. H. Mayaphi, T. M. Rossouw, D. P. Masemola, S. A. Olorunju, M. Jeffrey Mphahlele, and D. J. Martin, “HBV/HIV co-infection: the dynamics of HBV in South African patients with AIDS,” South African Medical Journal, vol. 102, no. 3, pp. 157–162, 2012.
[7]
A. Lukhwareni, R. J. Burnett, S. G. Selabe, M. O. Mzileni, and M. J. Mphahlele, “Increased detection of HBV DNA in HBsAg-positive and HBsAg-negative South African HIV/AIDS patients enrolling for highly active antiretroviral therapy at a tertiary hospital,” Journal of Medical Virology, vol. 81, no. 3, pp. 406–412, 2009.
[8]
C. P. Desmond, S. Gaudieri, I. R. James et al., “Viral adaptation to host immune responses occurs in chronic hepatitis B virus (HBV) infection, and adaptation is greatest in HBV e Antigen-Negative Disease,” Journal of Virology, vol. 86, no. 2, pp. 1181–1192, 2012.
[9]
R. K. Sterling, “Hepatitis B Virus in the Setting of HIV Infection: A Clinical Challenge,” Medical writers circle, 2003, http://www.hcvadvocate.org/hcsp/articles/Sterling-1.html.
[10]
N. J. Bodsworth, D. A. Cooper, and B. Donovan, “The influence of human immunodeficiency virus type 1 infection on the development of the hepatitis B virus carrier state,” The Journal of Infectious Diseases, vol. 163, no. 5, pp. 1138–1140, 1991.
[11]
C. L. Thio, E. C. Seaberg, R. Skolasky Jr. et al., “HIV-1, hepatitis B virus, and risk of liver-related mortality in the Multicenter Cohort Study (MACS),” The Lancet, vol. 360, no. 9349, pp. 1921–1926, 2002.
[12]
T. E. M. S. De Vriessluijs, J. G. P. Reijnders, B. E. Hansen et al., “Long-term therapy with tenofovir is effective for patients co-infected with human immunodeficiency virus and hepatitis b virus,” Gastroenterology, vol. 139, no. 6, pp. 1934–1941, 2010.
[13]
C. Stephan, A. Berger, A. Carlebach, et al., “Impact of tenofovir-containing antiretroviral therapy on chronic hepatitis B in a cohort co-infected with human immunodeficiency virus,” Journal of Antimicrobial Chemotherapy, vol. 56, no. 6, pp. 1087–1093, 2005.
[14]
M. B. Ristig, J. Crippin, J. A. Aberg et al., “Tenofovir disoproxil fumarate therapy for chronic hepatitis B in human immunodeficiency virus/hepatitis B virus-coinfected individuals for whom interferon-α and lamivudine therapy have failed,” Journal of Infectious Diseases, vol. 186, no. 12, pp. 1844–1847, 2002.
[15]
C. L. Thio, “Hepatitis B and human immunodeficiency virus coinfection,” Hepatology, vol. 49, no. 5, pp. S138–S145, 2009.
[16]
A. Ramezani, M. Banifazl, M. Mohraz, M. Rasoolinejad, and A. Aghakhani, “Occult hepatitis B virus infection: a major concern in HIV-infected patients,” Hepatitis Monthly, vol. 11, no. 1, pp. 7–10, 2011.
[17]
V. C. Kantelhardt, A. Schwarz, U. Wend, et al., “Re-evaluation of anti-HBc non-reactive serum samples from patients with persistent hepatitis B infection by immune precipitation with labelled HBV core antigen,” Journal of Clinical Virology, vol. 46, no. 2, pp. 124–128, 2009.
[18]
K. C. Kapembwa, J. D. Goldman, and S. Lakhi, “HIV, Hepatitis B, and Hepatitis C in Zambia,” Journal of Global Infectious Diseases, vol. 3, no. 3, pp. 269–274, 2011.
[19]
O. A. Ejele, C. A. Nwauche, and O. Erhabor, “The prevalence of hepatitis B surface antigenaemia in HIV positive patients in the Niger Delta Nigeria,” Nigerian Journal of Medicine, vol. 13, no. 2, pp. 175–179, 2004.
[20]
M. N. Mulders, V. Venard, M. Njayou et al., “Low genetic diversity despite hyperendemicity of hepatitis B virus genotype E throughout West Africa,” The Journal of Infectious Diseases, vol. 190, no. 2, pp. 400–408, 2004.
[21]
F. Rouet, M. L. Chaix, A. Inwoley et al., “HBV and HCV prevalence and viraemia in HIV-positive and HIV-negative pregnant women in Abidjan, Cote d'Ivoire: The ANRS 1236 study,” Journal of Medical Virology, vol. 74, no. 1, pp. 34–40, 2004.
[22]
J. J. Ott, G. A. Stevens, J. Groeger, and S. T. Wiersma, “Global epidemiology of hepatitis B virus infection: new estimates of age-specific HBsAg seroprevalence and endemicity,” Vaccine, vol. 30, no. 12, pp. 2212–2219, 2012.
[23]
GAVI ALLIANCE, “Investing in immunisation through the GAVI Alliance. The evidence base,” http://www.gavi.org/library/publications/the-evidence-base/investing-in-immunisation-through-the-gavi-alliance––the-evidence-base/.
[24]
E. A. Santos, M. V. Sucupira, J. Arabe, and S. A. Gomes, “Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine,” BMC Infectious Diseases, vol. 4, article 29, 2004.
[25]
N. J. Shire, S. D. Rouster, N. Rajicic, and K. E. Sherman, “Occult hepatitis B in HIV-infected patients,” Journal of Acquired Immune Deficiency Syndromes, vol. 36, no. 3, pp. 869–875, 2004.
[26]
D. Neau, M. Winnock, T. Galperine et al., “Isolated antibodies against the core antigen of hepatitis B virus in HIV-infected patients,” HIV Medicine, vol. 5, no. 3, pp. 171–173, 2004.
[27]
M. K. Osborn, J. L. Guest, and D. Rimland, “Hepatitis B virus and HIV coinfection: relationship of different serological patterns to survival and liver disease,” HIV Medicine, vol. 8, no. 5, pp. 271–279, 2007.
[28]
P. Kallestrup, R. Zinyama, E. Gomo et al., “Low prevalence of hepatitis C virus antibodies in HIV-endemic area of Zimbabwe support sexual transmission as the major route of HIV transmission in Africa,” AIDS, vol. 17, no. 9, pp. 1400–1402, 2003.
[29]
B. C. G?rtner, W. Jung, C. Welsch, et al., “Permanent loss of anti-HBc after reactivation of hepatitis B virus infection in an anti-HBs and anti-HBc-positive patient after allogeneic stem cell transplantation,” Journal of Clinical Virology, vol. 38, no. 2, pp. 146–148, 2007.
[30]
S. Awerkiew, M. D?umer, M. Reiser, et al., “Reactivation of an occult hepatitis B virus escape mutant in an anti-HBs positive, anti-HBc negative lymphoma patient,” Journal of Clinical Virology, vol. 38, no. 1, pp. 83–86, 2007.
[31]
V. Avettand-Fenoel, D. Thabut, C. Katlama, T. Poynard, and V. Thibault, “Immune suppression as the etiology of failure to detect anti-HBc antibodies in patients with chronic hepatitis B virus infection,” Journal of Clinical Microbiology, vol. 44, no. 6, pp. 2250–2253, 2006.