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Hepatitis B virus (HBV) infection, one of the major health priorities, accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus (HIV) in the world. Hepatitis B, one of the major health priorities, accounts approximately for 350 million chronic cases out of 2 billion people infected worldwide.1 An estimated 600,000 people die each year because of the acute or chronic consequences of hepatitis B.
Moreover in Iran, the prevalence of HBsAg has differed through the time and after mass vaccination in following years, the number of HBsAg positive individuals started to decrease. HBV, a prototype member of the Hepadnaviridae (hepatotropic DNA virus) family, is one of the Hepadnaviruses which strongly appeals to infect liver cells, but hepadnaviral DNA can be traced in pancreas, kidney, and mononuclear cells, as well.22,23 HBV virions are particles with double shells, 40 to 42 nm thick with an outer lipoprotein envelope. The HBV replication cycle is not directly cytotoxic to cells, as in, many HBV carriers show no symptoms and have minimal liver injury, however intrahepatic replication of the virus continues extensively.
There are also some cases of occult HBV infections which are described as the existence of HBV DNA without detectable HBsAg. Hepatitis B virus is a dynamic virus and its co-infection with HIV makes the diagnosis process significantly difficult. In a study performed by Matthews, patients receiving interferon therapy were shown to get significantly more improved with pegylated interferon compared to nucleosides and nucleotide analogues alone. Entecavir, a partial inhibitor of HIV replication along with lamivudine are applied to induce the YMDD mutation in HIV polymerase which is an indication of resistance to therapy. To initiate the treatment in co-infected patients, some factors such as combination antiretroviral therapy for HIV infection, the severity of liver disease, probability of various reactions, and potential adverse events should be taken into account.57 When treatment is necessary for both HBV and HIV infections, HAART is needed for HIV. We need styles that are quick and easy to maintain without having to wake up at the break of dawn every morning to get it right.
Its well known as an immune enhancer containing sterols and sterolins which have been shown to be beneficial at enhancing an under-active immune system or decreasing an overactive system. Co-infection with HIV and the HBV presents a significant challenge to health care providers, with different prevalence rates in different parts of the world. Human immunodeficiency virus (HIV)  is one of the other viruses in charge of infectious diseases.
Therefore, immune responses to viral antigens expressed by infected hepatocytes are the main signs of hepatocellular injury. Antibodies against hepatitis B core antigen (anti-HBc) are often the only serum markers in mono-infected patients with occult HBV. Increasing serum HBV DNA concentrations, decline in liver enzyme levels and developing faster liver cirrhosis, particularly in those with low CD4 counts, are some of the symptoms of this phenomenon (Table 2). However, proper diagnosis and monitoring of co-infection of hepatitis B and HIV, along with complete understanding of the mechanisms of drug resistance, will allow researchers and clinicians to manage co-infection cases more efficiently. Liver injuries are also more common in these patients for whom treatment options have widely developed. Tenofovir is another option to be chosen for resistance mutations in HIV polymerase.55 In coinfected patients who develop resistance to lamivudine, the recommended treatment is tenofovir plus entecavir (because there is no cross-reactivity between these two agents), tenofovir plus lamivudine or emtricitabine.
Using standard therapy for HIV, it is the main treatment strategy in co-infection whereas two effective agents should be selected against HBV infection.


Clinical observations also showed that patients who suffered from immune defects and were infected with HBV often had mild acute liver injury but were major chronic carriers.27,28 The immune responses to HBV and their role in the hepatitis B pathogenesis are still not completely understood. So in cases with high risk of hepatitis B where HBsAg is negative, it is needed to check anti-HBc level.
The most prominent issue among all these negative consequences is the faster progression of HBV-related liver disease. In general, there is a series of actions for the diagnosis or even prevention of co-infections which are mostly recommended to be accomplished in cases of new HIV infections. Levy and Grant have stated that using IFN-α once-weekly for about 16 weeks can be influential in treatment trend.
Some evidences suggest that entecavir resistance is inclined by lamivudine resistance, but the same studies were performed in patients with very high baseline viral loads; the efficiency of entecavir in patients who had low baseline viral loads is unknown. Because antiviral resistance is a probability in treatment, choosing active agents seems complicated, that is the choices for treatment of HBV infection are limited by resistance to HIV therapy. Ministries of Health of several African nations currently promote Hypoxis as a traditional medicine for the treatment of HIV and associated symptoms.
Infection with HBV becomes more violent in patients co-infected with human immunodeficiency syndrome.
Viral genome, a relaxed-circular, partially duplex DNA containing 3.2 kb, and a polymerase responsible for the synthesis of viral DNA in infected cells are included in the core.
Several clinical studies showed that in acute, self-limited hepatitis B, strong T-cell responses against many HBV antigens were proven to exist in the peripheral blood, including both major-histocompatibility-complex (MHC) class II, CD4+ helper T cells and MHC class I, CD8+ cytotoxic T lymphocytes.
The presence of anti-HBc is rarely coupled with occult infection in HIV-uninfected patients, though. Cirrhosis has been more commonly reported in HIV-HBV co-infection individuals despite lower alanine aminotransferase (ALT) levels than in HBV mono-infection, and it may be related to lower CD4+ T cell counts.50,51 Co-infection of HBV with HIV changes the natural history of HBV infection. First, all individuals diagnosed with HIV recently, should be examined for hepatitis B surface antigen (HBsAg) and anti-HBs. The first aim of therapy is to decrease the amount of HBV DNA to an undetectable level; so using less potent agents is not an option.
HBV virus seems to have multiple viral genotypes, according to the data acquired from DNA sequencing of many isolates of HBV, each of which with a characteristic geographic distribution.24-26 Other than virions, cells infected with HBV produce two different subviral lipoprotein particles of spheres and filamentous forms of about 20 nm.
The antiviral cytotoxic T-lymphocyte response which is against multiple epitopes within the HBV core, polymerase, and envelope proteins, and also strong helper T-cell - against C and P proteins- occur in acute infection.
HIV-HBV co-infected patients seroconvert from HBV e (precore) antigen (HBeAg) to HBV e antibody less frequently and have higher HBV DNA levels but lower levels of alanine aminotransferase (ALT). The most potent agent such as tenofovir plus lamivudine or tenofovir plus emtricitabine is recommended as the best choice (Figure 1).55,56 In a study performed by GERMIVIC Study Group, Piroth et al. In this review, the latest statistics on epidemiology of HIV, HBV and their co-infection has been presented along with prominent characteristics of HBV.
In this case, there is a co-infection rate of 5-10% which is 10 times higher than general population. In areas with low HBV endemicity, such as the United States, Australia, and Europe, HBV and HIV usually happened in adulthood either sexually or through percutaneous transmission.


HBeAg is an accessory protein of HBV and is not necessary for viral replication or infection. For HBsAg positive patients, HBeAg, anti-HBe and HBV DNA should be tested, otherwise it is recommended to apply HBV vaccination. Transmission routes which are the common between HBV and HIV are described and the most important ones are described according to the regional and age features.
Average prevalence of 2-7% HBsAg- has been reported in Japan, Middle East, Central America, and Latin America. Infection with HBV often follows HIV because HBV is nearly 100-fold more likely to be transmitted than HIV. In addition to a complete history and physical examinations, newly HIV infected patients’ bloods should be screened for complete blood pictures, clotting profiles including prothrombin time, international normalized ratio (INR), alpha-fetoprotein (AFP) and tests on liver and renal functions.
Professor Ben Smith, head of the department of oncology at Cape Town’s Tygerberg Hospital has treated patients suffering from advanced cancer and found it increased their life expectancy. Also, there is a series of actions being performed once HBV infections occur to prevent HIV or to diagnose if the HBV-infected individuals are also infected with HIV.
Finally, high HBV endemicity of 8-15% HBsAg exists in Sub-Saharan Africa, South East Asia, and China.
The prevalence of HBV co-infection in such low endemicity areas is 5-7% of HIV-infected individuals but it is affected by route of infection. Victims of cancer of the pancreas usually die within four to six months of diagnosis, but after plant sterol treatment they lived for a year or longer.
As in treatment case, some of the frequent treatment methods including applying interferon and using nucleoside and nucleotide analogues have been discussed. Although as yet there is no scientific evidence that Hypoxis rooperi eliminates cancer tumors, it does seem to slow down the growth of certain types of tumors.
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