geographical location established different rates. 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. Infection with HBV often follows HIV because HBV is nearly 100-fold more likely to be transmitted than HIV. 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. The highest frequency of co- infection is because of MSM (men who have sex with men), ranging from 9-17%, and the lowest was from heterosexual transmission.17 Whereas in countries with intermediate and high HBV endemicity, the main routes of HBV transmission were perinatal or in early childhood; so HBV infection usually preceded HIV infection by decades. In these countries, most studies suggested that HBV co-infection prevalence was 10- 20%, but some showed as low as 6%.18 Nowadays, around 1/3 of people in the world had a contact history with HBV infection presented with isolated anti-HBcAb during their lives. Among these, 350 million remained infected chronically and be- came carriers of the virus. Three quarters of the world’s population live in areas where there are high levels of infection.19 There is a new entity in co- infection of HBV/HIV that the HBs Ag is negative and occult HBV persists.20,21 The prevalence of OBI in HIV-positive patients varies considerably from 0% to 89.5% in different geographical regions.21 Virological Features Classification and Structure 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 pancre- as, 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 enve- lope has three envelope glycoproteins (or surface an- tigens) related to each other. The viral nucleocapsid which is also called core exists within the envelope. 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. HBV virus seems to have multi- ple viral genotypes, according to the data acquired from DNA sequencing of many isolates of HBV, each Epidemiology of HIV/HBV co-infections of which with a characteristic geographic distribu- tion.24-26 Other than virions, cells infected with HBV produce two different subviral lipoprotein particles of spheres and filamentous forms of about 20 nm. Enve- lope glycoproteins and host-derived lipids are the on- ly parts HBsAg particles and they are usually signifi- cantly more than virions in number (1000:1 to 10,000:1).25 Pathogenesis of Hepatitis B The HBV replication cycle is not directly cytotox- ic to cells, as in, many HBV carriers show no symp- toms and have minimal liver injury, however intrahe- patic replication of the virus continues extensively. Therefore, immune responses to viral antigens ex- pressed by infected hepatocytes are the main signs of hepatocellular injury. Clinical observations also showed that patients who suffered from immune de- fects 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 un- derstood. 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 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. By contrast, in chronic carri- ers of HBV, such virus-specific T-cell responses are greatly reduced, at least as examined in cells obtained from peripheral blood.29 Following the introduction of highly active antiretroviral therapy (HAART), liver disease is now the major cause of non-AIDS-related deaths in HIV-1-infected patients.30-32 Progression to cirrhosis seems to be more rapid and more common, and liver-related mortality is higher, in HIV/HBV co- infection than with either infection alone.33 Natural History and Transmission Routes Hepatitis B Virus Percutaneous and mucous membrane exposures to infectious blood and body fluids containing blood are the main routes of HBV transmission.34 Percutaneous exposure includes blood or blood products transfu- WWW.ircmj.com Vol 13 December 2011 857