Ranjbar et al. sion, using contaminated equipment in therapeutic injections and other health-care related practices, in- jectable drug use, and needle sticks or other injuries from sharp instruments occurred by hospital staff.35,36 Perinatal and sexual exposures to HBV are two other modes of transmission which are extremely efficient. HBV can also spread among household through con- tacts with a chronically infected person.37,38 Moreo- ver, tattooing and acupuncture have been in charge of some occasional outbreaks.36 Chronic HBV infection is considered as two distinct phases: HBeAg positive and HBeAg negative.39 In most cases, transmissions result from non-compliance with aseptic techniques and recommended infection control procedures that were designed to prevent post-practice infections due to cross-contamination of medical equipment and de- vices. In developing countries, donor testing for HBsAg is not common and, unsafe therapeutic injec- tion practices, including inadequately sterilized nee- dles and medical instruments, the reuse of disposable needles and syringes, and contamination of multiple dose medication vials are still responsible for trans- mission which has made it a significant problem.40-43 There are also some cases of occult HBV infec- tions which are described as the existence of HBV DNA without detectable HBsAg. Antibodies against hepatitis B core antigen (anti-HBc) are often the only serum markers in mono-infected patients with occult HBV. So in cases with high risk of hepatitis B where HBsAg is negative, it is needed to check anti-HBc level. The presence of anti-HBc is rarely coupled with occult infection in HIV-uninfected patients, though. Thus, HBV DNA should be measured.44 Co-Infection with HIV HBV and HIV have similar characteristics such as transmission modes; using a reverse transcriptase en- zyme in replication; the tendency to develop chronic infections, which are often difficult to treat; and final- ly, an immense capacity of mutation in their genome, causing rapid emergence of mutant strains, some of which are resistant to widely used anti-viral agents. In addition, both viral genomes can integrate within the host genome, a process which is obligatory for the life cycle of HIV, but not for HBV.45 Among the estimated 40 million persons infected with HIV worldwide, an estimated 2–4 million are chronically infected with HBV.31 In general, HBV tends to be more aggressive in HIV-positive individu- als than in mono-infected individuals, with higher HBV carrier rates, higher levels of HBV viremia, more frequent episodes of activation, and faster pro- gression to cirrhosis.46,47 Several factors are effective in estimating these co-infection rates, such as geo- graphic differences in the incidence of chronic infec- tion by age, the efficiency of exposures which is di- rectly responsible for most transmissions, and the prevalence of persons at high risk for infection.36 Co- infection with HBV and HIV follows a different course everywhere in the world. For example, neona- tal or childhood infection, with either vertical or hori- zontal transmission is the most common route of transmission in Africa and Asia after birth. In parts of Africa, ritual scarification seems to have a major role in the adolescent transmission of HBV.48,49 (ritual scarification is known as the practice of making small incisions in the skin of adolescents and rubbing black ash in the wounds to form scars; the instruments be- ing used for cutting are not sterilized between rituals). Co-infection with HIV alters the natural history of chronic hepatitis B. 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). The most prominent issue among all these negative consequences is the faster progression of HBV-related liver disease. Cirrhosis has been more commonly reported in HIV-HBV co- infection individuals despite lower alanine ami- notransferase (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. 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). HBeAg is an accessory protein of HBV and is not necessary for viral replica- tion or infection. Most studies on natural history of HIV- HBV co-infection until now have principally Table 2: Effects of HIV on the Natural History of Adult-Acquired HBV Infection.50 Effects Comment Increase risk for developing chronic HBV infection Studies in men who have sex with men. Lower CD4+ Decreased rate of HBeAg clearance T-cell count with higher risk of chronicity Increased HBV replication Demonstrated with higher HBV DNA levels Decreased inflammatory response to chronic hepatitis B Lower ALT levels Increased liver disease progression More cirrhosis and higher liver-related mortality 858 WWW.ircmj.com Vol 13 December 2011