Hepatitis B virus reactivation or reinfection associated with HIV-1 infection

Prevalence of hepatitis B e antigen among human immunodeficiency virus and hepatitis B virus co-infected patients in Jos, Nigeria

“…This is in agreement with other studies that found a strong association between younger age and HBeAg seropositivity in Taiwan [38] and the Gambia [39], both of which have similar HBV transmission epidemiology to Nigeria. In areas of high endemicity such as sub-Saharan Africa and Asia, horizontal and perinatal mechanisms are the most important means of HBV transmission, with most HBV-infected individuals acquiring the infection in early childhood, leading to high rates of chronic HBsAg carriage [8,40].…”

“…This finding is similar to other reports from Romania [21] and South Africa [38] that found no relationship between HBV replication markers and HIV viral load among coinfected patients. The reason for the lack of association between HIV viral load and HBV replication markers cannot readily be explained, especially because only a few studies have investigated this relationship.…”

“…In natural history studies of Asian HBsAg-positive children, the rate of spontaneous HBeAg seroconversion was less than 2% per year among children three years of age or younger and between 4% and 5% per year in older children [40]. Approximately 90% of HBsAg carriers who acquired HBV in early life remained HBeAg-positive at age 15-20 years, but HBeAg clearance increased with increasing age, such that the prevalence of HBeAg was less than 10% in patients older than 40 years [31,38]. These observations therefore explain our finding that age below 40 years was independently associated with HBeAg seopositivity.…”

“…Effective immunological control of HBV replication requires an intact immune system and involves the targeting of HBV antigens on infected hepatocytes through polyclonal, multi-specific CD8+ T-lymphocyte activity supported by CD4+ T-cells [35,36].In the early stages of HIV infection, CD4+ cell decline is often gradual, while CD8+ cells are relatively preserved, which could still maintain significant immunological control of HBV replication [36].However, with advanced HIV-induced immunosuppression, both CD4+ and CD8+ cells are depleted, leading to severe impairment in HBeAg clearance [36]. Beyond defective HBeAg clearance attributed to T-cell lymphopaenia, it has also been shown that HIV-induced immunosuppression favours HBV re-activation, which would make individuals who had previously experienced HBeAg seroconversion (i.e., had developed anti-HBe antibody and lost HBeAg) to become HBeAg seropositive again, a phenomenon known as reverseseroconversion [37,38].…”

Hepatitis B reactivation after chemotherapy: two decades of clinical research

“…This is particularly a problem in Asia owing to the high hepatitis B surface antigen carrier rate, compounded by the recent increase in use of cytotoxic or immunosuppressive therapy for the treatment of a wide variety of clinical diseases [21]. With the increasing prevalence of HIV infection, HBV reactivation has also been observed in HBV-infected subjects with advanced immune deficiency due to HIV infection [22][23][24][25][26][27]. Hepatitis due to HBV reactivation has not only been reported in HBsAg-positive patients, HBeAg-positive [6,[28][29][30] or HBeAg-negative [31][32][33][34][35][36][37][38][39][40][41] subjects who were treated with chemotherapy and transplantation but also in HBsAg-negative patients who had past HBV infection (hepatitis B surface antibody; antiHBs positive and hepatitis B core antibody; anti-HBc positive) [42][43][44][45][46][47][48][49], especially those treated with rituximab or alemtuzumab-containing chemotherapy [50][51][52][53][54][55].…”