Abstract
ContextSince the introduction of highly active anti-retroviral regimen for human immunodeficiency virus-1 infection, a significant increase in the incidence of hepatocellular carcinoma has been reported in patients already chronically infected with hepatitis B virus and then given this form of regimen for their retroviral infection.Evidence AcquisitionThis phenomenon was initially attributed to the far more prolonged survival of those patients who received this new regimen, which provided sufficient time, allowing hepatitis B virus-induced hepatocellular carcinoma to develop.ResultsThe current belief is that the increased incidence of hepatocellular carcinoma is because of co-infection with the two viruses, one known to be hepatocarcinogenic and the other suspected to increase the carcinogenic potential of the other. Because both hepatitis B virus and human immunodeficiency virus -1 are endemic in the Black population of sub-Saharan Africa and are transmitted in similar ways, as many as 20% of this population are co-infected with the two viruses. In this way, the already high risk of Black African patients developing hepatitis B virus-induced hepatocellular carcinoma is further increased.ConclusionsThe pathogenetic mechanism or mechanisms involved in the carcinogenic interaction between the hepatitis B virus and the human immunodeficiency virus-1 in sub-Saharan Black Africans and other populations co-infected with these viruses have yet to be determined.
Highlights
ResultsThe current belief is that the increased incidence of hepatocellular carcinoma is because of co-infection with the two viruses, one known to be hepatocarcinogenic and the other suspected to increase the carcinogenic potential of the other
The pathogenetic mechanism or mechanisms involved in the carcinogenic interaction between the hepatitis B virus and the human immunodeficiency virus-1 in sub-Saharan Black Africans and other populations co-infected with these viruses have yet to be determined
Two possible ways in which HIV-1 co-infection might indirectly increase the risk of Hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) should be taken into account
Summary
Two possible ways in which HIV-1 co-infection might indirectly increase the risk of HBV-induced HCC should be taken into account. High HBV loads are known to increase the risk of HCC development [53, 54]. Immune suppression of the host induced by HIV-1 infection could result in higher HB viral loads, thereby increasing the risk of HBV-induced hepatocellular carcinogenesis. HIV1-positive individuals co-infected with HBV in adulthood have been shown to have an increased rate of HBV replication, and progression to chronic hepatitis five times more than HIV-negative individuals, thereby accelerating progression to cirrhosis and to HCC [17, 26, 55]
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