Interactions between hepatitis B virus infection and exposure to aflatoxins in the development of hepatocellular carcinoma: a molecular epidemiological approach

Sylla, Abdoulaye; Diallo, Mamadou Samba; Castegnaro, Jean-Jacques; Wild, Christopher P.

doi:10.1016/s1383-5742(99)00046-0

Cited by 53 publications

(36 citation statements)

References 32 publications

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“…The use of aflatoxin biomarkers as efficacy endpoints in primary prevention trials has been recently reported (75). This work was built on earlier research that established high aflatoxin exposure in Guinea, West Africa, due to consumption of groundnuts as a dietary staple (11,70,74) and revealed that postharvest storage was correlated with increases in exposure (74). On the basis of these observations, a community-based intervention study was conducted among subsistence farmers in the Kindia region of Guinea, West Africa.…”

Section: Primary Preventionmentioning

confidence: 99%

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Groopman

Kensler

Wild

2008

Annu. Rev. Public Health

255

163

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The public health impact of aflatoxin exposure is pervasive in economically developing countries; consequently, we need to design intervention strategies for prevention that are practicable for these high-risk populations. The adverse health consequences of aflatoxins in populations are quite varied, eliciting acute effects, such as rapid death, and chronic outcomes, such as hepatocellular carcinoma. Furthermore, a number of epidemiological studies describe a variety of general adverse health effects associated with aflatoxin, such as impaired growth in children. Thus, the magnitude of the problem is disseminated across the entire spectrum of age, gender, and health status in the population. The aflatoxins multiplicatively increase the risk of liver cancer in people chronically infected with hepatitis B virus (HBV), which illustrates the deleterious impact that even low toxin levels in the diet can pose for human health. Thus other aflatoxin interactions, which likely contribute to the diesease burden, still remain to be identified. Therefore, many diverse and appropriate strategies for disease prevention are needed to decrease the incidence of aflatoxin carcinogenesis in developing countries.

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Section: Primary Preventionmentioning

confidence: 99%

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Groopman

Kensler

Wild

2008

Annu. Rev. Public Health

255

163

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“…Both epidemiological and experimental studies have demonstrated a synergistic interaction between chronic HBV infection and aflatoxin exposure in the development of HCC (Ross et al, 1992;Wang et al, 1996a;Sylla et al, 1999). Taken together, the degree that AFB 1 contributes to risk of HCC may be influenced by both genetic and environmental factors.…”

mentioning

confidence: 99%

Determinants of formation of aflatoxin-albumin adducts: a seven-township study in Taiwan

Ca¹,

Dm²,

Ly³

et al. 2002

Br J Cancer

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Dietary exposure to aflatoxins is one of the major risk factors for hepatocellular carcinoma. Individual susceptibility to aflatoxin-induced hepatocarcinogenesis may be modulated by both genetic and environmental factors affecting metabolism. A cross-sectional study was performed to evaluate determinants of the formation of aflatoxin covalently bound to albumin (AFB 1 -albumin adducts). A total of 474 subjects who were free of liver cancer and cirrhosis and were initially selected as controls for previous case -control studies of aflatoxin-induced hepatocarcinogenesis in Taiwan, were employed in this study. Aflatoxin-albumin adducts were determined by competitive enzyme-linked immunosorbent assay, hepatitis B surface antigen and antibodies to hepatitis C virus by enzyme immunoassay, as well as genotypes of glutathione S-transferase M1-1 and T1-1 by polymerase chain reaction. The detection rate of AFB 1 -albumin adducts was significantly higher in males (42.5%) than in females (21.6%) (multivariate-adjusted odds ratio=2.6, 95% confidence interval=1.4 -5.0). The formation of detectable albumin adducts was moderately higher in hepatitis B surface antigen carriers (42.8%) than in non-carriers (36.6%) (multivariate-adjusted odds ratio=1.4, 95% confidence interval=1.0 -2.1). In addition, the detection rate of AFB 1 -albumin adducts tended to increase with the increasing number of null genotypes of glutathione S-transferase M1-1 and glutathione Stransferase T1-1. In conclusion, this cross-sectional study has assessed the relative contributions of environmental exposure and host susceptibility factors in the formation of AFB 1 -albumin adducts in a well characterised Chinese adult population. This study further emphasises the necessity to reduce aflatoxin exposure in people living in an area endemic for chronic hepatitis B virus infection.

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“…There are also studies that have examined genotypes of enzymes thought to activate aflatoxin to the reactive epoxide form. This is important as there is a strong interaction between aflatoxin and hepatitis B in carcinogenesis [pic] (Sylla et al, 1999;Uwaifo and Bababunmi, 1984). In the African context we identified several publications on genetics of HBV-related liver disease relating to Gambians, Ghanaians, Sudanese and Moroccans, respectively.…”

Section: Genetic Factors In Hbv-related Liver Disease and Hccmentioning

confidence: 99%

Host genetic factors in hepatitis B infection, liver cancer and vaccination response: A review with a focus on Africa

Hennig

Hall

2012

Science of The Total Environment

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The disease burden due to hepatitis B virus (HBV) infection remains significant; 350 million people are infected world-wide, and around half a million deaths each year are due to HBVrelated liver disease and hepatocellular carcinoma (HCC). Infant immunisation against infection was introduced in the early 1980s, the vaccine is routinely administered across regions where the disease is endemic and has been shown to be safe and effective. However, the large number of older individuals with persistent infection means that disease will not be reduced significantly for several decades. Furthermore, failure to respond to the vaccination has been observed in about 5% of vaccinees and to date we have limited information on the durability of vaccine protection against infection. Hepatitis B infection and disease pathogenesis are known to be influenced by a number of factors including host genetics factors. This review aims to give an overview of the role of genetic variation in persistent HBV infection and the development of liver disease including HCC. Vaccine-induced immunity is, at least in part, heritable and we also discuss findings on the genetic control of responses to HBV vaccination. The epidemiology of HBV infection differs by world region, as does the genetic makeup of individuals originating from different regions. This review focuses on the situation in Africa, where hepatitis B is highly endemic.

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Interactions between hepatitis B virus infection and exposure to aflatoxins in the development of hepatocellular carcinoma: a molecular epidemiological approach

Cited by 53 publications

References 32 publications

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Determinants of formation of aflatoxin-albumin adducts: a seven-township study in Taiwan

Host genetic factors in hepatitis B infection, liver cancer and vaccination response: A review with a focus on Africa

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