No abstract

BackgroundChina is experiencing a dynamic HIV/AIDS epidemic. While serology based surveillance systems have reported the spread of HIV/AIDS, detailed tracking of its transmission in populations and regions is not possible without mapping it at the molecular level. We therefore conducted a nationwide molecular epidemiology survey across the country.MethodsHIV-1 genotypes were determined from 1,408 HIV-positive persons newly diagnosed in 2006. The prevalence of each genotype was estimated by weighting the genotype’s prevalence from each province- and risk-specific subpopulation with the number of reported cases in the corresponding subgroups in that year.ResultsCRF07_BC (35.5%), CRF01_AE (27.6%), CRF08_BC (20.1%), and subtype B' (9.6%) were the four main HIV-1 strains in China. CRF07_BC and CRF08_BC were the primary drivers of infection among injecting drug users in northeastern and southeastern China, respectively, and subtype B' remained dominant among former plasma donors in central China. In contrast, all four strains occurred in significant proportions among heterosexuals nationwide, pointing to an expansion of the HIV-1 epidemic from high-risk populations into the general population. CRF01_AE also replaced subtype B as the principal driver of infection among men-who-have-sex-with-men.ConclusionsOur study provides the first comprehensive baseline data on the diversity and characteristics of HIV/AIDS epidemic in China, reflecting unique region- and risk group-specific transmission dynamics. The results provide information critical for designing effective prevention measures against HIV transmission.

Objectives:We sought to comprehensively analyze the origin, transmission patterns and sub-epidemic clusters of the HIV-1 CRF01_AE strains in China.Methods:Available HIV-1 CRF01_AE samples indentified in national molecular epidemiologic surveys were used to generate near full-length genome (NFLG) sequences. The new and globally available CRF01_AE NFLG sequences were subjected to phylogenetic and Bayesian molecular clock analyses, and combined with epidemiologic data to elucidate the history of CRF01_AE transmission in China.Results:We generated 75 new CRF01_AE NFLG sequences from various risk populations covering all major CRF01_AE epidemic regions in China. Seven distinct phylogenetic clusters of CRF01_AE were identified. Clusters 1, 2 and 3 were prevalent among heterosexuals and IDUs in southern and southwestern provinces. Clusters 4 and 5 were found primarily among MSM in major northern cities. Clusters 6 and 7 were only detected among heterosexuals in two southeast and southwest provinces. Molecular clock analysis indicated that all CRF01_AE clusters were introduced from Southeast Asia in the 1990s, coinciding with the peak of Thailand's HIV epidemic and the initiation of China's free overseas travel policy for their citizens, which started with Thailand as the first destination country.Conclusion:China's HIV-1 epidemic of sexual transmissions, was initiated by multilineages of CRF01_AE strains, in contrast to the mono-lineage epidemic of B′ strain in former plasma donors and IDUs. Our study underscores the difficulty in controlling HIV-1 sexual transmission compared with parenteral transmission.

We assessed the separate and combined effects of hepatitis B virus (HBV), hepatitis C virus (HCV), and aflatoxin in causing hepatocellular carcinoma (HCC) in Qidong, China. A consecutive series of 181 pathologic-diagnosed HCC cases were studied for hepatitis B surface antigen (HBsAg), anti-HBc, HBV X gene sequence, anti-HCV, the 249ser-p53 mutation, and chronic hepatitis pathology. Each of the 181 incident HCC cases had markers for HBV infection and hepatitis pathology; only 6 of 119 cases were coinfected with HCV. The 249ser-p53 mutation was found in 54% (97/181) of HCC cases and in all 7 cases with tissue for analysis from the hepatitis cohort but in none of 42 matched cases from Beijing. The estimated cumulative dose of aflatoxin B1 in these 7 cases ranged from 0.13 to 0.49 mg/kg. Follow-up data through 13.25 years on a cohort of 145 men with chronic HBV hepatitis showed that the relative risk from aflatoxin exposure was 3.5 (1.5-8.1). A similar relative risk was found using 249ser-p53 mutation as a marker for aflatoxin exposure. In conclusion, HBV hepatitis is ubiquitous in Qidong HCC cases, whereas HCV contributes little to its risk. The 249ser-p53 mutation appears to result from coexposure to aflatoxin and HBV infection. Even modest levels of aflatoxin exposure tripled the risk of HCC in HBV-infected men. H epatocellular carcinoma (HCC) is the second most common cancer and kills 300,000 or more people each year in China. 1,2 The close linkage of hepatitis B virus (HBV) to HCC was largely established in epidemiologic studies based on the detection of HBV surface antigen (HBsAg) in sera. In Qidong, China, about 16% of the adult population are seropositive for HBsAg. This marker is not present in every person infected with HBV, however. Early studies had shown that many HBsAg seronegative HCC patients in Qidong had evidence of HBV infection determined by immunohistochemistry 3 or by molecular hybridization in European cases. 4 Fujimoto et al. 5 reported that 23 of 26 HCC cases from Qidong were HBV positive by Southern blot analysis, including 3 HBsAg seronegatives. Paterlini et al. 6 had shown by reverse transcriptase polymerase chain reaction assays that HBV X gene-related transcripts were often found in the diseased and normal hepatic tissues of HBsAg-negative HCC patients. In Japan, many HCC cases attributed to hepatitis C virus (HCV) were found to have markers of HBV infection. 7-9 Zhang et al. 10 reported that PCR analysis of 21 HBsAg seronegative HCC cases in Qidong revealed HBV X gene sequence in the HCC DNA of every case. A recent cohort study in Qidong also showed that HBV worked synergistically with aflatoxin, HCV, and family history to significantly enhance HCC incidence. 11 Using an extensive set of assays, we sought to determine whether HBV infection is virtually ubiquitous in HCC cases in Qidong. Such a finding would have implications for understanding the carcinogenic process