Résumé
@#Abstract: Chronic infection of hepatitis B virus (HBV) is the major cause of hepatocellular carcinoma (HCC) in China. The occurrence of HCC through chronic inflammation follows the Darwinian evolutionary law, known as "mutation-selection-adaptation". Inflammatory mutagenic molecules promote the generation of somatic mutations, and the most mutant cells are eliminated by inflammatory microenvironment. However, a minority of mutant cells survive the selective pressure and develop to tumor initial cells by activating oncogenic signaling pathway and acquiring "stemness" characteristics. Alongside this process, HBV also evolves under the pressure of inflammatory microenvironment, which is characterized by the accumulation of cancer-promoting viral mutations, reducing the ability to infect new individuals. The high-risk mutant strains are eliminated with the death of hosts, leading to a phenomenon termed as "dead-end evolution". HBV evolution contributes to cancer evolution by maintaining the inflammatory microenvironment, activating oncogenic pathways, inducing somatic cell mutations, and altering metabolic patterns. The combo mutations of HBV and HBV integrations can be applied to predict the occurrence and prognosis of HCC. Anti-viral treatment reduces the risk of HCC by relieving inflammation. This article reviews the molecular epidemiological evidence and mechanistic advances related to the co-evolution of HBV and HCC. Clarifying the co-evolutionary pattern of virus and cancer and the key molecular events involved, is beneficial for identifying new biomarkers and therapeutic targets, thus improving the prevention and treatment strategies for HCC.
Résumé
Purpose: The purpose of this study was to identify measles virus in Shanghai in 2012 and study the genotype trend of measles virus epidemic strains during 2000–2012. Methods: Nose and throat swab specimens were collected from 34 suspected measles cases in Shanghai. Measles virus was isolated using Vero-SLAM cells (African green monkey kidney cells/lymphoid signal activating factor-transfected African green monkey kidney cells). The 450 bp of C terminus of the N gene and the entire hemagglutinin gene sequence was amplified using RT-PCR. Phylogenetic analysis was performed by comparing the seven measles strains in Shanghai with the reference strains for H1a, H1b and D8 genotypes, as well as the Chinese measles virus vaccine strain. Results: Seven measles viruses strains were isolated from the 34 throat swap specimens. Six strains were genotype H1a, which is the predominant strain in China and one strain was genotype D8, which is the first imported strain since 2000. All these seven strains maintained most of the glycosylation sites except subtype H1a, which lost one glycosylation site. Conclusion: Since 2000, measles virus strains in Shanghai are consistent with measles virus from other provinces in China with H1a being the predominant genotype. This study is also the first report of genotype D8 strain in Shanghai. All strains maintained their glycosylation sites except H1a that lost one glycosylation site. These strains could still be neutralized by the Chinese measles vaccine. We suggest that Shanghai Center for Disease Control laboratories should strengthen their approaches to monitor measles cases to prevent further spread of imported strains. .