Release date: 2016-03-18
According to the World Health Organization (WHO), the number of hepatitis B virus (HBV) virus infections is nearly 240 million, and about 650,000 people die each year from malignant diseases such as liver failure, liver cirrhosis and liver cancer caused by HBV infection. In China, there are about 93 million people with chronic HBV infection, 20 million patients with chronic hepatitis B, and the virus infection rate is about 60%-70%.
HBV is mainly transmitted through blood, mother and baby, and sexual contact, and its infectious ability is 100 times higher than HIV HIV. Currently, the injection of hepatitis B vaccine is the most effective way to prevent HBV infection. About 90-95% of infected people can recover from acute infections, and most of the chronic infections are only carriers of the virus, and there will be no serious lesions. Only 5-10% of patients develop chronic hepatitis. The concern is that patients with chronic hepatitis B have no cure, but they need to be treated and nursed to ensure long-term stability.
The pathogenesis of HBV is complex and has not been studied so far. Studies have shown that HBV does not directly kill liver cells, but triggers an abnormal immune response, leading to secondary inflammation and liver cell damage. But there are still many unknowns about how to achieve immune escape with viruses.
Recently, the research team of the University of Geneva School of Medicine (UNIGE) published a new study on hepatitis B virus in the Nature Journal, revealing how cells can resist HBV infection and how the virus fights back. This latest study has deepened the understanding of HBV and is expected to provide new targets for the development of innovative drugs.
Hero and Reverse Thief: Battle between Host Cells and Viruses
Cells produce defense proteins that form the first line of defense against viral infections. These protective factors are an important part of the natural immune response. But little is known about how cells protect against HBV infection and which protective factors are involved. After HBV is infected with hepatocytes, the circovirus genome enters the nucleus and is independent of the cell chromosome. But what happens next?
Professor Michel Strubin, a microbiologist at the University of Geneva School of Medicine, and the University of Lyon, France, and the American Gilead Science Company, found that a protein complex Smc5/6 of the host cell recognizes the HBV genome and acts as a protective factor to inhibit viral gene expression and prevent new genes. Virus generation.
However, the virus also carries a "weapon" to protect itself. The defense of the Smc5/6 protein complex should have been able to control the virus, but the virus countered it. HBV is able to express a small protein, the X protein, which disrupts Smc5/6 and transports the protective protein to lysosomal degradation. After escaping the defensive line of Smc5/6, the virus can generate more new viruses, infect neighboring cells, and lead to disease progression.
A new drug target: inhibition of viral X protein This study provides a new target for hepatitis B virus therapeutic drugs, by targeting X protein, preventing viral immune escape. Gilead researcher Dr. Simon Fletcher said that the discovery of this new mechanism is expected to provide background support for X-protein inhibitors, which is also the significance of basic research.
In addition, the research team is interested in whether this mechanism is applicable to other infectious viruses. Considering that herpes virus, human papillomavirus, etc., like HBV, have a circular genome independent of the cell chromosome, the research team is conducting in-depth research to determine whether the Smc5/6 protein complex can target these viruses, and these viruses Whether it is possible to produce special proteins for counterattacks. If consistent with the results of the HBV study, stopping viral proteins from disrupting Smc5/6 may be an effective strategy to prevent these highly contagious diseases.
Source: Bio-Exploration
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