PNAS reveals hepatitis C marker molecule

Scientists from the National Institutes of Health have identified some marker molecules in people infected with hepatitis C virus. Based on these marker molecules, researchers may predict whether the disease will abnormally and rapidly develop into severe liver disease from the initial infection, such as liver hardening. Knowing whether the patient's disease is likely to deteriorate rapidly can help the doctor determine the best course of treatment. The research results were published in the Proceedings of the American Academy of Sciences (PNAS).

Dr. Patrizia Farci, head of the liver pathogenesis department of the Infectious Disease Laboratory of the National Institute of Allergy and Infectious Diseases (NIAID), a NIH affiliate, and Dr. Harvey Alter, deputy director of the research department and clinical research director of the Department of Transfusion Medicine at the NIH Clinical Research Center, jointly led this One study.

Dr. Anthony S. Fauci, Director of NIAID, said: "Treatment of hepatitis C is often quite expensive and difficult to tolerate. Having tools that enable doctors to better predict the course of disease in patients with hepatitis C will help guide treatment decisions. This small study may be a An important step forward in developing such tools. "

Hepatitis C virus is one of five viruses that can cause acute and chronic hepatitis diseases. The symptoms of acute infection with hepatitis C virus are fatigue, jaundice, and loss of appetite. 70-80% of people infected with hepatitis C virus will develop chronic infections, which can lead to serious liver diseases such as liver cancer and cirrhosis throughout their lives. The World Health Organization estimates that 130-170 million people worldwide are infected with hepatitis C virus. According to the Centers for Disease Control and Prevention, approximately 2.7-3.9 million people live in the United States.

After an individual is infected with hepatitis C virus, the virus will evolve and circulate in the body in the form of several closely related virus strains to adapt to drug treatment and avoid being cleared. Some of the genetic differences between these virus strains have caused certain proteins encoded by the virus to change, while others do not.

Dr. Farci said: “An important mystery in the study of hepatitis C is that the course of disease is highly variable. Some patients do not show symptoms for decades and will eventually die from other causes. Others quickly develop cirrhosis and liver cancer. It will cause liver-related deaths within ten years. "

Past research has found that weakening the immune system, such as HIV infection or organ transplantation, can aggravate hepatitis C-related diseases. But this does not fully explain which hepatitis C patients will eventually experience a more rapid health decline. Currently, there is no way to predict how the condition of all designated patients will develop.

The samples tested in the new study came from six patients with Hepatitis C who were infected with the Hepatitis C virus through contaminated blood transfusions in the 1970s. The virus had not been identified at the time. It was not until the 1990s that blood donation was routinely required to be tested for hepatitis C virus. The patients' symptoms and clinical results have been closely tracked for 30 years since they started receiving blood transfusions, ranging from mildly stable chronic hepatitis C to rapid disease progression and death.

Dr. Alter and his colleagues at the clinical center regularly collect serum samples from 6 patients. Colleagues from Farci and NIAID obtained and analyzed a total of 1,876 hepatitis C virus genetic sequences using up to 17 stored samples from each patient. The researchers used these genetic sequences to reconstruct two special isopropyl hepatitis genes, E1 and E2. The research team analyzed the types of genetic changes that occurred to understand their relationship to disease progression. They also studied the levels of 39 serum proteins in the acute and chronic stages of the disease.

"We have fully characterized the biological changes that occur in these patients. We found that patients with rapidly progressive disease have some specific changes in the blood that can be detected from the early acute stage of infection," Dr. Farci said. In patients with rapid disease progression, the level of a protein called MCP-1 is significantly higher, and it is believed to play an important role in the formation of liver fibrosis and eventually cirrhosis. In addition, in these patients, the virus has evolved its genetic changes over time and is unlikely to cause changes in viral proteins.

The researchers say that genetic and serum markers may one day allow doctors to determine the risk of rapid disease progression in hepatitis C patients and use this information to adjust their treatment. Farci believes that there may be other markers. The research team is working to increase the sample size by performing similar analysis on the remaining stored samples.

"Now that we know what to look for, we believe this is extremely important for extending our observations to a large number of patients," Farci said.

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