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Chinese scholars have discovered that humans have new anti-HIV proteins that help develop anti-AIDS drugs.
2019 03/06 10:39
Beijing Daily Client
For more than a decade, scientists have discovered several antiviral proteins known as restriction factors in viral host cells. Such proteins are capable of high expression by interferon, which in turn induces natural antiviral immunity, inhibiting viral replication from various stages of the viral life cycle.
After the "London Patient" became the second known adult to get rid of HIV in the world, another good news came from Chinese universities. Researchers at Tsinghua University, Fudan University and George Mason University in the United States passed high-sensitivity proteomics. A new anti-HIV protein PSGL-1 was first discovered and confirmed in human cells. Studying the binding inhibitors of the HIV accessory proteins Vpu and PSGL-1 will provide a new way to develop anti-AIDS drugs.
AIDS is a highly harmful infectious disease caused by HIV infection. HIV attacks the body's immune system, constantly destroying CD4-positive T lymphocytes in patients, and the patient loses immune function. Patients with extremely low immunity are prone to various concomitant diseases and eventually lead to death. Recently, Xinhua News Agency reported that since the first discovery of HIV in 1981, the AIDS pandemic has killed about 35 million people, and there are currently about 37 million people infected with HIV worldwide.
The existing combination therapy (cocktail therapy) can largely alleviate the patient's symptoms but cannot cure the disease, and long-term medication has the risk of developing resistance.
Studying the interaction between HIV and host cells has the potential to provide new targets for anti-HIV drugs. For more than a decade, scientists have discovered several antiviral proteins known as restriction factors in viral host cells. Such proteins are capable of high expression by interferon, which in turn induces natural antiviral immunity, inhibiting viral replication from various stages of the viral life cycle.
But "the road is one foot high and the devil is one foot tall." HIV has also evolved a corresponding antagonistic mechanism, and almost every limiting factor can be specifically antagonized by an accessory protein of HIV. By degrading these limiting factors, the virus subtly circumvents the natural immune system and eventually successfully infects the cells and completes replication. Therefore, it is a new research direction to explore new host restriction factors and study the interaction between viruses and them.
When HIV-infected cells, they can maintain some important protein degradation pathways in cells and affect the stability of proteins in host cells in a wide range. Therefore, it is difficult to fully reflect the transcriptome changes in the infection process only by second-generation sequencing. The relationship between the host and the host cells.
Tan Xu team of Tsinghua University School of Pharmacy used high-sensitivity protein mass spectrometry technology to compare the cellular protein levels of primary CD4 T cells before and after HIV infection. Among the approximately 14,000 proteins identified, nearly 1,000 proteins were found to be significant. Changes, by comparing with other databases, especially against a highly evolved list of human genes, screened for a protein that is not known to function in HIV infection, PSGL-1.
Previous studies have shown that PSGL-1 is present on the leukocyte membrane and can regulate the movement of white blood cells. When the body develops an inflammatory reaction, it can slow the movement speed of white blood cells and eventually adhere to the inflammatory reaction site, thus maintaining the body's homeostasis.
In this latest study, the researchers found that high levels of PSGL-1 inhibit DNA synthesis in the pre-infection of the virus, and that when the newly produced virus is released, PSGL-1 can be encapsulated into the released virus, further And more strongly inhibit a new round of viral infection. The researchers went on to verify that PSGL-1 was able to significantly reduce protein levels after infection with the virus. They also found that the HIV accessory protein Vpu escapes the body's natural immune system by recruiting ubiquitin ligase complexes in the body and specifically binding and degrading PSGL-1. Therefore, inhibition of Vpu antagonism of PSGL-1 is expected to become a new direction for the development of anti-HIV drugs.
The researchers also found that PSGL-1 is the main effector molecule of the antiviral function of type 2 interferon and an important component of human antiviral natural immunity.
The result was completed by Tan Xu's research group of Tsinghua University School of Pharmacy and Zhou Feng's research group of Fudan University and Wu Yuntao's research group of George Mason University. The related results were published on March 4th in the authoritative journal Microbiology, Nature - Microbiology.
Source: Beijing Daily Client
Author: Ren Min
Producer: Tong Yuquan, Liu Wei
Editor: Wang Haiping
Process Editor: Sun Yijie
https://new.qq.com/omn/20190306/20190306A0DY3D.html
2019 03/06 10:39
Beijing Daily Client
For more than a decade, scientists have discovered several antiviral proteins known as restriction factors in viral host cells. Such proteins are capable of high expression by interferon, which in turn induces natural antiviral immunity, inhibiting viral replication from various stages of the viral life cycle.
After the "London Patient" became the second known adult to get rid of HIV in the world, another good news came from Chinese universities. Researchers at Tsinghua University, Fudan University and George Mason University in the United States passed high-sensitivity proteomics. A new anti-HIV protein PSGL-1 was first discovered and confirmed in human cells. Studying the binding inhibitors of the HIV accessory proteins Vpu and PSGL-1 will provide a new way to develop anti-AIDS drugs.
AIDS is a highly harmful infectious disease caused by HIV infection. HIV attacks the body's immune system, constantly destroying CD4-positive T lymphocytes in patients, and the patient loses immune function. Patients with extremely low immunity are prone to various concomitant diseases and eventually lead to death. Recently, Xinhua News Agency reported that since the first discovery of HIV in 1981, the AIDS pandemic has killed about 35 million people, and there are currently about 37 million people infected with HIV worldwide.
The existing combination therapy (cocktail therapy) can largely alleviate the patient's symptoms but cannot cure the disease, and long-term medication has the risk of developing resistance.
Studying the interaction between HIV and host cells has the potential to provide new targets for anti-HIV drugs. For more than a decade, scientists have discovered several antiviral proteins known as restriction factors in viral host cells. Such proteins are capable of high expression by interferon, which in turn induces natural antiviral immunity, inhibiting viral replication from various stages of the viral life cycle.
But "the road is one foot high and the devil is one foot tall." HIV has also evolved a corresponding antagonistic mechanism, and almost every limiting factor can be specifically antagonized by an accessory protein of HIV. By degrading these limiting factors, the virus subtly circumvents the natural immune system and eventually successfully infects the cells and completes replication. Therefore, it is a new research direction to explore new host restriction factors and study the interaction between viruses and them.
When HIV-infected cells, they can maintain some important protein degradation pathways in cells and affect the stability of proteins in host cells in a wide range. Therefore, it is difficult to fully reflect the transcriptome changes in the infection process only by second-generation sequencing. The relationship between the host and the host cells.
Tan Xu team of Tsinghua University School of Pharmacy used high-sensitivity protein mass spectrometry technology to compare the cellular protein levels of primary CD4 T cells before and after HIV infection. Among the approximately 14,000 proteins identified, nearly 1,000 proteins were found to be significant. Changes, by comparing with other databases, especially against a highly evolved list of human genes, screened for a protein that is not known to function in HIV infection, PSGL-1.
Previous studies have shown that PSGL-1 is present on the leukocyte membrane and can regulate the movement of white blood cells. When the body develops an inflammatory reaction, it can slow the movement speed of white blood cells and eventually adhere to the inflammatory reaction site, thus maintaining the body's homeostasis.
In this latest study, the researchers found that high levels of PSGL-1 inhibit DNA synthesis in the pre-infection of the virus, and that when the newly produced virus is released, PSGL-1 can be encapsulated into the released virus, further And more strongly inhibit a new round of viral infection. The researchers went on to verify that PSGL-1 was able to significantly reduce protein levels after infection with the virus. They also found that the HIV accessory protein Vpu escapes the body's natural immune system by recruiting ubiquitin ligase complexes in the body and specifically binding and degrading PSGL-1. Therefore, inhibition of Vpu antagonism of PSGL-1 is expected to become a new direction for the development of anti-HIV drugs.
The researchers also found that PSGL-1 is the main effector molecule of the antiviral function of type 2 interferon and an important component of human antiviral natural immunity.
The result was completed by Tan Xu's research group of Tsinghua University School of Pharmacy and Zhou Feng's research group of Fudan University and Wu Yuntao's research group of George Mason University. The related results were published on March 4th in the authoritative journal Microbiology, Nature - Microbiology.
Source: Beijing Daily Client
Author: Ren Min
Producer: Tong Yuquan, Liu Wei
Editor: Wang Haiping
Process Editor: Sun Yijie
https://new.qq.com/omn/20190306/20190306A0DY3D.html
