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There is a virus that is very cunning.
It is hibernating when you are in good health.
When your immune system is weakened, it enters into it, causing blisters, ulcers and other painful symptoms on the skin, mouth, and eyes
.
All of this is caused by the herpes simplex virus (HSV), including type 1 (HSV-1) and type 2 (HSV-2)
.
HSV-1 can be transmitted through the mouth or skin that looks completely normal.
After transmission, it will basically not cause discomfort, but will dormant in the nerve cells of the peripheral nervous system; HSV-2 is mainly transmitted through sex and lives in seclusion.
In the reproductive tract
.
According to data from the official website of the World Health Organization, HSV-1 has been lurking in nearly 70% of the world's human body, and the number of people under the age of 50 infected reached 3.
7 billion in 2016
.
What is even more frustrating is that the herpes virus will remain latent in the peripheral nervous system of the host for life and will never be eradicated
.
Where is HSV sacred? Why can the spread range be so wide? The article "Herpesviruses assimilatekinesin to produce motorized viral particles" recently published by "Nature" uncovered the mystery of HSV and revealed the molecular mechanism of the virus' ) And type 2 (HSV-2) vaccines opened the way
.
Professor Greg Smith, who participated in the study, pointed out that the ultimate goal of viral infection is to expand infinitely and continuously expand the scope of infection.
The first condition for achieving this goal is to reach the nucleus, and this process cannot be separated from the participation of intracellular microtubules.
.
Microtubules are fibrous structures that exist in cells that can transport substances and maintain cell morphology
.
Microtubules alone are not enough.
Viruses also need the engines on the train tracks-kinesin and dynein
.
HSV-1 can encode a special protein pUL36, which can bind to dynein and promote the transport of virus particles into the cell during the initial infection
.
For example, after the influenza virus invades epithelial cells, it will carry these two proteins and move back and forth on the microtubules until it is close to the nucleus
.
The kinesin captured by the virus transports the capsid to the nucleus, but the study found that the bidirectional transport and peripheral accumulation of pUL36 not only indicate that the PRV protein binds to dynein, it also recruits an "important partner"-kinesin
.
Related experiments have also directly confirmed the necessity of kinesin: when there is no kinesin during the production of virions and subsequent infections, although a large number of virus particles are produced, most of the virus particles will accumulate in the center and the capsid The transport from the centrosome to the nucleus is significantly impaired, so the ability of these virus particles to spread infection is weak
.
In summary, the cellular proteins that assist HSV infection have a clear division of labor
.
Dynein carries HSV-1 from the end of the axon to the center of the neuron, while kinesin carries the virus particles to the nucleus
.
The presence of kinesin-1 during virus assembly promotes the transport of the capsid to the nucleus during subsequent infections.
It is worth noting that kinesin originates from previously infected epithelial cells rather than neuronal endogenous cells, and is affected by the herpes virus pUL36 protein.
The assimilated kinesin promotes the infection of all cells by shuttling virus particles from the centrosome to the nucleus
.
In this way, the infection of HSV can be said to be even more powerful, and the seemingly low-key HSV is not low-key at all
.
Kinesins are captured by virus particles and transmitted to other cells.
"This is the first time that viruses have been found to use cellular proteins to complete rounds of infections.
They seem to be one of the most successful pathogens that have evolved so far," the lead researcher Caitlin Dr.
Prgg said, “After understanding how the HSV virus achieves this incredible operation through this research, we can now consider how to take away their ability to invade the nervous system
.
This is useful for studying other viral infections and developing related prevention.
Sex vaccines can provide new ideas and directions
.
"In order to facilitate you to continue to receive our articles, you are welcome to set us as a "star" so that you can see our news in the future
.
End reference materials: [1]https://doi.
org/10.
1038/s41586-021-04106-w[2]https://zhuanlan.
zhihu.
com/p/434679338
It is hibernating when you are in good health.
When your immune system is weakened, it enters into it, causing blisters, ulcers and other painful symptoms on the skin, mouth, and eyes
.
All of this is caused by the herpes simplex virus (HSV), including type 1 (HSV-1) and type 2 (HSV-2)
.
HSV-1 can be transmitted through the mouth or skin that looks completely normal.
After transmission, it will basically not cause discomfort, but will dormant in the nerve cells of the peripheral nervous system; HSV-2 is mainly transmitted through sex and lives in seclusion.
In the reproductive tract
.
According to data from the official website of the World Health Organization, HSV-1 has been lurking in nearly 70% of the world's human body, and the number of people under the age of 50 infected reached 3.
7 billion in 2016
.
What is even more frustrating is that the herpes virus will remain latent in the peripheral nervous system of the host for life and will never be eradicated
.
Where is HSV sacred? Why can the spread range be so wide? The article "Herpesviruses assimilatekinesin to produce motorized viral particles" recently published by "Nature" uncovered the mystery of HSV and revealed the molecular mechanism of the virus' ) And type 2 (HSV-2) vaccines opened the way
.
Professor Greg Smith, who participated in the study, pointed out that the ultimate goal of viral infection is to expand infinitely and continuously expand the scope of infection.
The first condition for achieving this goal is to reach the nucleus, and this process cannot be separated from the participation of intracellular microtubules.
.
Microtubules are fibrous structures that exist in cells that can transport substances and maintain cell morphology
.
Microtubules alone are not enough.
Viruses also need the engines on the train tracks-kinesin and dynein
.
HSV-1 can encode a special protein pUL36, which can bind to dynein and promote the transport of virus particles into the cell during the initial infection
.
For example, after the influenza virus invades epithelial cells, it will carry these two proteins and move back and forth on the microtubules until it is close to the nucleus
.
The kinesin captured by the virus transports the capsid to the nucleus, but the study found that the bidirectional transport and peripheral accumulation of pUL36 not only indicate that the PRV protein binds to dynein, it also recruits an "important partner"-kinesin
.
Related experiments have also directly confirmed the necessity of kinesin: when there is no kinesin during the production of virions and subsequent infections, although a large number of virus particles are produced, most of the virus particles will accumulate in the center and the capsid The transport from the centrosome to the nucleus is significantly impaired, so the ability of these virus particles to spread infection is weak
.
In summary, the cellular proteins that assist HSV infection have a clear division of labor
.
Dynein carries HSV-1 from the end of the axon to the center of the neuron, while kinesin carries the virus particles to the nucleus
.
The presence of kinesin-1 during virus assembly promotes the transport of the capsid to the nucleus during subsequent infections.
It is worth noting that kinesin originates from previously infected epithelial cells rather than neuronal endogenous cells, and is affected by the herpes virus pUL36 protein.
The assimilated kinesin promotes the infection of all cells by shuttling virus particles from the centrosome to the nucleus
.
In this way, the infection of HSV can be said to be even more powerful, and the seemingly low-key HSV is not low-key at all
.
Kinesins are captured by virus particles and transmitted to other cells.
"This is the first time that viruses have been found to use cellular proteins to complete rounds of infections.
They seem to be one of the most successful pathogens that have evolved so far," the lead researcher Caitlin Dr.
Prgg said, “After understanding how the HSV virus achieves this incredible operation through this research, we can now consider how to take away their ability to invade the nervous system
.
This is useful for studying other viral infections and developing related prevention.
Sex vaccines can provide new ideas and directions
.
"In order to facilitate you to continue to receive our articles, you are welcome to set us as a "star" so that you can see our news in the future
.
End reference materials: [1]https://doi.
org/10.
1038/s41586-021-04106-w[2]https://zhuanlan.
zhihu.
com/p/434679338
