The key mechanism and structure of human herpes virus genome packaging are analyzed.

On May 30, the journal Nature published an online research paper by Dr. Liu Yuntao, Professor Bi Guoqiang and collaborators of the National Research Center for Microscale Matter Science in Hefei, China University of Science and Technology.
they used cryoscopic mirrors to analyze for the first time the key mechanisms of human herpes virus genome packaging and the DNA genome structure of the virus, helping to prevent and control a variety of diseases caused by the herpes virus, and modifying herpes viruses for targeted treatment.
herpes virus is a type of virus that is widely found in nature and can cause a variety of diseases after infection with the human body, including shingles, birth defects, multiple immune system diseases, and cancer.
herpes virus consists of cystic membranes, intermediate proteome, nucleosome sinshells and genomic four-layer structures, where the nucleosome is often considered a positive twenty-sided body with a unique DNA channel on which the viral genome is in and out.
lack of high-resolution structure sway from viral genomes and shell DNA channels, little is known about the genome packaging process of viral particles.
one of the most critical processes in the life cycle of herpes viruses is to "convene" DNA shearses into the unique DNA channels of the shell, identify, package and cut double-stranded DNA, and eventually produce viral particles containing the genome.
when the virus genome is filled in the virus's shell, it sends a signal that the redundant DNA will be removed for assembly.
researchers established a special algorithm, using cryoelectric mirrors to obtain the atomic resolution structure of DNA channels on the herpes virus shell, as well as the high-resolution 3D structure of most genomes, and found that the viral genome has a left-handed superhelix winding pattern and a disordered core, and revealed how the virus genome packaging signals are transmitted and how the genome passes through the DNA channel of the shell.
the study demonstrated the complete asymmetric structure of the herpes virus, obtaining an atomic model of the DNA channel of the first eyrevirus, and the first detection of the distorted state of DNA in the channel.
reviewer commented: "The author used the cutting-edge local classification method to perfectly analyze the structure of herpes virus, which is an ingenious work of 3D reconstruction of high-resolution cryoscopes."
" Bi Guoqiang said, by understanding the basic rules of herpes virus DNA transport and genomic packaging signal acquisition and transmission, on the one hand, targeted for the prevention and control of diseases caused by herpes virus, on the other hand, help to modify the herpes virus to become a more practical vector tool, and for tumor target ingress or brain neural loop tracing.
the research is another landmark achievement of the Integrated Imaging Center of the National Research Center of Hefei Microscale of the Chinese University of Science and Technology.
Integrated Imaging Center is an innovative research and public technology platform built by Hefei National Research Center for Microscale Material Science and The School of Life Sciences to promote the development of interdisciplinary disciplines.
study that reveals how the herpes virus accelerates the onset of Alzheimer's disease from researchers at Stockholm University and Karolinska School of Medicine, a new study describes the mechanism by which viral particles interact with proteins in biological fluids and become more infectious, while also accelerating the formation of plaques commonly associated with neurodegenerative diseases such as Alzheimer's disease.
In the 1980s, a series of studies found a strange link between herpes simplex virus and the onset of Alzheimer's disease.
suggested that the potential cause of this neurodegenerative disease may be the virus, but the amyloid hypothesis is more widely accepted.
after a series of failed clinical trials, some researchers are reconsidering these alternative viral hypothesis, which is designed to directly attack the accumulation of amyloid plaques.
one of the challenges in promoting the association of viruses with Alzheimer's disease is to understand possible mechanisms that can cause viruses such as herpes to accelerate neurodegenerative decline.
a new study of how viruses interact with proteins is the first to demonstrate how some viruses can accelerate the progression of Alzheimer's disease.
the study describes how viruses are covered in different protein layers based on the biological fluids they are living in.
the protein layer is called the protein crown, and the effect of a particular protein crown can vary depending on the given protein environment around the virus.
"Imagine tennis falling into a bowl of milk and cereal," says Kariem Ezzat, lead author of the new study.
" the ball is immediately covered with sticky particles in the mixture and remains on the ball when it is removed from the bowl.
the same thing happens when a virus comes into contact with blood or lung fluid sourcing thousands of proteins.
these proteins immediately adhere to the surface of the virus, forming a so-called protein crown. One of the viruses studied in
" study was the herpes simplex 1 virus (HSV-1).
Despite growing associated evidence linking HSV-1 to the accumulation of amyloid plaques and the onset of Alzheimer's disease, it is unclear how the virus induces this pathology.
new research shows that HSV-1 has the ability to catalyze amyloid proteins in its protein crown and induce the aggregation of these proteins.
basically, viral cells help accelerate the formation of larger plaque build-up of amyloid proteins.
to test the mechanisms in the organism, the researchers studied a mouse model that could develop rapidly amyloid in Alzheimer's disease.
the intracranial infection of HSV-1 in some animals, the results were very obvious.
infected animals develop significant pathological signs of Alzheimer's disease within 48 hours, while uninfected mice usually take months to reach the same degenerative point.
researchers caution that the study does not prove a causal link between the virus and Alzheimer's disease, but instead, it provides a compelling mechanism for many relevant studies to find these correlations.
because of the deep commonality of human HSV-1 infection, the virus may not be the only cause of Alzheimer's disease.
However, this may be an important factor that can accelerate the progression of the disease in individuals that have not been identified as a risk factor.
"... A physical mechanism that links the causes of viruses to amyloid proteins is described, increases interest in the study of the role of microorganisms in neurodegenerative diseases such as Alzheimer's disease, and opens up new avenues of treatment," Ezzat concluded.
Source: China Science Daily cnBeta.