host cell

Cells invaded by virus

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The cells invaded by the virus are called host cells. The virus generally has no formed nucleus, and it is usually wrapped in protein genetic material After the virus obtains the host, it uses the host's protein and other substances to make its own body, and then injects genetic material into the cell to infect the cell, some will kill the cell, and some will make the cell variation , which is the so-called canceration 。

Chinese name: host cell
Alias: Receptor cell

Composition: Prokaryotic receptor cell
host cell: Escherichia coli

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Cell Introduction

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host cell

Receptor cell Also called host cell. Receptor cells have Prokaryotic receptor cell (mainly Escherichia coli) Eukaryotic receptor cell (Mainly Yeast )、 Animal cell and insect cell (In fact, they are also eukaryotic receptor cells). Among the prokaryotic receptor cells, the most commonly used host cells are Escherichia coli 。

Infection process

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Host cell assay

Viruses are usually composed of genetic material It infects cells by penetrating the cell membrane and releasing a large amount of viral genetic material to the cells. Use the specific virus on the host cell to transport proteins into Infected A host cell that releases a large amount of viral genetic material to the cell and infects the cell. Because cells are asexual, they rely on the "body" of the replicating protein or host cell to replicate their DNA material. So as to usurp the cell function for its service. The result may be cell death. Virus controls cells. Or produce variation , normal cellular protein synthesis , cell division is affected by Structural gene , controlled by gene regulation system. Because the structural gene that controls cell proliferation mutates, the regulatory system loses control of it, resulting in unlimited cell proliferation. If it is relevant Regulatory gene When mutation occurs, it can no longer produce effective repressors, and the transcription and translation of structural genes that control proliferation will continue, resulting in unlimited proliferation of cells, cell mutation, and thus cell canceration 。

National research

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American Studies

host cell

Researchers from the University of Pennsylvania School of Medicine said they found that Kaposi sarcoma relevant Herpes virus （ KSHV ）Can cheat infected cells to complete the virus genetic material Copy. This means of KSHV replication can prevent it from being Human immune system detect. In the past, people believed that KSHV needed viral proteins to start replication. New research results showed that the virus could independently obtain proteins from host cells to achieve self replication. A virus is usually composed of genetic material with a protein coat. It infects cells by penetrating the cell membrane and releasing a large amount of viral genetic material to the cells. Because cells are asexual, they rely on the "body" of the replicating protein or host cell to replicate their DNA material. Previously, the researchers conducted a series of tests on patients infected with KSHV Human cells Research has determined that the virus genetic material One that started copying gene It is the coding gene of the viral protein latency associated nuclear antigen (LANA), which is bound to the viral DNA. To understand whether the replication of KSHV is completely dependent on LANA, the researchers used host cells without LANA. The results showed that KSHV DNA could replicate automatically by applying cell replication mechanism. Er Le, the chief author of the research report and professor of microbiology? Dr. Robertson pointed out that viruses have once again broken people's understanding of cells, and demonstrated the deceptive ability of viruses to replicate using cellular mechanisms. He believes that by studying how viruses usurp cell functions to serve them, people can gain new knowledge about human cell replication mechanisms. Robertson and his colleagues said that in the future, they will study whether other viruses also have the ability to replicate without the help of viral proteins, and further understand the mechanism of cell induced virus replication. In addition, to prevent virus suppression immune system To develop into disease, researchers will also seek ways to block KSHV replication without blocking cell replication. host cell

host cell

Johns Hopkins scientists published《 Public Science Library Biology 》(PLoS Biology), a new research discovery pointed out that, HIV Not as the scientific community has previously Retrovirus It is believed that the specific virus on the membrane of the host cell is used to transport proteins into the infected host cell, but the transport system of the host cell itself is used. This discovery is likely to develop new strategies to combat viruses in the future. How biological molecules, drugs or viral molecules are transmitted between cells has always been the focus of scientists' attention, because once the transport mechanism of specific molecules is mastered, relevant physiological behaviors can be regulated. In the case of viruses, analyzing the way of virus entering and leaving the cell is equivalent to mastering the method of blocking virus transmission. In the past, for retroviruses such as HIV, scientists always believed that they would invade and release host cells through specific protein receptors. However, this time, the research team of Dr. Stephen Gould of Johns Hopkins used high magnification microscopic equipment to observe the process of HIV virus moving in and out of human T cells, and researchers used the role of specific drug molecules, Observe and lock on the membranous vesicles exosomes released by the cells, and it is found that HIV leaves the original host cells by using the original secretory system of the cells, and then infects the next target, and this process also uses HIV A Gap protein in the body. Scientists suspect that this is one of the reasons for the rapid expansion of HIV by using the existing secretion system of cells. Now it is possible to design drugs with blocking paths for related pathways, so the goal of successfully blocking HIV is not impossible to achieve. How viruses integrate their DNA into host cells has always been a biological mystery. Now, a new study shows that viruses emit into host cells by controlling DNA under high pressure. For viruses, life is easy because they only need to trick host cells to complete all the work of assembling new viruses. However, a difficult task must be completed by the virus itself, which is to integrate its DNA into the nucleus inside the host cell. The cytoplasm in the cell is very thick, which is a salt mixture of proteins and other molecules, so insert a DNA molecule It's like squeezing a crack in an already crowded subway car. host cell

To find out whether it is possible for cells to shoot DNA into the nucleus of the host by maintaining high pressure, University of California Alex Evilevitch, a molecular biologist at the University of Los Angeles, and his colleagues designed a set of stress tests. First, they will Lambda bacteriophage -- A parasitic Escherichia coli 20% DNA virus -- put it into the solution containing the membrane protein that E. coli induces λ phage to emit DNA. They also gradually increase the concentration of an inert organic polymer in the solution osmotic pressure Until the virus cannot completely release its genome. By quantifying the residual DNA in the virus at different concentrations, scientists can determine the difficulty of λ phage releasing DNA, and thus estimate its internal pressure. The results of the study were published this week in the United States《 Journal of the National Academy of Sciences 》On the online version of PNAS, it is revealed that λ bacteriophage is a DNA "cannon", its internal pressure is about 40 times of the atmospheric pressure, and about 10 times higher than the pressure in the champagne bottle. The huge pressure is caused by the strong DNA bending Internal molecular force. This research result is related to how much pressure Lamda virus needs to release internal DNA to host cells theoretical model Is consistent. This method can be used to measure the internal pressure of several other viruses, including RNA viruses. This method will also be helpful to researchers who want to redesign viruses for drug delivery. Northwestern University Jonathan Widom, a molecular biologist based in“ Ballistics ”Our experimental method is "awesome".

German Studies

Cindy Rechner et al of Max Planck Institute of Infectious Biology in Germany found that the host glycoprotein Gp96 and Scavenger receptor SREC in neisseria gonorrhoeae When invading Specificity It interacts with some proteins of Neisseria gonorrhoeae. Neisser's Gonococcal infection The host will express many proteins to regulate bacterial adhesion and invasion. Rechner's study of Neisseria gonorrhoeae outer membrane protein PorBIA was taken from patients with severe infectious diseases. Under the condition of low concentration phosphate similar to systemic blood infection, PorBIA can effectively start the adhesion and invasion of invasive bacteria. At the same time, Rechner and other researchers found that human heat shock glycoprotein Gp96 and scavenger receptor SREC are specific receptors for PorBIA. The serum type A protein PorBIA (not the serum type B protein PorB) expressed by Neisseria gonorrhoeae specifically binds to the host or the recombinant human heat shock glycoprotein Gp96. The depletion of host cell Gp96 will prevent adhesion, but will effectively trigger the invasion of Neisseria gonorrhoeae. This invasion will be inhibited by chemical Scavenger receptor Blocking, scavenger receptor SREC can specifically block the invasion of PorBIA. Therefore, Rechner et al. believe that the heat shock glycoprotein Gp96 in host cells can resist the invasion of Neisseria, while the scavenger receptor SREC can mediate the entry of host cells, thereby blocking bacterial adhesion and invasion.

Exclusion method

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The host can expel pathogens in many ways. Common in respiratory tract, digestive tract, skin and blood（ Bloodsucking insect Bite). The way of excretion depends on the invasion portal, the specific location of pathogens and possible transmission conditions

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