The new study shows that the virus that infects the bacteria - called the bacterium - can decide whether to kill the host cell immediately after entering or entering a 'hidden' state , existing inside the cell. host
The study, published in the September 15 Biophysical magazine, shows that many viruses invade a cell increase the number of viral genes and thus increase viral gene expression. The change in viral gene expression can have a major effect on the network of genes that control whether the virus will disrupt the host cell or enter the 'hidden' phase .
Joshua Weitz, a professor at the Georgia Institute of Biotechnology, said: 'What upsets the community for studying the virus for quite a long time is the fate of a bacterium infected with a virus that is far away. when infected with two viruses. Our research suggests that the virus can decide, collectively, whether to kill the host, and that individual viruses 'exchange' with each other as a result of the gene-protein interaction that the virus forces. objects must create '.
To study viral infections, Weitz collaborated with colleagues Yurily Mileyko, graduate student Richard Joh and Eberhard Voit, Professor of Biomedical Engineering Wallace H, Coulter, who was also the director of the Biology Academy. Combined at Georgia Institute of Technology.
Most previous theoretical studies claim that the change between 'destroy' and 'temporarily hide' depends on changes in environmental conditions or random opportunities. However, new research suggests that the response to coinfection may be the evolutionary characteristic of the virus.
For this study, cycle analysis researchers decide whether the virus chooses to kill host cells - called lytic pathway - or choose how to live within a host cell - called a lysogenic pathway.
When the lytic patway is selected, the virus will copy itself and destroy the host cell, the newly released viruses continue to infect other cells. In contrast, for lysogenic pathways, the viral genome merges itself into the bacterial genome and replicates with the bacteria while restraining the gene that creates the ability to destroy the cell. The virus will not work until the condition inside the host body changes the line to lytic patway.
The decision of the genetic cycle to control a virus choosing to destroy or coexist is not accidental . Instead, the fate of the cells is decided by a group of viruses, according to new research, funded by the Defense Research Agency, the National Science Foundation and the Wellcome Buroughs Foundation.
Weitz, a member of the Integrated Biology Institute at the Georgia Institute of Technology, explains: 'In the case of the most widely studied bacteriophage, it is possible to colonize lambda, experimental evidence indicates that one can Single phage often leads to a decision to destroy the cell and release the virus, while if the number of phages is 2 or more, the result is usually temporary. We want to know why the two viruses are different from a single virus even though they have the same decision cycle. '
To understand this, scientists model complex gene systems that control the transition between the kill and temporary decisions in phage lambda. They studied three important genes - cro, cl and cll - as well as the proteins that were produced. The decision cycle consists of negative or positive feedback rings, different responses to the change in the number of viral genomes in a cell. Positive feedback is associated with lysogenic pathway and negative feedback associated with lytic patway.
With a single virus, the cro gen dominant and the lytic pathway prevailed. If the amount of co-infection virus exceeds a certain threshold, positive feedback is associated with cl overwhelming, light-passing lysogenic pathway. The difference of cell fate is entirely based on whether one or two viruses are within the cell.
Weitz explains: 'The decision cycle is the race between two pathways and in the case of a single virus, the outcome is directed towards the decision to destroy. In our model, when many viruses infect the same cell, the control protein formation increases. This short-lived process is temporarily shelved by the positive pathway of the pathway, allowing more lysogenic proteins to be produced, and thus a result of a temporary decision. "
The main idea of the model proposed by Weitz and colleagues is that an increase in the total amount of protein produced from multiple viral genomes may have a major effect on the network of offline genes that determine cell fate.
Weitz added: 'There are still many questions that need answers, for example, to what extent can the following virus change the results that have been decided, but have not yet been implemented, of the viruses that came first or at the level Any degree of microenvironment inside the host affects cell fate. However, this study proposes an explanation for the long-standing logic that when many viruses infect a cell, those viruses can make the same decision unlike their expression when operating separately. odd '