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The herpes virus can then exit this dormant stage and re-enter the lytic cycle, causing disease symptoms. Thus, while herpes viruses can enter both the lytic and lysogenic cycles, latency allows the virus to survive and evade detection by the immune system due to low viral gene expression. The model organism for studying lysogeny is the lambda ...
Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant within a cell, denoted as the lysogenic part of the viral life cycle. [1] A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which ...
Viruses may undergo two types of life cycles: the lytic cycle and the lysogenic cycle. In the lytic cycle, the virus introduces its genome into a host cell and initiates replication by hijacking the host's cellular machinery to make new copies of the virus. [12] In the lysogenic life cycle, the viral genome is incorporated into the host genome.
To enter the cells, proteins on the surface of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or its genetic contents are released into the host cell, where replication of the viral genome may commence.
To infect a host cell, the virus must first inject its own nucleic acid into the cell through the plasma membrane and (if present) the cell wall. The virus does so by either attaching to a receptor on the cell's surface or by simple mechanical force. The binding is due to electrostatic interactions and is influenced by pH and the presence of ions.
Another important area of interest is the control of prophage gene expression with many of the lysogenic conversion genes (gene conversion) being tightly regulated. [15] This process is capable of converting non-pathogenic bacteria into pathogenic bacteria that can now produce harmful toxins [15] such as in staph infections. Since the specific ...
Life-cycle of a typical virus (left to right); following infection of a cell by a single virus, hundreds of offspring are released. When a virus infects a cell, the virus forces it to make thousands more viruses. It does this by making the cell copy the virus's DNA or RNA, making viral proteins, which all assemble to form new virus particles. [37]
Virus tropism refers to the virus' preferential site of replication in discrete cell types within an organ. In most cases, tropism is determined by the ability of the viral surface proteins to fuse or bind to surface receptors of specific target cells to establish infection.