Unlike a lytic virus, a lysogenic virus does not cause the host cell to lyse away. A lysogenic virus can remain inactive for a period of time. Viral DNA multiplies as the host cell multiplies. Each new daughter cell created is infected with the virus' DNA. It then removes itself from the host cell's DNA and enters the lytic cycle. Directions: Watch Virus Lysogenic Cycle to see the complete process of the lysogenic cycle.
Directions : Study the Lysogenic Cycle Diagram. It shows the steps of the lysogenic cycle, starting with bacteriophage attachment to a host cell. The steps shown in the diagram are also outlined in the Lysogenic Cyle Overview. Skip to main content. Introducing Viruses. Cite Source. Virus Lytic Cycle. Viruses are so small that a microscope is necessary to visualize them, and they have a very simple structure. When a virus particle is independent from its host, it consists of a viral genome, or genetic material, contained within a protein shell called a capsid.
In some viruses, the protein shell is enclosed in a membrane called an envelope. The viral replication process begins when a virus infects its host by attaching to the host cell and penetrating the cell wall or membrane. The virus's genome is uncoated from the protein and injected into the host cell. Then the viral genome hijacks the host cell's machinery, forcing it to replicate the viral genome and produce viral proteins to make new capsids.
Next, the viral particles are assembled into new viruses. Attachment to the receptor can fore the viral envelope protein to undergo either changes that result in the fusion of viral and cellular membranes, or changes of non-enveloped virus surface proteins that allow the virus to enter. Penetration follows attachment. Virions enter the host cell through receptor-mediated endocytosis or membrane fusion. This is often called viral entry. The infection of plant and fungal cells is different from that of animal cells.
Plants have a rigid cell wall made of cellulose, and fungi one of chitin, so most viruses can get inside these cells only after trauma to the cell wall. However, nearly all plant viruses such as tobacco mosaic virus can also move directly from cell to cell, in the form of single-stranded nucleoprotein complexes, through pores called plasmodesmata. Bacteria, like plants, have strong cell walls that a virus must breach to infect the cell. However, since bacterial cell walls are much less thick than plant cell walls due to their much smaller size, some viruses have evolved mechanisms that inject their genome into the bacterial cell across the cell wall, while the viral capsid remains outside.
Uncoating is a process in which the viral capsid is removed: This may be by degradation by viral or host enzymes or by simple dissociation. In either case the end-result is the release of the viral genomic nucleic acid. Replication of viruses depends on the multiplication of the genome. Hepatitis C virus : A simplified diagram of the Hepatitis C virus replication cycle. Following the structure-mediated self-assembly of the virus particles, some modification of the proteins often occurs.
In viruses such as HIV, this modification sometimes called maturation occurs after the virus has been released from the host cell. Viruses can be released from the host cell by lysis, a process that kills the cell by bursting its membrane and cell wall if present. This is a feature of many bacterial and some animal viruses. The viral genome is then known as a provirus or, in the case of bacteriophages a prophage. Whenever the host divides, the viral genome is also replicated.
The viral genome is mostly silent within the host; however, at some point the provirus or prophage may give rise to active virus, which may lyse the host cells. Enveloped viruses e. The genetic material within virus particles, and the method by which the material is replicated, varies considerably between different types of viruses.
Viral infection involves the incorporation of viral DNA into a host cell, replication of that material, and the release of the new viruses. A virus must use cell processes to replicate. The viral replication cycle can produce dramatic biochemical and structural changes in the host cell, which may cause cell damage.
These changes, called cytopathic causing cell damage effects, can change cell functions or even destroy the cell. The symptoms of viral diseases result from the immune response to the virus, which attempts to control and eliminate the virus from the body and from cell damage caused by the virus. Many animal viruses, such as HIV Human Immunodeficiency Virus , leave the infected cells of the immune system by a process known as budding, where virions leave the cell individually.
During the budding process, the cell does not undergo lysis and is not immediately killed. However, the damage to the cells that the virus infects may make it impossible for the cells to function normally, even though the cells remain alive for a period of time.
Most productive viral infections follow similar steps in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release. Pathway to viral infection : In influenza virus infection, glycoproteins attach to a host epithelial cell. As a result, the virus is engulfed. RNA and proteins are made and assembled into new virions. A virus attaches to a specific receptor site on the host cell membrane through attachment proteins in the capsid or via glycoproteins embedded in the viral envelope.
The specificity of this interaction determines the host and the cells within the host that can be infected by a particular virus. This can be illustrated by thinking of several keys and several locks where each key will fit only one specific lock.
The nucleic acid of bacteriophages enters the host cell naked, leaving the capsid outside the cell. Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus.
Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane. Once inside the cell, the viral capsid is degraded and the viral nucleic acid is released, which then becomes available for replication and transcription. The replication mechanism depends on the viral genome.
The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and to assemble new virions. Of course, there are exceptions to this pattern. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the information to direct synthesis of the missing proteins. Reverse transcription never occurs in uninfected host cells; the needed enzyme, reverse transcriptase, is only derived from the expression of viral genes within the infected host cells.
The fact that HIV produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. This approach has led to the development of a variety of drugs used to treat HIV and has been effective at reducing the number of infectious virions copies of viral RNA in the blood to non-detectable levels in many HIV-infected individuals.
The last stage of viral replication is the release of the new virions produced in the host organism. They are then able to infect adjacent cells and repeat the replication cycle. As you have learned, some viruses are released when the host cell dies, while other viruses can leave infected cells by budding through the membrane without directly killing the cell.
A tropism is a biological phenomenon, indicating growth or turning movement of a biological organism in response to an environmental stimulus. In tropisms, this response is dependent on the direction of the stimulus as opposed to nastic movements which are non-directional responses.
Host tropism is the name given to a process of tropism that determines which cells can become infected by a given pathogen.
Host tropism is determined by the biochemical receptor complexes on cell surfaces that are permissive or non-permissive to the docking or attachment of various viruses. Various factors determine the ability of a pathogen to infect a particular cell.
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