Viruses are known to only reproduce within the confines of a host cell. The parental virus (virion) produces a large number of offspring, which are usually genetically and structurally identical to the parent virus.
The actions of the virus are determined by both its destructive tendencies toward a specific host cell and environmental conditions. The multiplication of progeny viruses during the vegetative cycle of viral infection can be rapid.
This infection cycle frequently results in cell death and the release of numerous virus progeny. Certain viruses, particularly bacteriophages, are referred to as temperate (or latent) and this is because the infection does not result in cell death right away.
The viral genetic material either remains dormant or is integrated into the host cell's genome. Lysogenic cells are those infected with temperate viruses that break down when exposed to some chemical or physical factor, such as ultraviolet light. Furthermore, many animal and plant viruses, whose genetic information is not integrated into the host DNA, can remain dormant in tissues for long periods of time without causing significant, if any, tissue damage. Viral infection does not always result in cell death or it doesn’t result in tissue injury; in fact, most viruses lie dormant in tissue without ever causing pathological effects, or they do so only under certain conditions, which are frequently environmental.
Viral Replication Steps: How Do Virus Replicate?
Let’s know the 5 steps of virus replication or the infection cycle of viruses.
Steps of Virus Infections
To replicate, a virus must use cell processes. The viral replication cycle can cause significant biochemical and structural changes in the host cell, which can lead to cell damage. These alterations, known as cytopathic (cell-damaging) effects, have the potential to alter cell functions or even destroy the cell. Some infected cells, such as those cells which are infected with rhinovirus, die by lysis (bursting) or apoptosis (programmed cell death or "cell suicide"), releasing all progeny virions at once. The symptoms of viral diseases are caused by the immune response to the virus, which attempts to control and eliminate the virus from the body, as well as by virus-caused cell damage.
Many animal viruses, including HIV (Human Immunodeficiency Virus), leave infected immune system cells via a process known as budding, in which virions leave the cell individually. The cell does not undergo lysis and is not immediately killed during the budding process. However, the virus's damage to the cells it infects may make normal cell function impossible, even if the cells remain alive for a period of time. In the virus replication cycle, most productive viral infections follow the same steps: attachment, penetration, uncoating, replication, assembly, and release.
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Attachment proteins in the capsid or glycoproteins embedded in the viral envelope allow a virus to attach to a specific receptor site on the host cell membrane. The host (and the cells within the host) that can be infected by a specific virus is determined by the specificity of this interaction. Consider several keys and several locks, each of which will only fit one specific lock.
The nucleic acid of a bacteriophage enters the host cell naked, leaving the capsid outside. Plant and animal viruses can enter through endocytosis, a process in which the cell membrane completely surrounds and engulfs the virus. When the viral envelope fuses directly with the cell membrane, some enveloped viruses enter the cell. Once inside the cell, the viral capsid is degraded and the viral nucleic acid is released, allowing replication and transcription to occur.
Replication and Assembly
The viral genome determines the replication mechanism. DNA viruses typically use host cell proteins and enzymes to generate more DNA, which is then transcribed to messenger RNA (mRNA), which is then used to direct protein synthesis. The RNA core is typically used as a template for the synthesis of viral genomic RNA and mRNA by RNA viruses. The viral mRNA instructs the host cell to produce viral enzymes and capsid proteins, as well as to construct new virions.
There are, of course, exceptions to this rule. If a host cell lacks the enzymes required for viral replication, viral genes provide the information to direct the synthesis of the missing proteins. Retroviruses, like HIV, have an RNA genome that must be reverse-transcribed into DNA before being incorporated into the host cell genome.
Retroviruses must contain genes that encode the virus-specific enzyme reverse transcriptase, which transcribes an RNA template to DNA in order to convert RNA into DNA. Reverse transcription does not occur in uninfected host cells; the required enzyme, reverse transcriptase, is only derived from viral gene expression within infected host cells. Because HIV produces some of its own enzymes that are not found in the host, researchers have been able to develop drugs that inhibit these enzymes. These drugs, such as the reverse transcriptase inhibitor AZT, prevent HIV replication by reducing the activity of the enzyme without interfering with the host's metabolism.
This approach has resulted in the development of a number of HIV-treatment drugs that have been effective in reducing the number of infectious virions (copies of viral RNA) in the blood to undetectable levels in many HIV-infected people.
The release of new virions produced in the host organism is the final stage of viral replication. They can then infect neighbouring cells and continue the replication cycle. As you know, some viruses, are released when the host cell dies, whereas others can leave infected cells by budding through the membrane without directly killing the cell.