How Does a Virus Infect a Cell? Stages & Dormant Phase Explained
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
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.
Entry
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.
Egress
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.
FAQs on Infection Cycle of Virus: Step-by-Step Guide for Students
1. What are the main stages of a viral infection cycle?
A typical viral infection cycle, for a lytic virus, involves six key stages. The primary goal of this process is for the virus to replicate itself using the host cell's machinery. The stages are:
- Attachment: The virus attaches to specific receptor sites on the surface of the host cell.
- Penetration: The virus or its genetic material enters the host cell. This can happen through endocytosis or by direct fusion of the viral envelope with the host cell membrane.
- Uncoating: The viral capsid is removed, releasing the viral nucleic acid (DNA or RNA) into the host cell's cytoplasm.
- Biosynthesis (Replication): The viral genome hijacks the host cell's machinery to replicate its own genetic material and produce viral proteins, such as capsid proteins.
- Assembly (Maturation): New viral particles are assembled from the newly synthesised genomes and proteins.
- Release: The newly formed viruses are released from the host cell, often causing the cell to burst (lysis), which kills the cell and allows the new viruses to infect neighbouring cells.
2. What is the difference between the lytic and lysogenic cycles of a virus?
The primary difference between the lytic and lysogenic cycles lies in the immediate outcome for the host cell. The lytic cycle is a rapid, active replication cycle that culminates in the destruction (lysis) of the host cell to release new virus particles. In contrast, the lysogenic cycle is a dormant phase where the viral DNA integrates into the host cell's chromosome, becoming a prophage. The virus does not immediately replicate or destroy the cell; instead, its genetic material is copied and passed on to daughter cells whenever the host cell divides. An external trigger, like UV radiation, can later induce the prophage to exit the host chromosome and enter the lytic cycle.
3. How does the infection cycle of a retrovirus like HIV differ from other viruses?
The infection cycle of a retrovirus, such as HIV, is unique because of a special enzyme it carries called reverse transcriptase. Unlike most viruses that use DNA to make RNA, retroviruses have an RNA genome. Upon entering a host cell, they use reverse transcriptase to create a DNA copy of their RNA. This viral DNA then integrates into the host cell's own DNA, where it can remain dormant for years before being activated to produce new viruses. This process of converting RNA back into DNA is a key feature that distinguishes retroviruses from most other viral types.
4. Why don't viruses have a cell wall like bacteria?
Viruses do not have a cell wall because they are not cells. They are simple, acellular infectious agents that lack the complex internal machinery (organelles) found in cellular organisms like bacteria. A bacterium is a complete, single-celled organism with cytoplasm, ribosomes, and a cell membrane, all protected by a rigid cell wall. A virus, on the other hand, consists only of genetic material (DNA or RNA) enclosed in a protein coat called a capsid. Some viruses also have an outer lipid layer called an envelope, but this is derived from the host cell membrane and is not a self-synthesised cell wall.
5. What determines which specific cells a virus can infect?
A virus's ability to infect specific cells is determined by a concept called host specificity. This specificity is based on a lock-and-key type of interaction between molecules on the virus's surface and receptors on the host cell's surface. The proteins or glycoproteins on the viral capsid or envelope must bind to specific receptor proteins on the host cell membrane. If a cell does not have the correct receptor for a particular virus, that virus cannot attach to and infect it. This is why, for example, the influenza virus primarily infects respiratory cells and the rabies virus targets nerve cells.
6. What is the importance of the capsid and viral envelope in the infection process?
Both the capsid and the viral envelope are crucial for a successful infection, but they serve distinct functions. The capsid is the protein shell that encloses the viral genetic material. Its primary importance is to protect the fragile DNA or RNA from environmental damage, such as enzymes or pH changes, when the virus is outside a host cell. The viral envelope, present in enveloped viruses like influenza and HIV, is an outer lipid membrane that contains viral proteins. Its main role is to facilitate entry into the host cell by fusing with the cell's membrane and helping the virus evade the host's immune system.
7. What happens during the 'dormant' or lysogenic phase of a viral infection?
During the dormant or lysogenic phase, the virus does not actively replicate or harm the host cell. Instead, its genetic material integrates directly into the host cell's chromosome. This integrated viral DNA is called a prophage. The host cell remains healthy and continues its normal functions, including cell division. Every time the host cell replicates its own DNA and divides, it also replicates the prophage's DNA, passing the viral genetic code to all its descendants. This allows the virus to spread silently without producing new virions until it is triggered to enter the active lytic cycle.
