# Life Cycle of a Virus – Stages, Lytic and Lysogenic Cycles > Explore the life cycle of a virus, stages of viral replication, lytic and lysogenic cycles, and how viruses multiply in bacterial, animal and plant cells. Canonical URL: https://biologynotesonline.com/life-cycle-of-a-virus/ Author: Sourav Pan Last updated: November 15, 2026 ![Life Cycle of a Virus – Stages, Lytic and Lysogenic Cycles](https://biologynotesonline.com/wp-content/uploads/2024/04/seven-stages-of-viral-life-cycle.webp) The life cycle of a virus involves several stages such as attachment, penetration, uncoating, biosynthesis, assembly and maturation, and release. The virus first attaches to the host cell followed by the entry of the virus particle or its genetic material into the cell. The viral genome is replicated and new viral proteins are synthesised within the host cell. The newly synthesised viral components are assembled to form new virus particles which are released from the cell. Viral replication is often described in five, six or seven stages. In some cases, uncoating is not described as a separate stage, while assembly and maturation may be considered as a single stage. The mechanism of viral multiplication also differs in viruses infecting bacterial, animal and plant cells. ## What is the Life Cycle of a Virus? The life cycle of a virus refers to the sequence of biological events involved in the infection and multiplication of a virus within a susceptible host cell. Viruses are obligate intracellular parasites and cannot multiply outside living host cells. They lack their own [ribosomes](https://biologynotesonline.com/ribosomes-structure-and-functions/) and depend upon the cellular machinery of the host for the synthesis of viral proteins. Both host cell proteins and virus-encoded proteins, including enzymes, may be involved in the replication of the virus. The viral life cycle is also referred to as the viral infection cycle or viral replication cycle. In a productive infection, multiple copies of the virus are produced within the host cell. These newly formed infectious virus particles are called progeny virions. However, infection of a susceptible host cell does not always result in viral multiplication. In an abortive infection, the virus enters the host cell but fails to produce infectious progeny virions. ## Stages of the Viral Life Cycle The stages of virus infection can be divided into seven stages- attachment, penetration, uncoating, biosynthesis, assembly, maturation and release. The number of stages may vary depending upon the grouping of different events involved in viral multiplication. - Five stages of viral replication- Attachment, penetration, biosynthesis, assembly and release. Uncoating is included under penetration where applicable and maturation is included under assembly. - Six stages of viral replication- Attachment, penetration, uncoating, biosynthesis, assembly and release. Assembly and maturation are described together. - Seven stages of viral replication- Attachment, penetration, uncoating, biosynthesis, assembly, maturation and release. Assembly and maturation are described as separate stages. Some of these phases of viral infection may take place simultaneously. The following are the different viral replication steps: ![Seven stages of viral replication in an animal cell showing attachment, penetration, uncoating, biosynthesis, assembly, maturation and release.](https://biologynotesonline.com/wp-content/uploads/2024/04/seven-stages-of-viral-life-cycle-1024x576.webp)Seven stages of viral replication in an animal cell showing attachment, penetration, uncoating, biosynthesis, assembly, maturation and release. ### 1. Attachment (Adsorption) Attachment is the first stage of viral infection in which the virus binds to specific receptors present on the surface of the host cell. The proteins of the virus involved in this process are known as viral attachment proteins (VAPs). In non-enveloped viruses, attachment takes place with the help of proteins present on the surface of the capsid, whereas in enveloped viruses, envelope glycoproteins are involved in attachment. The receptors on the host cell surface may be proteins, glycoproteins, lipids or carbohydrates. Some viruses require more than one receptor for entry into the host cell. For example, HIV binds to the CD4 receptor and requires a co-receptor (CCR5 or CXCR4) for entry. The specificity of binding between viral attachment proteins and cellular receptors is one of the factors responsible for the host range and tissue tropism of a virus. Host range refers to the types of hosts that can be infected by a virus, whereas tissue tropism refers to its ability to infect particular cells or tissues within a host. ### 2. Penetration (Entry) After attachment, the virus particle or its genetic material enters the host cell. Penetration of viruses takes place by different mechanisms. - Receptor-mediated endocytosis- The virus attached to the cellular receptor is taken up by the host cell in a membrane-bound vesicle called an endosome. - Membrane fusion- In enveloped viruses, the viral envelope may fuse with the plasma membrane or endosomal membrane of the host cell, releasing the viral nucleocapsid or core into the cytoplasm. - Direct penetration- Some non-enveloped viruses form pores or disrupt the cellular or endosomal membrane through which the viral genome or particle enters the cytoplasm. - Genome injection- In many bacteriophages, the viral nucleic acid is injected into the bacterial cell while the capsid remains outside the cell. ![Comparison of viral entry by receptor-mediated endocytosis, membrane fusion, direct penetration and bacteriophage genome injection.](https://biologynotesonline.com/wp-content/uploads/2024/04/mechanisms-of-viral-penetration-1024x524.webp)Comparison of viral entry by receptor-mediated endocytosis, membrane fusion, direct penetration and bacteriophage genome injection. ### 3. Uncoating During uncoating, the proteins of the viral capsid are removed or undergo structural changes to make the viral genome available for transcription, translation or replication. The process of uncoating may involve viral proteins, cellular enzymes and changes in the pH of endosomes. In some viruses, penetration and uncoating take place simultaneously. Complete removal of the capsid is not required in all viruses. For example, in rotavirus, the outer capsid layer is removed during entry into the host cell. The viral RNA-dependent RNA polymerase synthesises mRNA within the remaining double-layered particle, and the mRNA is released into the cytoplasm. ### 4. Biosynthesis (Genome Replication and Gene Expression) During this stage, new copies of the viral genome are produced along with the synthesis of viral proteins. The process involves transcription, translation and replication of viral nucleic acid. Viral mRNA is translated by the ribosomes of the host cell for the synthesis of structural and non-structural proteins. The structural proteins form different parts of the virus particle, whereas many of the non-structural proteins are involved in viral genome replication and regulation of viral gene expression. The nucleotides, amino acids and energy required for these processes are obtained from the host cell. The mechanism of genome replication and mRNA synthesis differs depending upon the type of nucleic acid present in the virus. ![Molecular pathways of genome replication and mRNA synthesis in DNA, positive-sense RNA, negative-sense RNA, double-stranded RNA and reverse-transcribing viruses.](https://biologynotesonline.com/wp-content/uploads/2024/04/viral-genome-replication-strategies-1024x341.webp)Molecular pathways of genome replication and mRNA synthesis in DNA, positive-sense RNA, negative-sense RNA, double-stranded RNA and reverse-transcribing viruses. DNA viruses - In conventional DNA viruses, the viral DNA is replicated with the help of host cell or virus-encoded DNA-dependent DNA polymerases. - Viral mRNA is synthesised from the DNA template by host or viral RNA polymerases. - In single-stranded DNA viruses, a complementary DNA strand is synthesised to form a double-stranded DNA intermediate. - Most animal DNA viruses replicate their DNA within the nucleus of the host cell. An exception is the poxvirus, in which DNA replication takes place in the cytoplasm. Positive-sense single-stranded RNA viruses - The positive-sense RNA genome functions as mRNA and is directly translated by the ribosomes of the host cell. - One of the proteins produced during viral gene expression is the RNA-dependent RNA polymerase (RdRp). - The enzyme synthesises a complementary negative-sense RNA strand using the viral RNA as a template. - The negative-sense RNA serves as a template for the synthesis of new positive-sense RNA genomes. Negative-sense single-stranded RNA viruses - The negative-sense RNA of these viruses cannot be directly translated by the ribosomes of the host cell. - These viruses contain RNA-dependent RNA polymerase within the virion, which synthesises positive-sense mRNA from the negative-sense RNA genome. - A full-length complementary positive-sense RNA (antigenome) is also synthesised. It acts as a template for the production of new negative-sense RNA genomes. Double-stranded RNA viruses - Double-stranded RNA viruses contain RNA-dependent RNA polymerase within the virus particle. - The enzyme uses the negative-sense strands of dsRNA as templates for the synthesis of positive-sense mRNA. - In viruses such as rotavirus, positive-sense RNA molecules are packaged into newly forming viral cores, within which complementary negative-sense RNA strands are synthesised to form dsRNA genomes. Reverse-transcribing viruses - In retroviruses such as HIV, the viral RNA is converted into double-stranded DNA with the help of the enzyme reverse transcriptase. - The viral DNA is integrated into the chromosomal DNA of the host cell by the enzyme integrase and is known as a provirus. - The host RNA polymerase II synthesises viral RNA from the proviral DNA. These RNA molecules are used for protein synthesis or packaged as viral genomes. - In hepatitis B virus, pregenomic RNA (pgRNA) is synthesised from viral DNA. The pgRNA is reverse transcribed into DNA within the newly formed nucleocapsid by the viral polymerase. ### 5. Assembly The newly synthesised viral structural proteins and copies of the viral genome associate with each other to form new virus particles. This stage is known as assembly. The capsid proteins associate with each other to form the viral capsid. In many viruses, specific nucleotide sequences or structures called packaging signals are involved in the selective incorporation of viral genomes into the developing virus particles. The complex formed by the viral nucleic acid and its associated capsid proteins is called a nucleocapsid. Certain viral enzymes required for the next cycle of infection are also incorporated into the virus particle during assembly. Assembly of viruses may take place in the nucleus, cytoplasm or at the cellular membranes depending upon the type of virus. ### 6. Maturation Maturation is the process in which an immature virus particle undergoes structural and biochemical changes necessary for infectivity. In some viruses, precursor proteins are cleaved into smaller functional proteins by viral or cellular proteases. Rearrangement of capsid proteins may also take place during maturation. An assembled virus particle is not necessarily a mature infectious virus particle. In HIV, the viral protease cleaves the Gag and Gag-Pol polyproteins during or shortly after budding. The capsid proteins (CA) rearrange to form the characteristic cone-shaped capsid of mature HIV. Maturation may occur within the host cell, during the release of the virus particle or after its release from the host cell. ### 7. Release Release is generally considered the final stage of the viral life cycle, although in some viruses maturation continues after release. The progeny viruses are released from the host cell by the following mechanisms: - Cell lysis- The plasma membrane or cell envelope of the host cell is disrupted, resulting in the release of virus particles and death of the host cell. It is commonly found in lytic bacteriophages and many non-enveloped animal viruses. - Budding- The viral nucleocapsid or assembling viral components become surrounded by a portion of the host cell membrane containing viral envelope proteins. The developing virus particle separates from the membrane and acquires its lipid envelope. Budding may take place at the plasma membrane or intracellular membranes. - Exocytosis- Virus particles present within intracellular vesicles are released when the vesicular membrane fuses with the plasma membrane of the host cell. This mechanism is also found in some non-enveloped viruses. Unlike cell lysis, budding and exocytosis do not necessarily result in the immediate death of the host cell. An infected cell may continue to produce and release viruses for a certain period of time. The infectious progeny virions released from the cell can infect other susceptible host cells and initiate another cycle of viral replication. ![Three mechanisms of viral release showing membrane rupture, acquisition of a viral envelope through budding and release from intracellular vesicles.](https://biologynotesonline.com/wp-content/uploads/2024/04/viral-release-lysis-budding-exocytosis-1024x524.webp)Three mechanisms of viral release showing membrane rupture, acquisition of a viral envelope through budding and release from intracellular vesicles. ## Lytic Cycle In the lytic cycle, the bacteriophage multiplies within the bacterial cell and causes lysis of the cell for the release of newly formed phages. Bacteriophage T4 is a virulent phage which undergoes the lytic cycle in susceptible strains of Escherichia coli. ### Stages of the Lytic Cycle The lytic cycle of bacteriophage T4 involves five major stages: - Attachment (Adsorption)- The bacteriophage attaches to specific receptors (lipopolysaccharides or OmpC proteins) present on the outer membrane of the bacterial cell with the help of its long tail fibres. The short tail fibres bind irreversibly to the bacterial cell surface. - Penetration- The tail sheath contracts and the tail tube penetrates the bacterial cell envelope. The tail-associated protein (gp5) contains a lysozyme domain which helps in the breakdown of peptidoglycan. The double-stranded DNA (dsDNA) is injected into the bacterial cytoplasm. The head and tail of the phage remain outside the bacterial cell. - Biosynthesis- The bacterial DNA is degraded by the nucleases encoded by the phage. The phage makes use of bacterial RNA polymerase and ribosomes for the synthesis of phage RNA and proteins. Phage DNA polymerase along with other replication proteins synthesises new copies of phage DNA. Proteins of the head, tail, baseplate and tail fibres are also synthesised at this stage. - Assembly and maturation- The newly synthesised DNA is packed into the phage heads by an enzyme complex called terminase, and the heads, tails and tail fibres are joined together to form mature bacteriophages. - Lysis and release- The two phage-encoded proteins involved in cell lysis are holin and endolysin. Holin forms pores in the cytoplasmic membrane through which the endolysin reaches the peptidoglycan layer and breaks it down. The bacterial cell ruptures and releases the newly formed bacteriophages into the surrounding medium. ![Bacteriophage T4 infecting Escherichia coli through attachment, DNA injection, biosynthesis, assembly and bacterial cell lysis.](https://biologynotesonline.com/wp-content/uploads/2024/04/lytic-cycle-bacteriophage-t4-1024x437.webp)Bacteriophage T4 infecting Escherichia coli through attachment, DNA injection, biosynthesis, assembly and bacterial cell lysis. ## Lysogenic Cycle The lysogenic cycle is a type of viral life cycle in which the genetic material of the virus remains within the host cell and is replicated during the reproduction of the host cell without causing cell lysis. Bacteriophages capable of establishing lysogeny are known as temperate bacteriophages. Bacteriophage lambda (λ), which infects Escherichia coli, is an example of a temperate bacteriophage. The different events of the lysogenic cycle can be described under establishment of lysogeny, maintenance of the prophage and prophage induction. ### Establishment of Lysogeny - The bacteriophage lambda attaches to the LamB receptor present on the outer membrane of the bacterial cell. - The double-stranded DNA of the bacteriophage is injected into the bacterial cell. - The two complementary cohesive ends (cos sites) of the phage DNA join together to form a circular DNA molecule. - The circular phage DNA is integrated into the bacterial chromosome by site-specific recombination with the help of the phage-encoded enzyme integrase. - The phage DNA present in the bacterial chromosome is known as a prophage. The bacterial cell containing the prophage is called a lysogen. - The CI repressor protein binds to specific operator regions of the phage DNA and inhibits the transcription of genes required for the lytic cycle. - In some bacteriophages (e.g. bacteriophage P1), the phage DNA is not integrated into the bacterial chromosome but remains within the cell as an extrachromosomal plasmid. ### Maintenance of the Prophage - The prophage DNA of bacteriophage lambda is replicated along with the chromosomal DNA of the bacterial cell. - When the bacterial cell divides by binary fission, the prophage is passed on to the daughter cells. - The expression of lytic genes remains inhibited by the CI repressor protein. - No new bacteriophage particles are produced during the maintenance of lysogeny. - Some prophages contain genes which on expression bring about changes in the characteristics of the bacterial cell. This is known as lysogenic conversion. - For example, the gene (tox) responsible for the production of diphtheria toxin in Corynebacterium diphtheriae is carried by the temperate bacteriophage β. ### Prophage Induction - Under certain environmental stress conditions, the prophage may enter the lytic cycle. This process is known as prophage induction. - DNA damage caused by ultraviolet radiation or certain chemicals (e.g. mitomycin C) activates the SOS response in the bacterial cell. - The activated RecA protein stimulates the self-cleavage of the CI repressor protein. - The inhibition of lytic gene expression is removed due to the inactivation of the CI repressor. - The prophage DNA of bacteriophage lambda is excised from the bacterial chromosome with the help of integrase and excisionase enzymes and forms a circular DNA molecule. - The phage DNA is replicated and the proteins required for the formation of new bacteriophages are synthesised. - The newly formed bacteriophages are released by lysis of the bacterial cell. ![Lysogenic cycle of lambda phage showing DNA integration, prophage inheritance during bacterial division, RecA-mediated induction and transition to the lytic cycle.](https://biologynotesonline.com/wp-content/uploads/2024/04/lysogenic-cycle-bacteriophage-lambda-1024x437.webp)Lysogenic cycle of lambda phage showing DNA integration, prophage inheritance during bacterial division, RecA-mediated induction and transition to the lytic cycle. ## Differences Between the Lytic and Lysogenic Cycles The lytic and lysogenic cycles are the two classical pathways of viral replication found in bacteriophages. Virulent bacteriophages undergo the lytic cycle, whereas temperate bacteriophages can undergo either the lytic or lysogenic cycle. These two cycles are not applicable to the life cycles of all viruses. The differences between the lytic and lysogenic cycles are given below: ParameterLytic CycleLysogenic CycleType of bacteriophageIt occurs in both virulent and temperate bacteriophages.It occurs in temperate bacteriophages.Viral genomeMultiple copies of the phage genome are synthesised for the production of new bacteriophages.The phage genome remains within the bacterial cell as a prophage.IntegrationIntegration of phage DNA into the bacterial chromosome is not required.The phage DNA may be integrated into the bacterial chromosome or maintained as an extrachromosomal element.Prophage formationA stable prophage is not formed during the lytic cycle.The phage genome is maintained in the form of a prophage.Viral gene expressionThe phage genes required for genome replication, formation of phage particles and cell lysis are expressed.The expression of genes required for the lytic cycle is inhibited. Some prophage genes are expressed during lysogeny.Progeny productionNew bacteriophages are produced and released from the bacterial cell.No new bacteriophage particles are produced as long as lysogeny is maintained.Host cell fateThe bacterial cell is destroyed by lysis.The bacterial cell remains alive and can undergo cell division.Genome inheritanceThe phage genome is not maintained and passed on to the daughter cells as a prophage.The prophage is replicated and passed on to the daughter cells during bacterial reproduction.Lysogenic conversionLysogenic conversion does not take place during the lytic cycle.Expression of certain prophage genes may result in changes in the characteristics of the bacterial cell.InductionProphage induction is not required for the initiation of the lytic cycle following direct infection.The prophage may enter the lytic cycle due to environmental stress or spontaneous induction.ExamplesBacteriophage T4.Bacteriophage lambda (λ) and P1. ## Life Cycle of Animal Viruses - Animal viruses attach to specific receptors present on the surface of susceptible animal cells, including human cells. In some viruses, co-receptors are also required for entry into the host cell. - The virus enters the host cell by receptor-mediated endocytosis, membrane fusion or other mechanisms depending upon the type of virus. - In enveloped viruses, fusion may take place between the viral envelope and the plasma membrane or the endosomal membrane of the host cell. - The viral genome becomes available for replication and gene expression after partial or complete uncoating of the virus particle. - Replication of the viral genome takes place in the nucleus or cytoplasm of the host cell. Some viruses form specialised compartments within the host cell known as viral replication factories. - The newly synthesised viral genomes and structural proteins are assembled in the nucleus, cytoplasm or at the cellular membranes to form new virus particles. - The progeny virions are released from animal cells by cell lysis, budding or exocytosis. During budding, the virus acquires its envelope from the cellular membrane. ### Replication of DNA Viruses - In most animal DNA viruses, replication of viral DNA takes place within the nucleus of the host cell. - The viral DNA is transported into the nucleus after entry and uncoating of the virus. - The DNA-dependent RNA polymerase of the host cell transcribes the viral DNA into mRNA, which is transported into the cytoplasm for protein synthesis. - The proteins synthesised during the early stages of infection are mainly involved in viral DNA replication and regulation of gene expression. - Replication of viral DNA may take place with the help of host or virus-encoded DNA polymerases. Papillomaviruses make use of the DNA polymerase of the host cell, whereas herpesviruses encode their own DNA polymerase. - Most of the structural proteins of viruses such as adenoviruses and herpesviruses are synthesised during the late stages of infection. - In adenoviruses, the capsid proteins are transported into the nucleus where assembly of the virus particles takes place. - An exception is the poxvirus (e.g. vaccinia virus), in which transcription and DNA replication take place in the cytoplasm of the host cell. These viruses carry their own DNA-dependent RNA polymerase and encode enzymes required for DNA replication. ### Replication of RNA Viruses - In most animal RNA viruses, replication of viral RNA takes place in the cytoplasm. - The enzyme RNA-dependent RNA polymerase (RdRp) is responsible for the synthesis of RNA from an RNA template. - In positive-sense RNA viruses (e.g. poliovirus), the viral RNA acts as mRNA and is directly translated by the ribosomes of the host cell. - The RNA-dependent RNA polymerase synthesises a complementary negative-sense RNA strand, which acts as a template for the synthesis of new positive-sense RNA genomes. - Negative-sense RNA viruses (e.g. rabies virus) contain RNA-dependent RNA polymerase within the virion for the synthesis of viral mRNA. A full-length complementary RNA strand (antigenome) is required for the synthesis of new negative-sense RNA genomes. - In double-stranded RNA viruses such as rotavirus, viral mRNA is synthesised with the help of RNA-dependent RNA polymerase present within the partially uncoated virus particle. - In some RNA viruses, the membranes of cellular organelles such as the endoplasmic reticulum are modified to form sites for viral RNA replication. - Unlike most RNA viruses, transcription and replication of influenza virus RNA take place within the nucleus of the host cell. The viral mRNA is transported into the cytoplasm for translation. - The newly formed influenza virus particles are assembled at the plasma membrane and released by budding. ### Replication of Retroviruses The replication of [retroviruses](https://biologynotesonline.com/retrovirus-definition-types-structure-replication/) can be explained with the help of the human immunodeficiency virus (HIV). - The envelope glycoprotein (gp120) of HIV binds to the CD4 receptor and a co-receptor (CCR5 or CXCR4) present on the host cell. - The viral envelope fuses with the plasma membrane of the host cell with the help of gp41 and the viral core is released into the cytoplasm. - The viral RNA is converted into double-stranded DNA (dsDNA) by the enzyme reverse transcriptase. - With the help of the enzyme integrase, the viral DNA is integrated into the chromosomal DNA of the host cell. This integrated viral DNA is known as a provirus. - The RNA polymerase II of the host cell transcribes the proviral DNA to produce viral RNA. - Viral proteins are synthesised by the ribosomes of the host cell. The full-length viral RNA also acts as the genetic material of the newly formed virus particles. - The viral envelope glycoproteins are transported to the plasma membrane of the host cell. - The viral RNA and proteins such as Gag and Gag-Pol assemble at the plasma membrane. - The newly formed immature virus particles are released from the host cell by budding. - During and after budding, the viral protease cleaves the Gag and Gag-Pol polyproteins into smaller functional proteins. Rearrangement of the capsid proteins takes place and mature infectious HIV particles are formed. ![HIV replication in a CD4-positive T cell showing receptor binding, fusion, reverse transcription, nuclear import, integration, protein synthesis, budding and maturation.](https://biologynotesonline.com/wp-content/uploads/2024/04/hiv-life-cycle-replication-maturation-1024x524.webp)HIV replication in a CD4-positive T cell showing receptor binding, fusion, reverse transcription, nuclear import, integration, protein synthesis, budding and maturation. ### Outcomes of Animal Virus Infection The different outcomes of viral infection in animal cells are given below: - Productive infection- The viral genome is replicated and infectious progeny virions are produced within the host cell. - Cytolytic infection- In this type of infection, viral multiplication results in the death of the host cell. It is commonly found in poliovirus infection. - Noncytolytic infection- The newly formed virus particles are released without causing immediate death of the infected cell. - Latent infection- The viral genome remains within the host cell with restricted expression of viral genes. No infectious virus particles are produced during latency. For example, herpes simplex virus (HSV) remains in a latent state within sensory neurons and may be reactivated under certain conditions. - Chronic productive infection- Infectious virus particles are produced continuously or intermittently over a prolonged period. It is found in chronic hepatitis B and hepatitis C virus infections. - Abortive infection- The virus enters the host cell but fails to complete its replication cycle due to the absence of certain cellular factors, cellular antiviral responses or defects in the viral genome. No infectious progeny virions are produced. In animal viruses, the genome of a latent virus may remain as an extrachromosomal DNA molecule (episome), as found in herpes simplex virus, or may be integrated into the host cell chromosome, as found in HIV. The term lysogeny is used for the maintenance of a prophage within a bacterial cell and is not used to describe viral latency in animal cells. ## Life Cycle of Plant Viruses Plant viruses cannot normally enter the host cell through an intact cell wall. They enter the plant cells through wounds or are introduced into the cells by vectors. [Tobacco mosaic virus (TMV)](https://biologynotesonline.com/tobacco-mosaic-virus-tmv-structure-life-cycle-infection-treatment/) is a positive-sense single-stranded RNA virus which is commonly used to study the replication and movement of viruses within plants. ### Entry and Multiplication in Plant Cells - Plant viruses enter through small wounds produced on the plant surface due to mechanical injury or during the feeding of vectors. Insects, nematodes and certain soil-borne organisms act as vectors of plant viruses. - Tobacco mosaic virus (TMV) enters the plant cells mainly through mechanical wounds. - After entering the cell, the coat proteins of TMV are gradually removed from the viral RNA. The separation of coat proteins from the RNA is associated with the translation of viral RNA. - The positive-sense RNA of TMV acts as mRNA and is translated by the ribosomes of the host cell to produce two replication proteins (126 kDa and 183 kDa). - Replication of TMV RNA takes place in the cytoplasm in association with cellular membranes, particularly the endoplasmic reticulum. - The viral RNA-dependent RNA polymerase synthesises a complementary negative-sense RNA strand using the viral genomic RNA as a template. - The negative-sense RNA acts as a template for the synthesis of new genomic RNA and subgenomic RNAs. - The movement protein (30 kDa) and coat protein (17.5 kDa) of TMV are synthesised by the translation of subgenomic RNAs. - The newly synthesised coat proteins associate with the genomic RNA to form rod-shaped virus particles. ### Cell-to-Cell Movement - The movement of plant viruses from one cell to another takes place through the [plasmodesmata](https://biologynotesonline.com/plasmodesmata/). These are small channels present in the cell walls which connect the cytoplasm of adjacent plant cells. - Normally, the size of the plasmodesmata restricts the movement of large molecules and virus particles between adjacent cells. - Plant viruses encode one or more proteins known as movement proteins (MPs), which are involved in the movement of viral genetic material between plant cells. - The movement protein of TMV binds to viral RNA and increases the size exclusion limit of plasmodesmata. - TMV RNA moves into adjacent cells in association with viral and cellular proteins. The formation of complete virus particles is not required for the cell-to-cell movement of TMV. - In some plant viruses, complete virus particles are transported through modified plasmodesmata. - The viruses do not normally require budding or lysis of the host cell for their movement from one plant cell to another. ### Systemic Movement and Transmission - By cell-to-cell movement, the virus reaches the vascular tissues of the plant. - Long-distance movement of most plant viruses takes place through the sieve elements of the phloem. - The viruses move along with the flow of organic substances from the source tissues (e.g. mature leaves) to the sink tissues (e.g. young leaves and roots). - Depending upon the type of virus, the viral genome is transported through the phloem in the form of complete virus particles or ribonucleoprotein complexes. - The coat protein of TMV is generally required for efficient long-distance movement within the plant. - The virus moves out of the phloem into the surrounding cells where further viral multiplication takes place. - Transmission of plant viruses from one plant to another may occur through insect vectors, mechanical contact, contaminated agricultural tools, seeds, pollen and vegetative propagation. - TMV is mainly transmitted through contact with infected plants, contaminated hands and agricultural tools. The virus particles remain infectious in dried plant materials for prolonged periods. ![Tobacco mosaic virus entering through a plant wound, replicating RNA in the cytoplasm, moving through plasmodesmata and spreading systemically through the phloem.](https://biologynotesonline.com/wp-content/uploads/2024/04/tobacco-mosaic-virus-life-cycle-1024x477.webp)Tobacco mosaic virus entering through a plant wound, replicating RNA in the cytoplasm, moving through plasmodesmata and spreading systemically through the phloem. ## Viral Growth Curve The viral growth curve or [one-step growth curve](https://biologynotesonline.com/one-step-growth-curve-of-virus/) represents the changes in the number of infectious virus particles with time during a single cycle of viral replication. The one-step growth curve is used to study the different periods of viral multiplication and to determine the average number of infectious virus particles produced per infected cell. - In a one-step growth experiment, the host cells are infected with viruses at approximately the same time (synchronised infection). - Initially, the virus particles attach to specific receptors present on the host cell surface. This is known as adsorption. - The unadsorbed virus particles are removed, neutralised or diluted sufficiently to prevent further infection of host cells. - Samples are collected at regular time intervals and the number of infectious virus particles is determined by a suitable method such as the plaque assay. The viral titre is expressed in plaque-forming units per millilitre (PFU/mL). - Extracellular infectivity is measured by determining the number of infectious virus particles present outside the host cells. - For viruses that mature within the cell, intracellular infectivity can be determined by disrupting the infected cells artificially and measuring the infectious virus particles released from them. - The total infectivity includes both intracellular and extracellular infectivity. - Unlike bacteria, viruses do not multiply by binary fission. The individual components of a virus are synthesised separately within the host cell and assembled to form new virus particles. ![One-step bacteriophage growth curve comparing total and extracellular infectivity during the eclipse, latent, rise and plateau periods.](https://biologynotesonline.com/wp-content/uploads/2024/04/one-step-viral-growth-curve-1024x524.webp)One-step bacteriophage growth curve comparing total and extracellular infectivity during the eclipse, latent, rise and plateau periods. ### Eclipse Period - The eclipse period is the time between the loss of infectivity of the parental virus following entry and the first appearance of newly formed infectious virus particles within the host cell. - The viral nucleic acid is exposed due to uncoating of the virus or injection of the viral genome into the host cell, as in bacteriophages. - Replication of viral nucleic acid and synthesis of viral proteins take place during this period. - No newly formed infectious virions can be detected within the host cell during the eclipse period, even after artificial disruption of the cell. - The eclipse period ends with the formation of the first infectious progeny virions. ### Latent Period - The latent period is the time between the initial infection of the host cell and the first release of infectious progeny virions into the surrounding medium. - In viruses that mature within the host cell, the latent period includes the eclipse period and a period during which infectious virions accumulate within the cell. - During the latter part of the latent period, infectious virus particles can be detected inside the host cell but not outside the cell as newly released progeny. - The latent period is longer than the eclipse period in typical lytic bacteriophages. In some enveloped viruses, maturation and release take place together, and the two periods may be nearly equal in duration. ### Rise Period - The rise period or burst period begins with the release of newly formed infectious virus particles from the host cells. - In a lytic bacteriophage infection, the bacterial cells undergo lysis and a large number of bacteriophages are released into the surrounding medium. - As more infected cells undergo lysis, there is a rapid increase in the extracellular virus titre. - In viruses released by budding, the release of progeny virions may take place gradually over a longer period. ### Plateau Phase - The plateau phase is the period during which the extracellular virus titre becomes relatively constant. - In a typical one-step growth experiment with lytic bacteriophages, most or all of the initially infected bacterial cells have undergone lysis by this stage. - No further increase in the number of infectious virus particles due to secondary infection occurs under the conditions of a one-step growth experiment. - Unlike the stationary phase of a [bacterial growth curve](https://biologynotesonline.com/bacterial-growth-curve/), the plateau phase of a one-step viral growth curve does not represent an equilibrium between microbial cell division and cell death. ### Burst Size - Burst size refers to the average number of infectious progeny virus particles produced per infected host cell during a single cycle of viral replication. - It is calculated from the increase in extracellular infectious virus particles after the completion of the rise period and the number of host cells initially infected. - The burst size varies depending upon the type of virus, host cell and physiological condition of the host cell. 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