# Replication of Viruses – Steps, Strategies and Life Cycles > Replication of viruses involves several stages of viral multiplication. Explore viral replication steps, DNA and RNA replication strategies, and phage cycles. Canonical URL: https://biologynotesonline.com/replication-of-virus/ Author: Sourav Pan Last updated: November 15, 2026 ![Replication of Viruses – Steps, Strategies and Life Cycles](https://biologynotesonline.com/wp-content/uploads/2024/04/seven-stages-of-viral-replication.webp) The replication of viruses generally takes place in seven stages- attachment, penetration, uncoating, biosynthesis, assembly, maturation and release. In some textbooks, the viral replication cycle is divided into six stages, where assembly and maturation are considered a single stage. The mechanism of replication of the viral genome and the expression of viral genes depends upon the type of nucleic acid present in the virus. In most animal DNA viruses, genome replication takes place in the nucleus of the host cell, whereas in most animal RNA viruses it takes place in the cytoplasm. However, there are exceptions in both groups of viruses. ## What is Viral Replication? Viral replication is the process by which viruses produce new viral particles within suitable host cells. Viruses are obligate intracellular parasites and cannot multiply independently outside the host cell. They depend on the cellular machinery of the host for protein synthesis and also utilise the energy and other cellular resources of the host cell for viral multiplication. A cell which can be infected by a particular virus is known as a susceptible cell. The cells which support the complete replication cycle of the virus are called permissive cells. During a productive infection, new infectious virus particles (progeny virions) are produced. In virus reproduction, new viral particles are formed by the assembly of viral components and not by the division of pre-existing virus particles. Viral genome replication refers to the production of new copies of the viral nucleic acid (DNA or RNA). It is a part of the complete viral replication cycle, which also involves the synthesis of viral proteins, formation of virions and their release from the host cell. ## Requirements for Viral Replication The following are the requirements for viral replication: - The host cell must be susceptible and permissive to the virus. Susceptibility refers to the ability of a cell to be infected by a virus, whereas permissiveness refers to its ability to support viral replication. - In viruses that depend on receptor-mediated entry, specific receptors must be present and accessible on the surface of the host cell. - A susceptible cell may or may not be permissive to the virus. The virus may enter a non-permissive cell but fails to produce infectious progeny virions due to the absence of essential cellular factors or the presence of inhibitory factors. - The virus requires functional genetic material (DNA or RNA) containing the genetic information necessary for viral multiplication. - Viruses do not possess ribosomes. They utilise the ribosomes and other components of the protein-synthesising machinery of the host cell. - The energy required for viral replication is obtained from the host cell in the form of nucleoside triphosphates such as ATP and GTP. - Nucleotides and amino acids are required for the synthesis of viral nucleic acids and proteins, respectively. - Viral replication requires both cellular and, in many viruses, virus-encoded enzymes. The types of enzymes required depend upon the nature of the viral genome. - Suitable intracellular conditions such as temperature, pH and ionic concentrations are required for the activity of the enzymes involved in viral replication. Some viruses also require the host cell to be at a particular stage of the cell cycle. ## Steps of Viral Replication The productive replication cycle of a virus is generally divided into seven stages. In the six-stage model of viral replication, assembly and maturation may be considered a single stage. In the five-stage model, penetration and uncoating are grouped together, and release and maturation are considered another stage. The number of stages described in these models differs due to the grouping of the events involved in viral replication. ![Seven stages of viral replication showing attachment, penetration, uncoating, biosynthesis, assembly, maturation and release from a host cell.](https://biologynotesonline.com/wp-content/uploads/2024/04/seven-stages-of-viral-replication-1024x576.webp)Seven stages of viral replication showing attachment, penetration, uncoating, biosynthesis, assembly, maturation and release from a host cell. The following are the seven stages of viral replication: ### 1. Attachment (Adsorption) - The virus attaches to the surface of the host cell with the help of specific viral attachment proteins. - In enveloped viruses, the attachment proteins are generally present in the form of glycoproteins in the viral envelope, whereas in non-enveloped viruses these proteins form part of the capsid or its associated structures. - The viral attachment proteins recognise and bind to specific receptors present on the surface of the host cell. Some viruses also require co-receptors for successful entry into the cell. - The distribution of these receptors in different cells and tissues is one of the factors responsible for the host range and tissue tropism of a virus. ### 2. Penetration (Entry) ![Comparison of enveloped virus entry by plasma membrane and endosomal fusion with non-enveloped virus entry by endosomal membrane penetration.](https://biologynotesonline.com/wp-content/uploads/2024/04/mechanisms-of-viral-entry-1024x576.webp)Comparison of enveloped virus entry by plasma membrane and endosomal fusion with non-enveloped virus entry by endosomal membrane penetration. - After attachment, the viral particle or its genetic material enters the host cell. - In receptor-mediated endocytosis, the virus is taken up by the host cell within a membrane-bound vesicle (endosome). - Enveloped viruses may enter the cell by fusion of the viral envelope with the plasma membrane or by endocytosis followed by fusion with the endosomal membrane. - Non-enveloped viruses lack a lipid envelope and cannot enter the cell by membrane fusion. They may enter by endocytosis and subsequently form pores in or disrupt the endosomal membrane. In some viruses, penetration takes place directly across the plasma membrane. ### 3. Uncoating - During uncoating, the viral capsid is partially or completely removed or undergoes structural changes. - The viral genome becomes available for transcription, translation or replication, depending upon the type of virus. - Host cell receptors, cellular proteases, changes in pH and certain viral proteins are involved in the uncoating of different viruses. - In some viruses, complete removal of the capsid does not take place. For example, in reoviruses, the viral RNA remains within the inner capsid (core), from which viral mRNA is synthesised. ### 4. Biosynthesis - Biosynthesis involves the replication of the viral genome, transcription of viral genes and synthesis of viral proteins. - During genome replication, new copies of the viral genetic material (DNA or RNA) are produced, whereas transcription involves the synthesis of viral RNA transcripts, including messenger RNA (mRNA). - The viral mRNA is translated with the help of ribosomes, tRNA and other components of the protein-synthesising machinery of the host cell. In positive-sense RNA viruses, the viral genomic RNA itself can act as mRNA. - Two major types of viral proteins are synthesised during viral replication: Structural proteins, which form the structural components of new viral particles. - Non-structural proteins, which are mainly involved in viral genome replication, regulation of gene expression and other intracellular processes. - The enzymes required for the replication of the viral genome and transcription may be encoded by the virus or the host cell. - The viral replicase is an enzyme or enzyme complex involved in the synthesis of new copies of the viral genome. - In many viruses, the viral and cellular proteins involved in genome replication are associated with each other to form replication complexes. These complexes may be associated with modified intracellular membranes in the host cell. ### 5. Assembly - The newly synthesised viral structural proteins and viral genomes are assembled to form new viral particles. - The capsid proteins associate with each other to form the viral capsid. In many viruses, specific sequences or structures present in the viral nucleic acid help in its recognition and packaging. - The capsid may be formed before the packaging of the viral genome or may be assembled around the viral nucleic acid. - The viral genome along with its associated capsid proteins forms the nucleocapsid. - Depending upon the type of virus, assembly takes place in the nucleus, cytoplasm or at the plasma membrane or other intracellular membranes of the host cell. ### 6. Maturation - During maturation, the newly assembled viral particles undergo certain structural and biochemical changes and acquire infectivity. - In some viruses, precursor viral proteins are cleaved by viral or cellular proteases to form functional proteins. Changes may also occur in the arrangement of the viral structural proteins. - Maturation may take place before, during or after the release of the virus from the host cell. For example, in HIV, the cleavage of viral precursor proteins and rearrangement of the viral core take place during or after budding. ### 7. Release The newly formed viral particles (progeny virions) are released from the host cell by different mechanisms: - Cell lysis- The plasma membrane of the infected cell is disrupted, resulting in the release of viral particles and death of the host cell. It is a common mechanism of release in non-enveloped viruses. - Budding- The virus acquires its lipid envelope from the plasma membrane or intracellular membranes of the host cell containing viral envelope proteins. Budding does not necessarily result in the immediate death of the host cell. - Exocytosis- Viral particles present within intracellular vesicles are transported to the plasma membrane and released when the vesicular membrane fuses with the plasma membrane. Some non-enveloped viruses, such as hepatitis A virus and poliovirus, may also be released from the host cell within membrane-bound vesicles without cell lysis. Enveloped viruses may also cause damage and eventual death of the infected host cell. ![Three mechanisms of viral release showing cell membrane rupture, acquisition of a viral envelope during budding and vesicular release by exocytosis.](https://biologynotesonline.com/wp-content/uploads/2024/04/mechanisms-of-viral-release-1024x524.webp)Three mechanisms of viral release showing cell membrane rupture, acquisition of a viral envelope during budding and vesicular release by exocytosis. ## Viral Replication Strategies The mode of replication of viruses depends upon the type of genetic material present in the virus and the mechanism by which the viral mRNA is produced. On the basis of these properties, viruses are divided into seven groups by the Baltimore classification system. - DNA viruses (Group I and II). - RNA viruses (Group III, IV and V). - Reverse-transcribing viruses (Group VI and VII). The viral genome replication strategies of these seven groups are described below. ### Replication of Double-Stranded DNA (dsDNA) Viruses — Group I - The viruses belonging to this group contain double-stranded DNA as their genetic material. - In most animal dsDNA viruses, both DNA replication and transcription take place in the nucleus of the host cell. - The viral DNA is transcribed into mRNA by DNA-dependent RNA polymerase, which in most nuclear DNA viruses is the RNA polymerase II of the host cell. - In viruses such as adenoviruses and herpesviruses, the expression of viral genes occurs in different phases. The early genes mainly code for enzymes and regulatory proteins required for viral DNA replication, whereas the late genes mainly code for viral structural proteins. - The viral DNA acts as a template for the synthesis of new DNA molecules with the help of DNA-dependent DNA polymerase. - Adenoviruses and herpesviruses encode their own DNA polymerases, whereas smaller DNA viruses such as papillomaviruses and polyomaviruses utilise the DNA polymerases of the host cell. - Poxviruses are an exception among the dsDNA viruses. Their DNA replication and transcription take place in the cytoplasm. They encode their own DNA-dependent DNA polymerase and DNA-dependent RNA polymerase. Examples: Adenovirus, herpes simplex virus, papillomavirus, vaccinia virus. ### Replication of Single-Stranded DNA (ssDNA) Viruses — Group II - These viruses contain single-stranded DNA as their genetic material. - In parvoviruses, the viral ssDNA is converted into dsDNA in the nucleus by the DNA polymerase of the host cell. This double-stranded DNA is known as the replicative form (RF). - The double-stranded DNA acts as a template for the synthesis of viral mRNA by the cellular RNA polymerase II. - The viral mRNA is translated into viral proteins in the cytoplasm. - The replicative form of DNA is also involved in the production of new single-stranded viral DNA molecules. - Parvoviruses do not encode their own DNA polymerase. They depend upon the cellular DNA replication machinery and certain viral non-structural proteins for the synthesis of viral DNA. - The replication of most autonomous parvoviruses depends on cellular factors present during the S phase of the cell cycle. Examples: Human parvovirus B19, canine parvovirus. ![Comparison of Group I dsDNA virus replication and Group II ssDNA virus replication through a double-stranded DNA intermediate.](https://biologynotesonline.com/wp-content/uploads/2024/04/dna-virus-replication-strategies-1024x683.webp)Comparison of Group I dsDNA virus replication and Group II ssDNA virus replication through a double-stranded DNA intermediate. ### Replication of Double-Stranded RNA (dsRNA) Viruses — Group III - The double-stranded RNA of these viruses cannot be directly translated by the ribosomes of the host cell. - These viruses possess an RNA-dependent RNA polymerase (RdRp) within the virion, which is required for the synthesis of viral mRNA. - The negative-sense strand of the dsRNA acts as a template for the synthesis of positive-sense RNA by the viral RNA-dependent RNA polymerase. - In rotaviruses, transcription takes place within the double-layered viral particles. The newly synthesised positive-sense RNA molecules are released into the cytoplasm through channels present in the capsid. - The positive-sense RNA molecules act as mRNA for the synthesis of viral proteins and as templates for the production of complementary negative-sense RNA strands. - During genome replication, the positive-sense RNA molecules are incorporated into developing viral cores, where the complementary negative-sense RNA strands are synthesised to form dsRNA. - In rotaviruses, genome replication takes place in specialised structures present in the cytoplasm known as viroplasms. Examples: Rotavirus, mammalian orthoreovirus. ### Replication of Positive-Sense Single-Stranded RNA (+ssRNA) Viruses — Group IV - The RNA genome of these viruses has the same polarity as that of mRNA. - The viral genomic RNA acts directly as mRNA and is translated by the ribosomes of the host cell. - Among the proteins synthesised from viral RNA are the RNA-dependent RNA polymerase and other proteins involved in viral RNA replication. - The viral RNA-dependent RNA polymerase synthesises a negative-sense RNA strand complementary to the positive-sense genomic RNA. - The negative-sense RNA acts as a template for the synthesis of several copies of positive-sense viral RNA. - The newly synthesised positive-sense RNA molecules may be used for further protein synthesis or incorporated as genetic material into new viral particles. - In viruses such as poliovirus and coronavirus, the proteins involved in RNA replication are associated with modified intracellular membranes in the cytoplasm, where viral replication complexes are formed. - Some positive-sense RNA viruses, such as coronaviruses, also produce subgenomic mRNAs for the synthesis of certain viral proteins. Examples: Poliovirus, coronavirus, hepatitis C virus, dengue virus. ### Replication of Negative-Sense Single-Stranded RNA (−ssRNA) Viruses — Group V - The RNA genome of these viruses is complementary to positive-sense RNA and cannot act directly as mRNA. - The RNA-dependent RNA polymerase is present within the viral particle and is required for transcription of the incoming viral RNA. - The viral polymerase transcribes the negative-sense RNA into positive-sense mRNA, which is translated by the ribosomes of the host cell. - During genome replication, a full-length positive-sense RNA complementary to the viral genomic RNA is synthesised. This RNA is known as the antigenome. - The antigenome acts as a template for the synthesis of new negative-sense viral RNA molecules by the viral RNA-dependent RNA polymerase. - The synthesis of viral mRNA and the synthesis of antigenomic RNA are two different processes. Antigenomic RNA serves as a replication intermediate for the production of new viral genomes. - In most negative-sense RNA viruses, such as rabies virus, both transcription and genome replication take place in the cytoplasm. - However, in influenza viruses, transcription and RNA genome replication take place in the nucleus of the host cell. The viral RNA polymerase obtains short capped RNA fragments from cellular RNA transcripts for the initiation of viral mRNA synthesis. This process is known as cap-snatching. Examples: Rabies virus, influenza virus, measles virus. ![Comparison of Group III dsRNA, Group IV positive-sense RNA and Group V negative-sense RNA virus replication, showing mRNA synthesis and genome replication intermediates.](https://biologynotesonline.com/wp-content/uploads/2024/04/rna-virus-replication-strategies-1024x683.webp)Comparison of Group III dsRNA, Group IV positive-sense RNA and Group V negative-sense RNA virus replication, showing mRNA synthesis and genome replication intermediates. ### Replication of RNA Reverse-Transcribing Viruses (ssRNA-RT) — Group VI - The viruses belonging to this group are mainly retroviruses, which contain positive-sense single-stranded RNA as their genetic material. - Unlike Group IV viruses, the incoming retroviral RNA is used for the synthesis of DNA rather than directly initiating viral protein synthesis. - The enzyme reverse transcriptase is present within the viral particle. - Reverse transcriptase synthesises a DNA strand complementary to the viral RNA. The RNA strand of the RNA-DNA hybrid is degraded by the RNase H activity of reverse transcriptase. - A complementary DNA strand is then synthesised to form double-stranded viral DNA. - The viral DNA is integrated into the chromosomal DNA of the host cell with the help of the viral enzyme integrase. The integrated viral DNA is known as the provirus. - The proviral DNA is transcribed by the RNA polymerase II of the host cell in the nucleus. - The viral RNA transcripts are used for the synthesis of viral proteins. In HIV, the full-length unspliced viral RNA also acts as the genome of the progeny virions. - In HIV, reverse transcription may begin in the cytoplasm and continue within the nucleus, where integration and transcription of the proviral DNA take place. Examples: Human immunodeficiency virus (HIV), human T-cell leukaemia virus (HTLV). ### Replication of DNA Reverse-Transcribing Viruses (dsDNA-RT) — Group VII - Hepatitis B virus (HBV) belongs to this group and contains partially double-stranded relaxed circular DNA (rcDNA) as its genetic material. - The viral DNA is transported to the nucleus, where the incomplete DNA strand and other discontinuities in the viral DNA are repaired by cellular DNA repair enzymes. - A covalently closed circular DNA (cccDNA) molecule is formed, which remains in the nucleus as an extrachromosomal DNA molecule. - The cccDNA acts as a template for the synthesis of viral mRNAs and pregenomic RNA (pgRNA) by the RNA polymerase II of the host cell. - The viral mRNAs are translated into viral proteins in the cytoplasm. - The pregenomic RNA along with the viral polymerase is incorporated into the developing viral capsid. - The reverse transcriptase activity of the viral polymerase is responsible for the synthesis of a negative-sense DNA strand complementary to the pregenomic RNA. The RNA template is degraded by its RNase H activity. - The negative-sense DNA strand acts as a template for the synthesis of the positive-sense DNA strand. The synthesis of the positive-sense DNA strand is usually incomplete in the progeny virions. - Unlike retroviruses, hepatitis B virus does not require the integration of viral DNA into the genome of the host cell for its replication. Integration of HBV DNA may occur during infection but is not an essential step in its replication cycle. Example: Hepatitis B virus (HBV). ![Comparison of HIV replication through an integrated DNA provirus and hepatitis B virus replication through cccDNA, pregenomic RNA and reverse transcription inside the capsid.](https://biologynotesonline.com/wp-content/uploads/2024/04/reverse-transcribing-virus-replication-1024x524.webp)Comparison of HIV replication through an integrated DNA provirus and hepatitis B virus replication through cccDNA, pregenomic RNA and reverse transcription inside the capsid. ### Comparison of Viral Replication Strategies Baltimore groupGenome typeReplication intermediateMode of mRNA productionMajor enzymes involvedTypical site of replication in animal cellsExamplesGroup IDouble-stranded DNA (dsDNA)dsDNA replication intermediatesTranscription of viral dsDNAHost or viral DNA-dependent DNA polymerase and DNA-dependent RNA polymeraseNucleus (cytoplasm in poxviruses)Adenovirus, herpesvirusGroup IISingle-stranded DNA (ssDNA)Double-stranded DNA replicative formTranscription of the dsDNA replicative formHost DNA polymerase, host RNA polymerase II and viral replication proteinsNucleusParvovirusGroup IIIDouble-stranded RNA (dsRNA)Positive-sense RNATranscription of the negative strand of dsRNA by viral RdRpVirion-associated RNA-dependent RNA polymeraseCytoplasmRotavirusGroup IVPositive-sense single-stranded RNA (+ssRNA)Complementary negative-sense RNA (−RNA)Genomic RNA acts directly as mRNA; subgenomic mRNAs are produced in some virusesViral RNA-dependent RNA polymeraseCytoplasmPoliovirus, coronavirusGroup VNegative-sense single-stranded RNA (−ssRNA)Full-length positive-sense RNA (antigenome)Transcription of negative-sense RNA by viral RdRpVirion-associated RNA-dependent RNA polymeraseMainly cytoplasm (nucleus in influenza viruses)Rabies virus, influenza virusGroup VIRNA reverse-transcribing genome (ssRNA-RT)Double-stranded DNA and integrated proviral DNATranscription of proviral DNA by host RNA polymerase IIReverse transcriptase, RNase H, integrase and host RNA polymerase IICytoplasm and nucleusHIVGroup VIIDNA reverse-transcribing genome (dsDNA-RT)cccDNA and pregenomic RNA (pgRNA)Transcription of cccDNA by host RNA polymerase IIHost DNA repair enzymes, host RNA polymerase II, viral reverse transcriptase and RNase HNucleus (cccDNA formation and transcription), cytoplasm (reverse transcription)Hepatitis B virus ## Replication of Bacteriophages Bacteriophages are viruses that infect and multiply within bacterial cells. The virulent bacteriophages reproduce through the lytic cycle, whereas temperate bacteriophages can undergo both lytic and lysogenic cycles. In the lytic cycle, the bacterial cell undergoes lysis after the formation of new bacteriophages. In the lysogenic cycle, the phage genetic material remains within the bacterial cell and is passed on to its daughter cells. Some bacteriophages also cause chronic infections, where new phage particles are released without lysis of the bacterial cell. ![Branching diagram of lambda bacteriophage infection showing productive phage replication and bacterial lysis, prophage integration and inheritance, and induction into the lytic cycle.](https://biologynotesonline.com/wp-content/uploads/2024/04/bacteriophage-lytic-and-lysogenic-cycles-1024x524.webp)Branching diagram of lambda bacteriophage infection showing productive phage replication and bacterial lysis, prophage integration and inheritance, and induction into the lytic cycle. ### Lytic Cycle T4 bacteriophage is a virulent bacteriophage which infects Escherichia coli. The steps involved in the lytic cycle of T4 bacteriophage are as follows: - Attachment (Adsorption)- The bacteriophage attaches to specific receptors present on the surface of the bacterial cell with the help of its tail fibres. - Penetration- The tail sheath contracts and the DNA of the bacteriophage is injected into the bacterial cell through the tail tube. The protein coat remains outside the bacterial cell. - Biosynthesis- The RNA polymerase of the host cell transcribes the phage DNA. The bacterial ribosomes are used for the translation of phage mRNA and the phage DNA is replicated with the help of phage-encoded enzymes. The proteins required for the formation of the head, tail and tail fibres are also synthesised. - Assembly and maturation- The head, tail and tail fibres of the bacteriophage are formed separately. The newly synthesised DNA molecules are packed into the phage heads. The heads and tails along with the tail fibres are joined together to form mature bacteriophages. - Lysis and release- The bacterial cell undergoes lysis with the help of phage-encoded proteins (holins and endolysins) and the newly formed bacteriophages are released into the surrounding environment. ### Lysogenic Cycle The lysogenic cycle is found in temperate bacteriophages such as lambda (λ) bacteriophage of Escherichia coli. The steps involved in the lysogenic cycle of lambda bacteriophage are given below: - The bacteriophage attaches to the receptors present on the bacterial cell surface and injects its DNA into the cell. - The linear double-stranded DNA of the bacteriophage becomes circular. - The circular phage DNA is integrated into the bacterial chromosome at a specific site with the help of integrase and other proteins of the host cell. - The phage DNA integrated into the bacterial chromosome is known as a prophage and the bacterium containing the prophage is called a lysogen. - The CI repressor protein of the lambda bacteriophage inhibits the expression of genes involved in the lytic cycle. - The prophage DNA is replicated along with the bacterial DNA. - When the bacterial cell divides by binary fission, the prophage is passed on to the daughter cells. No new bacteriophage particles are formed during the maintenance of lysogeny. - Under certain conditions, such as damage to the bacterial DNA due to ultraviolet radiation, the repressor protein is inactivated and the prophage enters the lytic cycle. This is known as prophage induction. - The phage DNA is excised from the bacterial chromosome and the genes required for the production of new bacteriophages and lysis of the bacterial cell are expressed. In some temperate bacteriophages, the prophage DNA is not integrated into the bacterial chromosome. E.g., the prophage DNA of bacteriophage P1 is present in the form of a circular plasmid, whereas in bacteriophage N15 it is present in the form of a linear plasmid. ### Differences Between Lytic and Lysogenic Cycles CharacteristicsLytic CycleLysogenic CycleType of bacteriophageVirulent and temperate bacteriophages.Temperate bacteriophages.Fate of phage DNAThe phage DNA is used for the production of new bacteriophages.The phage DNA remains within the bacterial cell as an integrated or extrachromosomal prophage.Production of progenyNew phage particles are produced.New phage particles are not produced during lysogeny.Host cell survivalThe bacterial cell undergoes lysis.The bacterial cell remains viable and can divide.Replication of phage DNAThe phage DNA is replicated with the help of enzymes involved in productive phage replication.The phage DNA is replicated along with the bacterial chromosome or as a plasmid.InheritanceNo stable inheritance of a prophage.The prophage is inherited by the daughter cells.PersistenceThe infection ends with the lysis of the bacterial cell.The prophage may remain within the bacterial population for several generations.Expression of lytic genesThe genes involved in the lytic cycle are expressed.The expression of genes involved in the lytic cycle is generally inhibited.InductionNot required when the bacteriophage directly enters the lytic cycle.The prophage may enter the lytic cycle by induction.ExamplesT4 bacteriophage, lambda bacteriophage during lytic infection.Lambda bacteriophage, P1 bacteriophage and N15 bacteriophage. ## Viral Growth Curve The viral growth curve represents the changes in the number of infectious virus particles with time following infection of the host cells. The one-step growth curve is used to study the production of infectious virus particles during a single cycle of viral replication. - In a one-step growth experiment, susceptible bacterial cells are infected with a lytic bacteriophage at nearly the same time (synchronized infection). - Secondary infection of bacterial cells by the newly released bacteriophages is prevented or minimised. - The number of infectious bacteriophages is determined at different time intervals by the plaque assay and expressed in plaque-forming units per millilitre (PFU/mL). - The extracellular infectious phages are measured in the medium, whereas the total infectious phages are measured after the artificial disruption of the infected cells. The difference between these two values gives an estimate of intracellular infectivity. - The time required for viral replication varies with the type of virus, host cell and environmental conditions. Many bacteriophages complete their replication cycle within several minutes to an hour, whereas the replication of animal viruses may take several hours or days. The different periods of the one-step viral growth curve are described below. ![One-step bacteriophage growth curve showing total and extracellular infectivity, eclipse period, latent period, rise period and plateau phase.](https://biologynotesonline.com/wp-content/uploads/2024/04/one-step-viral-growth-curve-1-1024x683.webp)One-step bacteriophage growth curve showing total and extracellular infectivity, eclipse period, latent period, rise period and plateau phase. ### Eclipse Period - After the penetration and functional uncoating of the virus, the infectivity of the parental virus particle is lost. - The replication of viral nucleic acid and synthesis of viral proteins take place during this period, but no newly formed infectious virus particles can be detected within the host cell. - Even if the infected cells are artificially lysed during this period, no newly formed infectious bacteriophages are obtained. - The eclipse period ends with the formation of the first detectable intracellular infectious virus particles. ### Latent Period - The latent period is the time interval between the beginning of infection and the appearance of newly formed infectious virus particles in the extracellular medium. - In a typical lytic bacteriophage, the latent period is longer than the eclipse period as the mature bacteriophages accumulate within the bacterial cell for some time before their release. - The latent period ends when the infected bacterial cells start undergoing lysis and release infectious progeny bacteriophages. - The latent period of the viral growth curve should not be confused with viral latency or lysogeny, in which the viral genome may persist within the host cell without the continuous production of infectious virus particles. ### Rise Period - During the rise period, the number of infectious bacteriophages in the extracellular medium increases rapidly due to the lysis of infected bacterial cells. - As more bacterial cells undergo lysis, more bacteriophages are released into the surrounding medium. - The time required for lysis may vary slightly among the infected bacterial cells. ### Plateau Phase and Burst Size - The plateau phase occurs when the infected bacterial cells have completed the replication cycle and released their progeny bacteriophages. - The extracellular infectious virus titre remains relatively constant during this phase in the absence of secondary infections and appreciable loss of viral infectivity. - The total and extracellular infectivity curves coincide when all the intracellular infectious bacteriophages have been released. - The average number of infectious bacteriophages released per infected bacterial cell is known as the burst size. 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