Herpesvirus Lytic Replication
Herpesvirus Lytic Replication - Related Videos
11:28
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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Cited by 2 •
2011
We describe a protocol to identify key roles of host signaling molecules in lytic replication of a model herpesvirus, gamma herpesvirus 68 (γHV68). Utilizing genetically modified mouse strains and embryonic fibroblasts for γHV68 lytic replication, the protocol permits both phenotypic characterization and molecular interrogation of virus-host interactions in viral lytic replication.
07:10
Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
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2025
This protocol describes an in vitro system to model de novo lytic infection of Kaposi's sarcoma-associated herpesvirus using BAC16-derived virions. The method enables investigation of early viral replication and dissemination. Infectious virus production is quantified by GFP-based infectious units assays and real-time PCR of encapsidated viral genomes.
02:52
Inducing the Prophage Lytic Replication for Transcriptomic Analysis
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2026
Source: Krishnamurthi, R., et al. Understanding the Impact of Temperate Bacteriophages on Their Lysogens Through Transcriptomics. J. Vis. Exp. (2024)This video demonstrates the induction of lytic replication in a prophage integrated into the bacterial genome and the capture of gene expression changes through timed sampling for transcriptomic analysis.
01:20
Viral Replication: Lytic Cycle
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2025
Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.Attachment and DNA InjectionThe infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage...
01:30
Lytic Cycle of Bacteriophages
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2019
Bacteriophages, also known as phages, are specialized viruses that infect bacteria. A key characteristic of phages is their distinctive “head-tail” morphology. A phage begins the infection process (i.e., lytic cycle) by attaching to the outside of a bacterial cell. Attachment is accomplished via proteins in the phage tail that bind to specific receptor proteins on the outer surface of the bacterium. The tail injects the phage’s DNA genome into the bacterial cytoplasm. In the lytic replication...
FAQs
The cascade assigns different tasks to successive stages. Immediate-early proteins activate viral programs, early proteins support viral DNA replication, and late proteins produce capsids and other structural components. This ordering links genome use to particle construction, so disruption of an earlier stage can affect later production. It also provides a framework for interpreting where infection is progressing within a cell.
The nucleus provides the setting in which the delivered viral genome is used to initiate the regulated gene-expression cascade. It is also where viral DNA replication is supported by early proteins. Consequently, successful nuclear delivery connects entry with genome amplification and later particle production. Examining this transition helps explain how infection progresses from cell entry to formation of new virions.
Capsids package the newly generated viral genome, while later envelopment supplies the membrane-bound form needed for exit from the infected cell. These are coordinated late-stage events rather than independent outcomes. If assembly or acquisition of the envelope is impaired, production or release of newly formed particles can be affected. This link helps explain spread to neighboring cells.
Analysis can follow a staged path: first, determine whether the viral genome reaches the nucleus; next, examine immediate-early activation and early support for viral DNA replication; finally, assess late structural production, capsid assembly, envelopment, and exit. Tracking these events in order distinguishes failures in gene regulation, genome replication, particle formation, or release.
Productive replication can damage infected cells and provoke inflammation, making the cycle relevant to both viral pathogenesis and immunology. Newly released virions can infect neighboring cells, extending the local infection and exposing additional tissue to virus-associated injury. Studying these linked outcomes helps connect intracellular replication events with tissue-level disease and host immune responses.
Viral DNA polymerase is positioned at the genome-replication stage, which follows immediate-early activation and precedes late structural production. Targeting this enzyme or related replication steps can interfere with the transition from viral gene regulation to generation of genomes for new particles. The stage-specific logic helps researchers relate drug action to reduced particle production.