Herpes simplex virus replication Steps - Microbiology Animations

Summary

The video script discusses the herpes simplex virus (HSV), a DNA virus causing conditions like cold sores and genital herpes. It details the virus's structure, including its double-stranded DNA and icosahedral capsid, surrounded by viral proteins. The script explains the infection process, from binding to host cell receptors to viral replication and assembly. It distinguishes between lytic and latent infections, highlighting the virus's ability to remain dormant in nerve cells for years before reactivating. The video also touches on how stress or immune suppression can trigger viral outbreaks.

Takeaways

• 🧬 Herpes simplex virus (HSV) is a DNA virus that causes conditions like cold sores and genital herpes.
• 🔬 The HSV virion includes a double-stranded DNA chromosome enclosed in an icosahedral capsid.
• 🛡️ The capsid is enveloped by tegument proteins and a host-derived lipid membrane with spike proteins.
• 🔗 The virus can bind to various host cell receptors, leading to the fusion of the viral envelope with the host cell membrane.
• 🚀 After fusion, the capsid is released into the cytoplasm and travels to the nuclear membrane along microtubules.
• ⏳ The tegument protein VHS degrades host cell mRNA, reducing competition for cellular machinery.
• 🛡️ Another tegument protein, VP-16, protects viral mRNA and activates viral gene expression.
• 🔄 The viral DNA circularizes to form a plasmid-like structure within the nucleus.
• 🌀 The virus can follow a lytic infection pathway, leading to the production of new viral particles, or a latent infection pathway, where the virus remains dormant.
• 🧩 In lytic infection, immediate early genes are activated, leading to a cascade of events that result in new virus production.
• 🔄 The viral DNA is replicated using a rolling circle mechanism, and late-stage mRNAs encode for capsid and envelope proteins.
• 🚫 Latent infections can persist in nerve cells for long periods, potentially reactivating under stress or immune system depression.

Q & A

What is an example of a DNA virus mentioned in the script?

An important example of a DNA virus mentioned in the script is the herpes simplex virus (HSV), which includes strains that cause cold sores and genital herpes.

What is the structure of the herpes simplex virus (HSV)?

The HSV virion consists of a double-stranded DNA chromosome packed within an icosahedral capsid, which is surrounded by tegument, a collection of about 15 different kinds of virus-encoded proteins.

How does the HSV virion enter the host cell?

The HSV virion can bind to several alternative receptor molecules in the host cell membrane, after which the envelope fuses with the host membrane, releasing the capsid into the cytoplasm.

What is the role of the tegument protein called 'virion host shut off' (vhs)?

The vhs protein degrades the host cell's mRNA molecules, eliminating competition for ribosomes and other cellular machinery.

What is the function of the tegument protein vp-16 in the HSV?

The vp-16 protein protects viral mRNAs and acts as a transcriptional activator of gene expression in the viral genome at a nuclear pore.

How does the herpes chromosome enter the nucleus?

The herpes chromosome enters the nucleus where it circularizes to form a plasmid-like intermediate.

What is the difference between lytic and latent infections in the context of HSV?

In a lytic infection, a cascade of events leads to the production of new virus variants, while in a latent infection, latency genes are transcribed to keep the cell from committing suicide and producing new variants.

How does the HSV DNA replicate during a lytic infection?

The circular viral DNA replicates using a viral DNA polymerase and other proteins, with the production of new genomes for progeny viruses occurring by the rolling circle method.

What are the steps for the assembly and release of new HSV virions?

The newly synthesized DNA expresses late-stage mRNA, which is translated into capsid and envelope proteins. Capsids form in the nucleus, and the developing virions bud through the nuclear membrane, acquiring an envelope. They move through the endoplasmic reticulum, bud off, and eventually fuse with the Golgi apparatus before budding off and fusing with the plasma membrane to release the completed virions.

Where does the primary infection of HSV occur and what triggers new outbreaks?

The primary infection occurs in epithelial cells, followed by latent infection within neurons of ganglia near the original site of infection. New outbreaks are often triggered by stress, sunlight exposure, or depression of the immune system.

How does the HSV establish a latent infection, and where does this typically occur?

The script does not provide a clear mechanism for how a latent infection initiates in neurons, but it is known that a latent infection most commonly occurs in nerve cells.

Outlines

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🦠 Herpes Simplex Virus Lifecycle

The paragraph describes the lifecycle of the herpes simplex virus (HSV), a DNA virus known for causing cold sores and genital herpes. It details the structure of the virus, which includes a double-stranded DNA chromosome within an icosahedral capsid surrounded by tegument proteins. The virus enters the host cell through binding to receptors and fusing its envelope with the host cell membrane. Once inside, the capsid moves to the nuclear membrane, and tegument proteins like virion host shut off (vhs) degrade host mRNA, while vp-16 protects viral mRNA and activates gene expression. The viral DNA enters the nucleus and circularizes to form a plasmid-like intermediate, leading to the activation of immediate early genes. Depending on the infection pathway, the virus can either enter a lytic infection, leading to new virus production, or a latent infection, where the viral DNA persists within the cell for long periods without producing new viruses. The lytic infection involves the expression of early genes, replication of viral DNA, and assembly of new virus particles, which are then released from the cell. Latent infections, which commonly occur in nerve cells, can lead to reactivation and new outbreaks triggered by various factors.

Keywords

💡Herpes simplex virus (HSV)

Herpes simplex virus (HSV) is a type of DNA virus that causes infections around the mouth (cold sores) and on the genitals (genital herpes). The video script describes HSV as having strains that can lead to these specific conditions. HSV is significant in the video's theme as it is the primary virus being discussed, and understanding its structure and behavior is crucial to grasping the video's content.

💡Virion

A virion is the complete, infectious form of a virus, consisting of a nucleic acid genome enclosed within a protein coat called a capsid. In the script, the HSV virion is described as containing a double-stranded DNA chromosome within an icosahedral capsid, which is essential for understanding how the virus is structured and how it can infect host cells.

💡Capsid

The capsid is the protein shell of a virus that encloses its genetic material. In the context of the video, the HSV capsid is mentioned as being icosahedral in shape and plays a role in protecting the viral DNA and facilitating entry into host cells.

💡Tegument

The tegument is a layer of proteins found between the capsid and the envelope of some enveloped viruses, including HSV. In the script, the tegument is described as containing about 15 different kinds of virus-encoded proteins, which are crucial for the virus's interaction with the host cell and its ability to hijack the host's machinery.

💡Envelope

An envelope is a lipid membrane that surrounds some viruses, derived from the host cell's membrane. In the video script, the HSV envelope is mentioned as containing spike proteins that allow the virus to bind to and enter host cells, highlighting the importance of the envelope in the virus's infectivity.

💡Viral receptor binding

Viral receptor binding refers to the process by which a virus attaches to specific molecules on the surface of a host cell, allowing it to enter the cell. The script explains that the HSV virion can bind to several alternative receptor molecules, which is a critical step in the infection process.

💡VHSO protein

The virion host shut off (VHS) protein is a tegument protein of HSV that degrades host cell mRNA, as mentioned in the script. This action allows the virus to redirect the host cell's resources towards viral replication, illustrating the strategic ways viruses can manipulate host cells to their advantage.

💡VP-16

VP-16 is a tegument protein of HSV that has multiple roles, including protecting viral mRNAs and acting as a transcriptional activator. The script describes how VP-16 works at a nuclear pore to activate viral gene expression, which is essential for the virus's replication and production of new viral particles.

💡Lytic infection

Lytic infection is a type of viral infection where the virus replicates and causes the host cell to lyse, or break open, releasing new virus particles. The script discusses the lytic infection pathway of HSV, detailing the cascade of events that lead to the production of new viral variants and the eventual destruction of the host cell.

💡Latent infection

Latent infection is a state in which the virus remains dormant within host cells for long periods, potentially reactivating later. The script explains that HSV can enter a latent state in nerve cells, where specific genes are transcribed to maintain the viral genome without producing new virus particles, allowing the virus to persist for decades.

💡Immediate early genes

Immediate early genes are the first set of viral genes activated during a lytic infection. The script describes how, upon entering the nucleus, the viral chromosome activates these genes, which are then transcribed and translated into proteins that initiate the viral replication process, marking the beginning of the cascade of events leading to new viral particle production.

Highlights

Herpes simplex virus (HSV) is an example of a DNA virus causing cold sores and genital herpes.

The HSV virion is composed of a double-stranded DNA chromosome within an icosahedral capsid.

The capsid is surrounded by tegument, a layer of 15 different virus-encoded proteins.

The tegument is enclosed within a host-derived membrane envelope with spike proteins.

HSV can bind to several alternative receptor molecules on the host cell membrane.

The envelope fuses with the host membrane, releasing the capsid into the cytoplasm.

Capsid travels along microtubules to the nuclear membrane, facilitated by the tegument.

VHS protein degrades host cell mRNA, eliminating competition for cellular machinery.

VP-16 protects viral mRNAs and acts as a transcriptional activator in the viral genome.

The herpes chromosome enters the nucleus and forms a plasmid-like intermediate.

VP-16 activates a set of viral genes called immediate early genes.

The virus can enter a lytic infection pathway, leading to the production of new virions.

Alternatively, the virus can enter a latent infection, with latency genes preventing cell suicide.

Latent infections can persist within nerve cells for decades before reactivating.

In lytic infection, immediate early gene proteins return to the nucleus to activate early genes.

Early proteins include a viral DNA polymerase, which replicates the viral DNA using the rolling circle method.

Late-stage mRNA encodes for capsid and envelope proteins, synthesized in the cytoplasm and ER.

Capsids form and capture DNA genomes, then bud through the nuclear membrane to acquire an envelope.

The virion matures by moving through the endoplasmic reticulum and Golgi apparatus before being released.

Primary infection occurs in epithelial cells, followed by latent infection in nearby ganglia neurons.

Latent infections can lead to new outbreaks, often triggered by stress or immune system depression.

Transcripts

[Music]

an important example of a DNA virus is

herpes simplex virus or HSV strains of

which cause cold sores and genital

herpes the virion consists of a

double-stranded DNA chromosome packed

within an icosahedral capsid the capsid

is surrounded by about 15 different

kinds of virus encoded proteins

collectively called tagged ument the

tagamet is contained within a host

derived membrane envelope with several

kinds of spike proteins

the herpes very on can bind to several

alternative receptor molecules in the

host cell membrane after which the

envelope fuses with a host membrane

releasing the capsid into the cytoplasm

the capsid travels down a scaffold of

microtubules to the nuclear membrane at

the same time a protein from the tagamet

called virion host shut off or VHS

protein degrades the host cell's mRNA

molecules and thereby eliminates the

competition for ribosomes and other

cellular machinery

another tagamet protein called vp-16

ultimately protects viral mRNAs it also

acts as a transcriptional activator of

gene expression in the viral genome at a

nuclear pore the herpes chromosome

enters the nucleus the DNA then circular

Isis to form a plasmid like intermediate

vp-16 works in concert with host factors

to activate a set of viral genes called

immediate early genes these immediate

early mRNAs leave the nucleus for the

cytoplasm where ribosomes translate them

into proteins

in expressing these immediate early

genes the virus has entered a pathway

called oolitic infection in which a

cascade of events culminates in the

production of new variants however the

virus could have entered a pathway

called a latent infection in which genes

called latency or l80 genes are

transcribed and keep the cell from

committing suicide and from producing

new variants in a latent infection the

DNA circle can persist within the cell

for decades before switching to a

litigant latent infection most commonly

occurs in nerve cells

in the lytic infection the translated

proteins of the immediate early genes

return to the nucleus where they turn on

the expression of another set of genes

called

early genes the mRNAs traveled to the

cytoplasm where ribosomes translate them

into proteins

[Music]

these early proteins include a viral DNA

polymerase the DNA polymerase and other

proteins replicate the circular viral

DNA the production of new genomes for

progeny viruses occurs by the rolling

circle method which generates akincana

myrrh of many copies of the viral DNA

the newly synthesized DNA expresses

late-stage mRNA which exits the nucleus

for translation some of the mRNAs encode

capsid proteins and are translated on

free ribosomes in the cytoplasm some of

the late mRNAs encode envelope proteins

which are translated on ribosomes on the

endoplasmic reticulum many late-stage

proteins re-enter the nucleus to form

capsids and these capsids capture DNA

genomes

a capsid buds through the internuclear

membrane becoming enveloped by a single

membrane the developing virion moves

through the endoplasmic reticulum and

buds off after which it fuses with the

Golgi apparatus the virion eventually

buds off the Golgi apparatus and fuses

with the plasma membrane the completed

virion is now outside the cell

the primary infection occurs in

epithelial cells followed by latent

infection within neurons of ganglia near

the original site of infection how a

latent rather than lytic infection

initiates in neurons is not well

understood the latent infection of the

ganglia later leads to new outbreaks of

virus often triggered by stress sunlight

exposure or depression of the immune

system progeny variants travel back to

the epithelia causing lytic infection