Herpes simplex virus replication Steps - Microbiology Animations
Summary
TLDRThe 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
🦠 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.
Mindmap
Keywords
💡Herpes simplex virus (HSV)
💡Virion
💡Capsid
💡Tegument
💡Envelope
💡Viral receptor binding
💡VHSO protein
💡VP-16
💡Lytic infection
💡Latent infection
💡Immediate early genes
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
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