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Medical virology > Herpesvirus > Flashcards

Herpesvirus Flashcards

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USMLE® Step 1 flashcards
1
Q

What is herpesvirus?

A
  • family of dsDNA viruses
  • infect a wide range of species
  • 8 cause disease in humans some life theratening
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2
Q

What is the structure of a herpesvirus particle?

A
  • core contains a genome
  • this is surrounded by a proteinaceous core which is surrounded by a complex icosahedral capsid
  • a layer of tegument proteins resides outside the capsid
  • envelope on the outside
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3
Q

What is the tegument?

A
  • protein filled region
  • when the virus attaches all the tegument proteins are released into the cell and can begin to have effects on the cell immediately after entry
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4
Q

What are the 2 herpes lifecycles?

A
  • lytic replication involves the production of infectious virions, cell destruction and transmission
  • latent infection allows virus to persist in cells indefinitely without producing many proteins
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5
Q

What are the 3 families of herpesvirus?

A
  • alpha
  • beta
  • gamma
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6
Q

What are the characteristics of alpha herpesviruses? Give an example of one

A
  • wide host range
  • spread rapidly and cause efficient cell death in culture
  • latently infects sensory ganglia
  • e.g. HSV1/2
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7
Q

What are the characteristics of Beta herpesviruses? Give an example of one

A
  • more limited host range
  • slow cell to cell spread
  • CMV
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8
Q

What are the characteristics of Gamma herpesviruses? Give an example of one

A
  • most limited host range
  • latently infect B or T cells
  • EBV
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9
Q

What is HSV1?

A
  • herpes simplex virus 1
  • alpha herpes virus
  • causes encephalitis and necorsis of the temporal lobe
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10
Q

Describe the genome of a herpes simplex virus

A
  • composed of 2 covalently linked segments flanked by inverted repeats
  • short and long segments
  • repeats allow rearrangements of the regions into 4 different isomers
  • 80 gene products 40 of which arent essential for replication
  • lots of unspliced genes
  • very complex genome
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11
Q

Where do herpes simplex viruses replicate when in lytic life cycles?

A
  • nucleus of epithelial cells
  • infectious virions are produced and cell destruction occurs
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12
Q

Describe the latent stage of a herpes virus infection

A
  • reversible and non-productive
  • infects immune privileged sensory ganglia
  • can be life long
  • to maintain a latent state the virus must evade host responses and limit its gene expression
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13
Q

Describe the lytic replication of herpes simplex virus

A
  • attachment, fusion and release of tegument into the cell
  • nucleocapsid enters the nucleus via microtubule transport and releases the viral DNA
  • genome is replicated by the rolling circle method of replication
  • then gets enveloped and released
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14
Q

How does herpes simplex virus enter the host cell?

A
  • interaction of viral glycoproteins with host cell receptors
  • gB and gC bind cell surface proteoglycans
  • gD binds further herpes entry mediators to stabilise attachment
  • pH dependent fusion of the viral envelope with the plasma membrane
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15
Q

How are herpes simplex virus genes expressed during lytic infection?

A
  • tightly reagulated
  • IE, E and L genes expressed in a temporal fashion where the expression of the previous set is required for expression of the nect
  • interrupting one stage means the later ones arent expressed
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16
Q

What do HSV IE, E and L genes encode for in lytic gene expression?

A
  • intermediate early is involved in the expression of viral genes
  • early is involved in DNA metabolism and replication
  • late is involved in assembly and encodes structural proteins
17
Q

How are the herpes IE gene expression initiated?

A
  • transcription initiation is due to the recruitment of cellular factors to IE promoters
  • this is enhanced by VP16 in the tegument that recruits transcription factors and pol II to start transcription of IE genes
18
Q

Describe HSV early gene expression

A
  • replication occurs in replication compartments formed in the nucleus
  • 7 E genes are essential for genome replication
  • origin binding, DNA binding, helicase and polymerase important
19
Q

What are the specific roles of the IE proteins of herpes virus?

A
  • ICP0 allows transcription of early promoters
  • ICP22 enhances ICP0 expression
  • provide an environment conducive to viral genome synthesis
  • stabilise viral mRNA to enhance translation
  • can also affect MHC I presentation on cell surfaces
20
Q

How is HSV genome replication initiated?

A
  • binds to 1 of 3 origins of replication causing a bend in the DNA that forms a stem-loop and unwinds the DNA
  • helicase/primase complex binds to ssDNA and synthesises RNA primers
  • virla polymerase binds these and starts DNA synthesis
21
Q

What is a rolling circle intermediate in HSV1 replication?

A
  • circular replication structure is nicked after initiation to form a rolling circle
  • replication forms long strands of viral progeny with multiple copies wound like a spool of ribbon
  • cleaved at packaging sites to form single DNA genomes which are then packaged into virions
22
Q

How is the HSV assembled after replication?

A

procapsid is formed around scaffold proteins which then get degraded to form an empty capsid for the genome to be packaged into

23
Q

How does the assembled HSC capsid exit the host cell nucleus?

A
  • too big for a nuclear pore so must bud through the membrane
  • associates with the inner membrane by breaking through the nuclear lamina and buds into the perinuclear space - gains an envelope here
  • its envelope then fuses with the outer nuclear membrane and exits into the cytoplasm
24
Q

How and where does virion maturation of herpes virus occur?

A
  • in the cytoplasm
  • mature capsids associate with tegument proteins and bud into Golgi-derived vesicles that contain the glycoproteins produced during transcription
  • second envelopment takes place here - unique double-envelopment process
  • can alternatively recover memrbanes from the surface of the cell on its way out
25
Q

What kinds of proteins can be found n the HSV tegument? give 4 example

A
  • those important in initial infection
  • VP16 associates with host cell proteins such as TFs to activate IE genes
  • VHS (virion host shut off) degrades host mRNA
  • ICP0 disrupts PML bodies and allows transcription of early gene promoters
  • others interact with microtubules to facilitate virion transport to the nucleus
26
Q

What are PML bodies?

A
  • nuclear foci containing cellular proteins involved in transcription, DNA repair and apoptosis
  • stored in the nucleus to be readily available to associate with viral DNA and restrict its expression
27
Q

Where do herpes viruses travel to to become latent?

A
  • enter the sensory neuronal axons
  • migrate along the axon to the cell body of neuronal ganglions in the CNS
  • during this migration most of the tegument proteins are lost
28
Q

Why is loss of the tegument proteins important in herpes virus latency?

A
  • no activation of IE genes from the lytic cycle can occur
  • viral genomes become associated with methylated host histones to further repress transcription
29
Q

In herpes virus latency, all transcription is silent apart from the expression of what?

A
  • LAT
  • keeps the genome silent and avoids host immune surveillance
  • can be processed into 4 miRNAs that prevent the expression of lytic regulatory proteins and limit cytotoxic effects in doing so
30
Q

How does herpes virus reactivate from latency?

A
  • latent episome must reorganise its chromatin to ensure levels of IE gene expression are sufficient to overcome virus-encoded miRNAs
  • nuclear accumulation of viral VP16
  • demethylation of histones
  • mature virions are produced and transport to axonal terminuses where they mature and release
31
Q

What kind of stimuli can cause herpes virus to reactivate from latency?

A
  • poorly understood
  • physical stresses such as illness and exposure to UV light
  • leads to demethylation of histones associated with viral DNA
32
Q

What is Varicella Zoster virus?

A
  • alpha herpes virus that causes chicken pox or shingles
33
Q

Describe the basic life cycle of Varicella zoster virus

A
  • enters mucosal epithelium
  • spread to the tonsils and other lymphoid organs where it encounters and infects T cells
  • establishes latency as in HSV-1
  • reactivation from latency allows a second phase of replication in the skin
34
Q

Are there vaccines for herpesviruses?

A
  • live attenuated vaccine for chicken pox is 70-90% effective
  • vaccines for HSV-1, EBV etc are in development
35
Q

What kind of antiviral drugs are there for herpes viruses?

A
  • nucleoside analouges such as Acyclovir
  • helicase-primase inhibitors
36
Q

How do nucleoside analogues (Acyclovir) work against herpes virus?

A
  • analogues get phosphorylated by viral proteins and incorporated into viral DNA
  • prevents chain elongation by pol and leads to cell death
  • resistance is occuring
37
Q

How do helicase-primase inhibitors against herpes virus work?

A
  • inhibit the enzymes in the helicase-primase complex
  • stops it from forming properly
  • some can enhance DNA binding so much that the complex can’t move along the DNA

Medical virology (15 decks)

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