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MICR 221 Final exam > Lecture 6 > Flashcards

Lecture 6 Flashcards

1
Q

What are 5 shared properties of all herpesviruses?

A
  • spherical enveloped virions, 120-200nm in diameter
  • icosahedral capsid, can have glycoproteins forming spikes
  • linear double stranded DNA genome
  • 100-240 kbp
  • 70-200 genes
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2
Q

Where do all herpesviruses replicate?

A

replicate in the nucleuc with sequential transcription of immediate early a, early B, and late genes (y)

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3
Q

What are a (alpha) proteins for herpesviruses?

A
  • include DNA binding proteins important for the regulation of virus gene expression
  • some proteins involved in immune invasion fall into this kinetic class
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4
Q

What is meant by “kinetic class”

A

s a grouping of genes in a viral genome that are expressed at the same time during the viral replication cycle.

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5
Q

What are the B (beta) proteins for herpesviruses?

A

include enzymes involved in nucleotide metabolism as well as those required for genomic DNA replication

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6
Q

what are the Y proteins for herpesviruses?

A

consist mainly of structural proteins produced after the initiation of virus genome replication

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7
Q

True or False: herpes viruses can cause lifelong infections

A

true

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8
Q

what type of productive infection occurs for herpesviruses in permissive cells?

A

cytocidal

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9
Q

True or False: intranuclear infections, sometimes cytomegalic cells, or syncytia formation is never observed in herpesviruses?

A

false, it can be observed

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10
Q

What type of infections do herpesviruses establish?

A

latent infections

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11
Q

what are latent infections?

A
  • the virus genome persists in the nucleus of specialized cells, but only a small subset of genes is expressed during latency
  • think of this as “dormant” not active
  • it is present, but does not cause the symptoms we would see that are associated with the disease until activated
  • because of this it can “evade” detection, and be harder to treat because of it
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12
Q

What does reactivation for latency period trigger?

A

replication and shedding of infectious virus, leading to the symptoms seen with the disease

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13
Q

do herpes particles survive well outside the body?

A

no, they are fragile and don’t survive well outside of the body

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14
Q

How does transmission occur for herpesviruses?

A

transmission requires close contact, typically intimate contact that brings mucosal surfaces in direct contact

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15
Q

In crowded environments where animals are closely confined how does the herpesvirus quickly transmit?

A

sneezing, which causes short distance droplet spread, leading to transmission

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16
Q

What is alphaherpesvirinae?

A
  • one of the subfamilies of herpesviruses
  • grows rapdily and lyses infected cells
  • establish latent infections in neurons of the peripheral nervous system
  • some, but not all, have a broad host range (ex. HSV can infect a wide variety of species, whereas VZV infection is restricted to humans)
17
Q

What are the human alphaherpesviruses?

A

HSV-1, HSV-2, VZV

18
Q

What is betaherpesvirinae?

A
  • one of the subfamilies of herpesviruses
  • restructed host range
  • grows very slowly (80-120 hours)
  • cell lysis does not occur until several days after infection
  • latency established primarily in monocytes and lymphocytes
  • activation and replication of the virus in the kidney and secretory glands promote its secretion in urine and other bodily secretions, including semen and milk
19
Q

what are gammaherpesvirinae?

A
  • a subfamily of herpesvirus
  • narrow host range
  • establishes latency in and is capable of transforming B lymphocytes
  • other gammaherpesviruses are also capable of causing cancer
20
Q

How many herpesviruses are there for which humans are the natural host?

A

nine

21
Q

how many proteins can the herpesviruses that humans are the natural host encode?

A

70-200 proteins

22
Q

Can herpesviruses occur simulataneously?

A

yes, many can be infected with four+

23
Q

What is “B Virus”?

A
  • this is a tenth herpesvirus that can infect humans
  • it is a type of alphaherpesvirus
  • it is a monkey virus that causes a disease similar to HSV in macaques, however it is extremely pathogenic fo humans
  • mortality rate is 80%
  • causes acute CNS disease
24
Q

What are poxviruses?

A

large viruses with DNA genomes that replicate in the cytoplasm of infected cells

25
Q

what is the most “famous” poxvirus?

A

smallpox

26
Q

What virus has killed the most humans ever than all other infectious diseases combined?

A

smallpox

27
Q

True or False: the world is not free of smallpox

A

false

28
Q

over concerns of bioterrorism, what vaccine stockpile does the US have?

A

over concerns of bioterrorism, the US now has a stockpile of vaccine to vaccinate every person in the US in the event of a smallpox emergency

29
Q

Can poxviruses cause infections outside of a specific species?

A

some are restructed to only one host species and don’t cause infections out of that species. for other poxviruses, they can infect multiple zoonotic host species

30
Q

what is meant by “zoonotic”?

A

when a virus can jump from one species to another

31
Q

what is monkeypox?

A
  • can cause fatal disease in humans, similar to smallpox, but a lot less serious
  • occurs near tropical rainforests
  • it is transmitted to people from a variety of wild animals and it spreads in human populations through human-to-human transmission
32
Q
A
33
Q

is there a treatment/vaccine for monkeypox?

A

no specific one, but the smallpox vaccination has been proven to be 85% effective in preventing monkeypox

34
Q

what are the steps in poxvirus DNA replication?

A
  1. the poxvirus DNA duplex, it is linear double stranded DNA with closed ends (what we start with)
  2. a nuclease nicks on end, to start the process of replication. knows where to nick due to inverted repeat sequences.
  3. the terminal repeats (ATATATA…) fold-over as hydrogen bonds from between complementary bases on the same strand form a hairpin loop (the ends fold back on each other due to complementary inverted repeat sequences)
  4. the free 3’ end, folded over on itself in the hairpin loop to make it appear double stranded so it can act as a primer for dna synthesis (the next nucleotide gets added to 3’ end)
  5. DNA synthesis occurs around the other terminal loop, resulting in two genomes joined end-to-end (now we have two copies of the genome, making the molecule a dimer- this process can be repeated again to make more copies of the genome due to the head to tail repeats)
  6. the process may begin again to produce a concatemer of 4 genomes and so on. the concatemers formed contained copies of the genome separated by cruciform structures of dna
  7. the concatemer is cleaved into individual genomes
  8. the ends are ligated (sealed by formation of a covalent bond) as the two strands are bonded together at the ends, forming terminal loops
35
Q

what is a concatemer structure?

A

serves as signals when dna packaging is requires so something can come along and nick them to be seperated for packaging.

36
Q

where does poxvirus replication occur?

A

in cytoplasm

37
Q

if the replicated poxvirus has two membranes, what happens to the cell?

A

the cell does not undergo lysis, and the virus can be delivered to the cell surface to be driven into adjacent cells (by polymerizing actin) for infection

38
Q

what happens if the poxvirus cell only has one membrane after replication?

A

the cell will undergo lysis

39
Q

Describe HSV lytic cycle entry into nucleus

A
  • virus absorbs to absorption receptors on membrane
  • virus envelope fuses at membrane, releases nucleocapsid and integument proteins
  • nucleocapsid moves down microtubules towards nucleus
  • too large to go through nuclear core complex, reorients itself so that the portal binds and because of high pressure DNA goes shooting into nucleoplasm

MICR 221 Final exam (16 decks)

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