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Unit 2 > Unit 2 - Week 2 - Moffat 3,4,5,6 > Flashcards

Unit 2 - Week 2 - Moffat 3,4,5,6 Flashcards

1
Q

What is MERS?

A

Middle East Respiratory Syndrome

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2
Q

What is the only virus that has tegument?

A

Herpesvirus

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3
Q

What is a picornavirus?

A

A small RNA virus

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4
Q

Name some common RNA viruses?

A 
HIV
Ebola
Rabies
Flu
Croup
MERS
Dengue Fever
Hepatitis C
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5
Q

What important viral enzyme is used for both transcription and replication?

A

RDRP, RNA-dependent RNA Polymerase

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6
Q

mRNA is always what “sense”?

A

(+) or sense strand

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7
Q

Why do all RNA viruses encode an RNA polymerase?

A

Because a host cell cannot take RNA and transcribe it, therefore the virus needs to be able to transcribe its own RNA to make mRNA

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8
Q

Where does RDRP do its job?

A

Cytoplasm, except for influenza

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9
Q

Where does virus replication often take place?

A

On cell membranes of endosomes, lysosomes, ER vesicles…this concentrates the components (*not floating free in cytoplasm) and increases their efficiency.

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10
Q

What is the estimated error rate of RDRP?

A

1 in 10^3 to 1 in 10^4 nucleotides, sloppy, therefore all RNA virus stocks are a mixture of the starting genome and random mutations, not to mention recombination…

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11
Q

What are some effects of viral recombination?

A

Antigen changes, virulence changes, host range changes etc.

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12
Q

Name the segmented RNA viruses

A 
Reoviridae
Bunyaviridae
Retroviridae
Arenaviruses
Orthomyxo viruses
Influenza virus
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13
Q

What is a quasispecies?

A

Every virus is a mixture of genes, “a cloud,” therefore mutants arise frequently, new variants cause new diseases, and drugs and vaccines can lose effectiveness

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14
Q

Name this virus:
(+) ssRNA genome, linear mRNA molecule
enterovirus, picornavirus
can spread to muscles and nerves causing flaccid paralysis

A

Poliovirus

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15
Q

What is the mode of transmission for poliovirus?

A

Fecal-oral, can exist in water systems without dying, infected but asymptomatic people can shed virus readily, difficult to contain even with good sanitation

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16
Q

What is the pathogenesis profile for poliovirus?

A

95% get a an acute GI infection
5% get a mild, disseminated disease
1% get paralytic infection of motor neurons

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17
Q

CD155 receptor is also known as:

A

PVR, “poliovirus” receptor

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18
Q

What is the method of cell entry of poliovirus?

A

Endocytosis, only genome fully enters cell

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19
Q

3D^pol is poliovirus’s:

A

RDRP

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20
Q

True or False: RDRP copies only (+) strands.

A

False, RDRP copies both (+) and (-) strands.

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21
Q

When capsid proteins accumulate, mRNA is:

A

packaged instead of translated. This is a switch from mRNA to genome RNA synthesis.

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22
Q

What are some issues encountered with (+) sense RNA?

A
  1. Collisions between RDRP and ribosomes can occur
  2. If RDRP is scarce, translation happens first
  3. If RDRP is abundant, (-) RNA synthesis comes later
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23
Q

All RNA viruses encode __1__ and retroviruses encode __2__.

A
  1. RDRP

2. reverse transcriptase

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24
Q

(-) RNA and dsRNA viruses __1__ package RDRP in the virion. (+) RNA viruses __2__ package RDRP in the virion. If RDRP is not present in the virion, what must happen before replication can begin?

A
  1. must
  2. may or may not
    If RDRP is not present in the virion, then protein synthesis is necessary to make the RDRP before replication can begin.
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25
Q

What are the treatments for polio?

A

Supportive care, control breathing if paralysis has affected breathing.

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26
Q

What are the characteristic identifiers of rotavirus?

A

Reovirus
dsRNA
segmented
icosahedron

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27
Q

What are the characteristic identifiers of influenza virus?

A

Orthomyxovirus
(-) ssRNA
segmented
enveloped

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28
Q

What are the characteristic identifiers of HIV?

A

Retrovirus
(+) ssRNA, 2 copies
enveloped

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29
Q

What are the symptoms of rotavirus?

A

Severe vomiting and diarrhea
Peaks in winter
Maladsorption
Kills >1/2 million people yearly

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30
Q

What is a viroplasm?

A

An area of the cytoplasm that is being heavily occupied by replicating and assembling virions

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31
Q

In rotavirus, after viral proteins are translated, __1__ and genome segments are synthesized in the __2__.

A
  1. New virions

2. Cytoplasm

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32
Q

Where do rotavirus virions gain their coat proteins before leaving the cell?

A

ER

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33
Q

How does rotavirus leave the cell?

A

Lysis OR exocytosis

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34
Q

What kinds of influenza virus infections exist?

A
  1. Uncomplicated

2. Complicated - flu + pneumonia, myositis, rhabdomyolysis

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35
Q

What RNA virus traffics to the nucleus to release its genome using a ribonucleoprotein?

A

Influenza virus

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36
Q

How does influenza virus leave the host cell?

A

Budding

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37
Q

Neuraminidase is also known as:

A

N antigen

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38
Q

What is the function of N antigen?

A

N antigen, or neuraminidase, releases influenza virions from sialic acid on cell surface.

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39
Q

What are the components of the influenza vaccine?

A

It is a trivalent vaccine that contains 3 of the most expected strains antigens.

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40
Q

The HIV virion contains 2 copies of:

A

RNA genome

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41
Q

How does the HIV virus attach to the host cell?

A

HIV env protein binds to CD$+ and chemokine co-receptors on cell surface

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42
Q

What is the first step in HIV replication after uncoating?

A

Reverse transcriptase takes RNA and “transcribes” it back to dsDNA

43
Q

What is unique about HIV’s actions in the host nucleus?

A

The DNA, once formed in the cytoplasm, moves into the nucleus and inserts itself into host DNA, an irreversible event.

44
Q

What do types of HIV drugs target?

A
  1. Nucleoside reverse transcriptase inhibitors (NRTIs)
  2. Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
  3. Protease Inhibitors (PIs)
  4. Integrase strand transfer inhibitors (INSTIs)
  5. CCR5 antagonists
45
Q

Trivalent influenza vaccine is made of:

A

2 strains of A and 1 strand of B

46
Q

True or False: RDRP synthesizes mRNA AND dsRNA genome segments in the cytoplasm.

A

True

47
Q

While retroviruses use host RNA Pol to replicate their genome, DNA viruses can use:

A

Either host or viral DNA polymerase replicates the genome

48
Q

Herpesviruses and Adenovirus have what kind of DNA?

A

dsDNA

49
Q

In the transcription of mRNA of a DNA virus, whose polymerase is used?

A

Host RNA Polyermase

50
Q

True or False: Our transcription factors can be recruited to viral promoters.

A

True, as well as RNA Polymerase II

51
Q

Viral TF’s are important _____ and may even be essential proteins.

A

virulence factors

52
Q

Small DNA viruses do not encode their own ____ for replication of the genome.

A

polymerase

53
Q

Large DNA viruses encode their own __1__ and __2__.

A
  1. polymerase

2. accessory proteins

54
Q

Name two large DNA viruses:

A

Adenovirus

Herpesvirus

55
Q

DNA Polymerases have higher replicative fidelity than:

A

RDRP

56
Q

What is one effect of DNA viruses being more genetically stable?

A

They must interact with the immune system more.

57
Q

What DNA viruses are the most common causes of disease?

A

Adenovirus
Papillomavirus
Herpesvirus

58
Q

Adenovirus has the following sequelae:

A

A bad cold with a fever
Pharyngoconjuctival fever
Laryngitis, cough
Pneumonia

59
Q

What is the transmission of adenovirus?

A

Aerosol, fecal-oral, objects, poorly chlorinated swimming pools

60
Q

Talk me through the cycle of adenovirus.

A
  1. Highly toxic adenovirus fiber protein binds to cell receptor.
  2. Endocytic entry to host cell.
  3. Endosome acid causes fibers to come off the adenovirus and lyse the vesicle.
  4. Capsid traffics to nucleus and DNA genome uncoats through the nuclear pore.
  5. Genome replicates inside the nucleus.
  6. Host RNA Pol II makes mRNA
  7. There are 3 gene expression phases: immediate early, early and late
  8. Gene replication by viral DNA Pol
  9. Capsid assembly in nucleus
  10. Virions egress by lysis
61
Q

Does the adenovirus capsid enter the host nucleus?

A

No, the NLS brings the capsid to the nuclear membrane to fuse, and the genome is injected into nucleus. The genome inside the capsid is under pressure.

62
Q

What are the first viral proteins made in adenovirus replication and transcription?

A

Host RNA Pol II makes mRNA for transcription factors

63
Q

What is the recommended treatment (for emergencies) for treating Adenovirus? What is the risk?

A

Cidofovir, very bad for kidneys

64
Q

The adenovirus vaccine is only allowed for:

A

military personnel

65
Q

What is the major version of adenovirus controlled by the vaccine?

A

Ad4

66
Q

Human papilloma viruses attack only:

A

epithelial cells

67
Q

What kinds of cancers have been traced back to HPV?

A
  1. Head and neck cancer
  2. Cervical cancer
  3. Penile cancer
68
Q

Where in the epidermis does HPV infection settle?

A

Basal epidermis

69
Q

The HPV genome maintains itself in the host cell as:

A

Loops, kind of like bacterial plasmids

70
Q

Viral factors __1__ and __2__ are oncogenes.

A
  1. E6
  2. E7
    These modify host cells and force them to continually divide.
71
Q

Hoes does HPV replicate?

A
  1. HOST RNA Pol transcribes viral mRNA

2. HOST DNA Pol synthesizes viral genomes

72
Q

What is a VLP?

A

Virus-like particles composed of empty capsids, used in Guardasil,

73
Q

Guardasil covers what strains of HPV?

A

6, 11, 16, 18

74
Q

What is the most common STI in the US?

A

HPV

75
Q

Most people are infected with >3 _____.

A

Herpesviruses

76
Q

What is a dense body?

A

A herpesvirus with no capsid, just a ball of tegument.

77
Q

In herpesvirus replication, the first mRNAs made are for the:

A

immediate early stage genes

78
Q

In herpesvirus, genome replication is by:

A

viral polymerase and accessory factors (huge genome, capable of doing this on its own)

79
Q

The herpesvirus life cycle is most like:

A

Adenovirus

80
Q

What is the method of egress of herpesvirus?

A

Exocytosis

81
Q

What is the major barrier to creating a herpesvirus vaccine?

A

Latency. HVs establish latency prior to a host becoming symptomatic, or replication occurs. Vaccine trials failed.

82
Q

What is the definition of latency?

A

As seen in HV, the genome is present in a cell but infectious virions are absent. In this way, the genome is maintained for the life of the infected host.

83
Q

In HV, children often have this, which adults rarely do:

A

Primary infection. Most adults have recurrent disease.

84
Q

True or False: Lesions in a recurrent outbreak of HV are not contagious.

A

False. They are contagious! This is shedding.

85
Q

HSV-1 and 2 primary infections can cause:

A

Meningitis

86
Q

Ulcers on the sacral region, caused by HSV-2, are often mistaken for:

A

shingles

87
Q

How do you distinguish between HSV 1 and 2?

A

Serology or PCR

88
Q

What is the most contagious herpesvirus?

A

VZV

89
Q

Where is the latency of VZV maintained?

A

Dorsal root ganglia

90
Q

What is a bacterial complication of VZV?

A

Infection of pustules by MRSA or strep etc.

91
Q

What are some complications of HZ (shingles)?

A

Bell’s palsy
Postherpetic neuralgia
Retinitis

92
Q

What is the method of transmission of Epstein Barr Virus?

A

Saliva

93
Q

Where does Epstein Barr virus establish latency?

A

B cells

94
Q

EBV is associated with what long-term effects?

A

Lymphomas, oral hairy leukoplakia

95
Q

Where does CMV establish latency?

A

Stem cells

96
Q

What is the highest risk associated with CMV?

A

If a pregnant woman has a primary infection of CMV, 2%

97
Q

Hearing loss is one bad complication of:

A

Congenital CMV

98
Q

What is the method of transmission of CMV?

A

Body fluids/close contact

99
Q

HHV6b and HHV7 are the causes of:

A

Roseola. Every baby will get this 2x.

100
Q

What is the method of transmission of roseola?

A

Saliva

101
Q

Where do the roseola viruses, HHV6b and HHV7 establish latency?

A

CD4+

102
Q

True or False: Roseola viruses have no seasonality.

A

True.

103
Q

_______ is a risk for all HV’s to reactivate or cause malignancy.

A

Immunosuppression

Unit 2 (11 decks)

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