Viral Infections Flashcards

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1
Q

What are the 7 groups of viruses

A

dsDNA, ssDNA, dsRNA, +ssRNA, -ssRNA, rtDNA, rtRNA

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2
Q

The Baltimore classification system is based on…

A

Nucleic acid present in the virion particles and the pathway for expression of the genetic material

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3
Q

+ssRNA vs -ssRNA: infectivity

A
\+ssRNA = infectious right away, directly translated into proteins
-ssRNA = not infectious right away, needs to be converted to +ssRNA first
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4
Q

Ambisense ssRNA

A

Virus resembles a negative sense RNA virus, but they can also translate genes from the positive strand

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5
Q

Viral entry is initiated by… (3)

A
  1. Conformational changes in virus that expose receptors for membrane fusion and penetration
  2. Transmit signals through membrane to prepare cell for invasion
  3. Induction of endocytic pathway
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6
Q

2 ways RNA viruses replicate their genomes

A
  1. RNA dependent RNA synthesis

2. RNA dependent DNA synthesis (RT) followed by DNA replication and transcription (Retroviruses)

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7
Q

What is a downside of a high error rate for RNA viruses

A

Error rates impose an upper limit on genome size (most are 5-15kb)

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8
Q

Virus assembly: non-enveloped vs enveloped

A

Non-enveloped can assemble in the cytoplasm or nucleus

Enveloped must get a lipid bilayer from a host cell membrane during assembly

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9
Q

4 steps of non-enveloped virus assembly

A
  1. Macromolecules form empty capsids
  2. Viral DNA is inserted via packaging sequence at one end
  3. Precursor core proteins are also packaged
  4. Proteolytic cleavage of precursors proteins by proteinase makes infectious virion
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10
Q

3 pathways of enveloped virus assembly

A
  1. Proteins transported to PM and capsid assembly and envelopment occur simultaneously
  2. Capsid assembly happens in cytoplasm and virus buds from PM to get its membrane
  3. Capsid assembly happens in ER, gets its envelop from ER and is exocytosis
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11
Q

Enteric viruses do not multiply in…

A

Food systems

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12
Q

What is poliovirus associated with

A

Milk and milk products

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13
Q

What kills polio in milk

A

Pasteurization above 70C for 30 seconds

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14
Q

How is polio transmitted

A

Fecal oral route, it multiplies in the intestine

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15
Q

What does polio do in the body

A

It invades the nervous system and can cause total paralysis in hours

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16
Q

Initial symptoms of polio in the body

A

Fever, fatigue, headache, vomiting, stiffness of neck

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17
Q

Genome and capsid of polio

A
RNA genome (+ssRNA)
Non-enveloped
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18
Q

What are the 3 serotypes of the polio and what is different about them

A

PV1, PV2 and PV3

Each has a slightly different capsid

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19
Q

What is the most common polio serotype

A

PV1, localized in Pakistan and Afghanistan

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20
Q

Polio: 5’ NTR region

A

Harbors 2 domains, cloverleaf and internal ribosome entry site
Covalently linked to viral protein VPg

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21
Q

What does the cloverleaf structure do

A

Regulates viral RNA replication and the initiation of translation

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22
Q

What does the IRES domain do

A

Mediates translation of viral mRNA

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23
Q

How is polio mRNA translated

A

As one long polypeptide, later cleaved into mature structural and non-structural proteins by proteolytic processing

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24
Q

P1 precursor protein of polio is cleaved into what

A

VP1, VP3 and VP0

25
Q

What does HAV effect

A

The liver

26
Q

Duration and symptoms of HAV

A

8 weeks

Nausea, vomiting, diarrhea, jaundice, fever, abdominal pain

27
Q

How is HAV spread

A

Fecal oral route, and undercooked contaminated seafood

28
Q

If you get HAV once…

A

You are immune for life

29
Q

Genome and capsid of HAV

A
RNA genome (+ssRNA)
Non-enveloped
30
Q

How many proteins does HAV encode

A

A single polyprotein

31
Q

What part of the HAV polyproteins codes for the major capsid proteins

A

The N-terminal (the rest encodes series of nonstructural proteins required for HAV RNA replication)

32
Q

What is the function of VPg on the 5; end of HAV genomic RNA

A

A protein primer for RNA synthesis

33
Q

How does HAV spread in the body

A

By secretion from infected hepatocytes via the biliary system

34
Q

When does fecal shedding of the virus reach its max

A

Just before the onset of hepatocellular injury (individual is most infectious)

35
Q

What accompanies fecal shedding in HAV infection

A

Extended viremia, but at a lower magnitude

36
Q

What is indicative of hepatocellular injury

A

Serum alanine aminotransferase

37
Q

When are norovirus outbreaks most common

A

In fall and winter months

38
Q

What is the contagious period of norovirus

A

The moment they feel ill to 3 days after recovery (sometimes two weeks)

39
Q

Where is norovirus found in human secretions

A

The stool and vomit

40
Q

3 ways someone can be infected with norovirus

A
  1. Direct contact
  2. Touching surfaces
  3. Eating/drinking contaminated sources
41
Q

How is norovirus spread

A

Fecal oral route, sometimes shellfish

42
Q

Main symptoms of norovirus

A

Diarrhea, vomiting, nausea, stomach cramps (less common can be headache, chills, fever)

43
Q

Genome and capsid of norovirus

A
RNA genome (+ssRNA)
Non-enveloped virus
44
Q

What norovirus genogroup is the most prevalent in humans

A

Genogroup II

45
Q

What NoV genogroups infect: humans, bovine, mice

A

Humans: I, II, IV
Bovine: III
Mice: V

46
Q

What does ORF1 in NoV encode

A

A single nonstructural polyprotein

47
Q

What does ORF2 in NoV encode

A

VP1 capsid protein (divided in shell and protruding domains)

48
Q

What does ORF3 in NoV encode

A

Minor structural protein VP2

49
Q

What does ORF4 in NoV encode and where is it found

A

Only in mice NoV

Encodes virulence factor 1 (newly defined)

50
Q

Why are rotavirus infections rare in adults

A

Because you get it as a kid (before the age of 5) and immunity develops with each infection so subsequent infections are less severe

51
Q

How is rotavirus transmitted

A

Fecal oral route

52
Q

Treatment for rotavirus

A

Oral rehydration and vaccination to prevent infection

53
Q

Rotavirus symptoms

A

Nausea, vomiting, watery diarrhea and low-grade fever

54
Q

What is the most common cause of death related to rotavirus infection

A

Diarrhea

55
Q

Genome and capsid of rotavirus

A
RNA genome (dsRNA) - segmented, linear
Non-enveloped virus
56
Q

How does rotavirus achieve rapid evolution through genetic reassortment

A

If someone is co-infected with two strains, the segmented genome allows them to be mixed and packaged into a new virion

57
Q

What is the surface of the rotavirus made of

A

The VP7 glycoproteins and embedded with the VP4 spike attachment protein

58
Q

Why is the dsRNA genome of the rotavirus never completely uncoated

A

To prevent activation of the an antiviral state by the cell in response to the dsRNA