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Micro Patho > Virology > Flashcards

Virology Flashcards

1
Q

What are the key characteristics of HIV retroviridae?

A
  • RNA genome
  • reverse transcriptase (RNA to DNA)
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2
Q

What is the envelope of HIV retroviridae?

A

host-derived envelope surrounds capsid

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3
Q

What are the proteins of HIV retroviridae?

A

nucelocapsid (NC), capsid (CA), and matrix (MA) proteins

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4
Q

What are the two types of pathogenic human retroviruses?

A
  • HIV
  • Human T cell lymphotrophic virus (HTLV)
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5
Q

What are the symptoms of HIV during acute infection?

A
  • sore throat and fever
  • immune system recovers and destroys most virions
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6
Q

What are the symptoms of HIV during clinical latency?

A
  • skin issues (dermatitis, eczema, psoriasis)
  • T cell count continues to drop
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7
Q

What are the symptoms of HIV during secondary infection?

A

chronic infections common bc immunocompromised
- oral/vaginal thrush
- gastrointestinal illnesses
- cancers

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8
Q

What does Gag’s function? (1 of the 4 common genes that all retroviruses have)

A

Encodes polyprotein that contains MA, CA, and NC proteins
all 4 package into HIV virion

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9
Q

What does Pro’s function? (1 of the 4 common genes that all retroviruses have)

A

Encodes protease to cut Gag and Pol into separate proteins
all 4 package into HIV virion

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10
Q

What does Env’s function? (1 of the 4 common genes that all retroviruses have)

A

Encodes 2 diff envelope glycoproteins
all 4 package into HIV virion

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11
Q

What does Pol’s function? (1 of the 4 common genes that all retroviruses have)

A

Encodes 2 diff enzymes as polymerase
all 4 package into HIV virion

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12
Q

Which HIV protein are used to attach?

A

gp120 surface protein and CD4 protein on target cells

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13
Q

Which receptors do the HIV attachment protein (gp120) bind to?

A

CCR5 or CXCR4 coreceptors

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14
Q

How is the nucleocapsid in HIV released and where?

A
  • How: after gp41 dissociates and changes confirmation
  • Where: released into the cytosol
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15
Q

What happens if the virion in HIV enters via endocytosis?

A

It’s a dead end and non productive

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16
Q

Where does uncoating occur and which proteins are released in HIV?

A
  • Disassembles into cytosol
  • Viral and cellular proteins
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17
Q

What is the final outcome of reverse transcription in HIV?

A

Double stranded DNA viral genome

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18
Q

Where does RT occur in HIV?

A

in cytosol while synthesizing complimentary copy of ssDNA

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19
Q

How does the HIV viral genome get into the nucleus?

A

semi-intact capsids attach to MT (and actin MF and vimentin IF) to move towards nucleus

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20
Q

What happens once the HIV viral genome is in the nucleus? (i.e. enzymes involved?)

A

Inserted into the host genome by cutting from LTR and chromosome to ligate strands together

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21
Q

Which enzymes are used for gene expression and replication in HIV?

A

LTR, Tat, and Rev

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22
Q

Are the enzymes are used for gene expression and replication viral or host enzymes?

A

All 3 are viral enzymes

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23
Q

What is the role of LTR enzyme in HIV?

A

Promoter region where transcription begins

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24
Q

What is the role of Tat enzyme in HIV?

A

Transcription factor that guides RNA polymerase to host genome

(more transcription of HIV)

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25
Q

What is the role of Rev enzyme in HIV?

A

Viral mRNA’s are capped and transported out of nucleus

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26
Q

How are new virions replicated and released in HIV?

A

HIV replicated with CD4+ helper T cells and enhanced by Vpu protein

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27
Q

Which enzymes are involved in HIV maturation and what is their role?

A
  • Vpu protein: Envelope on HIV is enhanced and removed CD4 helper from membrane
  • Nucleocapsid coats RNA
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28
Q

How is HIV transmitted?

A
  • Sexually
  • Blood exposures (needles, IV drugs)
  • Vertically (mother to child)
    must penetrate through tissue
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29
Q

Which cell types does HIV bind to?

A

CD4+ Th cells and macrophages

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30
Q

How does HIV spread and where?

A

Moves through blood, and reach brain (dementia) and immune cells

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31
Q

What type of damage does HIV cause directly vs. damage caused by our own immune system?

A

HIV causes: Inactivation of monocytes/macrophages = death of helper T cells

Our body: Infected macrophages release inflammatory cytokines (dementia)

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32
Q

What strategies does HIV use to evade the host immune response?

A
  • HIV nef: binds to plasma membrane and triggers endocytosis
  • Hiding in macrophages and stem cells
  • Kills Th cells and inactivated macrophages
  • Mutations in RT
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33
Q

How is HIV diagnosed?

A

ELISA or PCR, confirmed with Western blot

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34
Q

How is HIV treated?

A

HAART (Highly active antiretroviral therapy)

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35
Q

What types of drugs are currently available for HIV and what do they target?

A
  • Reverse transcripterase: blocks active site or allosteric inhibition
  • Protease inhibitors: Blocks virion maturation and spread
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36
Q

How is HIV prevented?

A

Safe sex, don’t share needles, treat mothers with anti-retrovirals, don’t recap needles

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37
Q

Common features of negative sense RNA viruses

A
  • Size: small genetically
  • Structure: enveloped negative-sense RNA genome
  • Replication: only in cytosol (NO DNA INVOLVED)
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38
Q

What do Rhabdoviruses look like structurally and genetically?

A

Structure: bullet shaped helical capsid
Genetically: single pieces of neg sense RNA

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39
Q

Two main types of Rhabdoviruses that cause human disease

A

VSV and Rabies

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40
Q

Location of Nucleoprotein in structure of Rhabdoviruses virions

A

Nucleocapsid

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41
Q

Function of Nucleoprotein in structure of Rhabdoviruses virions

A

Protects RNA genome

42
Q

Location of Polymerase phosphoprotein in structure of Rhabdoviruses virions

A

Associated w nucleocapsid

43
Q

Function of Polymerase phosphoprotein in structure of Rhabdoviruses virions

A

RNA polymerase subunit

44
Q

Location of Matrix in structure of Rhabdoviruses virions

A

Between nucleocapsid and envelope

45
Q

Function of Matrix in structure of Rhabdoviruses virions

A

Virion assembly

46
Q

Location of glycoprotein in structure of Rhabdoviruses virions

A

Transmembrane envelope glycoprotein

47
Q

Function of glycoprotein in structure of Rhabdoviruses virions

A

Viral attachment protein

48
Q

Location of large protein in structure of Rhabdoviruses virions

A

Associated with nucleocapsid

49
Q

Function of large protein in structure of Rhabdoviruses virions

A

RNA polymerase

50
Q

What specific viral proteins are involved in replication of Rhabdoviridae and what do they do?

A
  • G protein: binds to host receptors
  • L/P: uses genome to make gene into full length
  • G and M: newly made G and M get sent to plasma membrane
51
Q

Characteristic symptoms of early Rabies infection

A

Fever, headache, twitching tingling at site of infection

52
Q

Characteristic symptoms of later Rabies infection

A

Confusion, increased salvation (frothing), hydrophobia, eventual coma and death

53
Q

How is Rabies acquired (and what types of animals)?

A

Contact with saliva from infected animal following a bite

Can get from cats and dogs, bats, raccoons, foxes, etc

54
Q

What are the two major clinical forms of Rabies seen in dogs?

A
  • Excitable form: animals become irritable and hyperactive (frothing), prone to attacking other animals
  • Dumb form: Animals stop eating, throat closes and dies
55
Q

How does the Rabies virus attach to our cells (receptor, viral protein, cell type(s))?

A

Virus attaches to unknown cell receptors on muscle tissue and connective tissue

56
Q

After initial replication, where does the Rabies virus go in the body and how?

A

Virus binds to peripheral neuron axon terminus and enters cytosol

Attaches to NAR and moves from peripheral to CNS

57
Q

After replicating in that new location, where does the Rabies virus go next and how?

A

Replicates well in brain and spinal cord, then spreads to all the tissue in the body and salivary glands

58
Q

How does the Rabies virus evade destruction by Tc cells?

A

FasL kills invading T cells

Leads to virally infected cells surviving

59
Q

What causes damage during Rabies infection and how does that occur?

A

Infected cells have cytosolic inclusions (metabolic products)

60
Q

What are Negri bodies?

A

Round inclusions in the cytoplasm of nerve cells in animals infected with Rabies

61
Q

What is special about the viral N protein in Rabies?

A

Can function as a superantigen (excessive activation of immune system)

62
Q

How is Rabies diagnosed?

A
  • Remove brain from infected and do cross section to look for Negri bodies. Inject brain tissue into mice
  • Interstitial fluid of brain tagged for anti-rabies antibodies
  • PCR from saliva
63
Q

How is Rabies prevented?

A

Prevent bites, stay away from wild animals, vaccinate pets and wild animals

64
Q

How is Rabies treated?

A

NO treatment exists once symptoms appear!

65
Q

General structure of Influenza virion

A
  • Segmented RNA genome
  • Encapsulated by NP protein
  • Nucleocapsid surrounded by matrix protein
66
Q

What is different about Influenza genome (when compared to other Rhabdoviruses)?

A

Influenza is segmented (contains multiple pieces of RNA)

67
Q

Differences between Influenza A vs B/C viruses

A

Flu A: major pathogen that infects, multiple mutations can occur

Flu B and C: Minor outbreaks, no animal reservoir, rare mutations

68
Q

What are the symptoms of Influenza disease?

A

Fever, headache, muscle ache, dry cough

Secondary illnesses can occur (pneumonia, bronchitis, encephalitis)

69
Q

Basic history of major flu pandemics

A
  • First epidemic: 1500
  • Spanish Flu: 1918
  • Asian Flu: 1957
  • Hong Kong Flu: 1968
70
Q

How is Influenza virus transmitted?

A

Person to person contact, through respiratory droplets

71
Q

How does the Influenza virus attach to our cells?

A

HA protein binds to sialic acid linked to galactose found in respiratory epithelial cells

72
Q

What viral protein and host receptors are involved in Influenza?

A

HA must recognize sialic acid-gal linkage

73
Q

What is different about the receptor in birds, humans, and pigs in Influenza?

A

Humans have A2-6 receptors

Birds and pigs have A2-3

74
Q

How does the receptor affect NA and HA compatibility in Influenza?

A

NA must match HA for infectivity

75
Q

How does the Influenza virus enter the cell?

A

Endocytosis occurs, allowing for acidification of the endoscope

76
Q

In Influenza, once in a phagosome, acidification takes place. What are two affects of that acidification?

A
  • Causes HA to do conformational change (Fusion of envelope with endoscope)
  • M2 protein allows H+ to trigger uncoating
77
Q

Where do released genomic pieces go and why does it go there (and why is that unique to Influenza)?

A

Genomes transported out via nuclear pore

78
Q

What role does NS2 play in viral replication of Influenza?

A

Export viral mRNA to cytosol

79
Q

What role does NA play in the release process of Influenza?

A

Cuts and releases into surface, also cuts of SA off of envelope

80
Q

How do the viruses spread in Influenza?

A

Particals released from apical surface inject into respiratory epithelial tissue

81
Q

What type of tissue damage is observed (and what tissue is primarily affected)?

A

Extensive damage to alveoli, massive edema (pneumonia), necrosis and hemorrhage

82
Q

What is unique about H5N1 in Influenza?

A

It’s a strain that is neurotrophic and can spread to CNS (not typical)

83
Q

What is meant by antigenic drift vs shift in Influenza?

A

Drift: MUTATIONS

Shift: COMPLETELY DIFF GENE MADE

84
Q

Why are pigs special and what is meant by a sentinel animal in Influenza?

A

Pigs have sialic acid found in humans and are reservoir for diff flus mixing together

85
Q

How is Influenza diagnosed?

A

RT-PCR, rapid flu, and immunofluorescense

86
Q

Structure of the measles virus

A

Genome = single RNA strand
Found within helical capsid

87
Q

What are symptoms of Measles?

A

1-2 weeks post infection: fever, cough, conjuctivitis, rash, and Koplik spots

88
Q

What are Koplik spots in Measles?

A

Raised white spots on the tongue with irregular redness (can’t be scraped off)

89
Q

How is Measles transmitted between hosts?

A

Inhalation of respiratory droplets, can also be acquired from eye exposure to respiratory droplets

90
Q

How does Measles attach (viral proteins and host receptors involved?) and what occurs as a result?

A
  • H protein attaches to receptors on epithelium
  • Binds to CD46 protein and unknown receptor
  • Binding triggers endocytosis
91
Q

What role does the F protein play in the Measles process?

A

Causes membrane fusion

92
Q

What are multinucleated giant cells (syncytia) and how do they arise in Measles?

A

Multiple cells fused together to make one big cell, HELPS VIRUS SPREAD

93
Q

Where does Measles spread initially and what happens as a result?

A

Virions released spread into bloodstream, can cause primary veremia

94
Q

Where does Measles spread during the second viremia?

A

GI tract, skin, CNS

95
Q

How does Measles damage our tissue?

A

Mediated cell death, inflammation and cell-mediated immunity can lead to Encephalitis

96
Q

How is Measles diagnosed?

A

Immunofluorescence and ELISA

97
Q

How is Measles treated?

A

No actual treatment besides waiting it out (give vitamin A and treat symptoms)

98
Q

How is Measles prevented?

A

Vaccine

99
Q

How is Influenza treated?

A

Inhibit M2 and uncoating and inhibit neuraminidase

100
Q

How is Influenza prevented?

A

Vaccine

Micro Patho (2 decks)

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