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BIO 435: Virology > Viral Pathogenesis > Flashcards

Viral Pathogenesis Flashcards

1
Q

What are the Six steps that viruses employ to propagate and survive?

A
  1. Enter the cell and translocate the genome to the site of replication
  2. Replicate its genome and produce mRNA
  3. Generate viral proteins
  4. Assemble progeny viruses and then emerge from the cell
  5. Evade host defenses
  6. Disperse and persist in the environment
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2
Q

What are the Basic requirements for the initiation of infection?

A
  1. Sufficient virus must be present
  2. Cells at the site of infection must be accessible, susceptible, and permissive for the virus
  3. Host antiviral defense must be absent or lacking
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3
Q

How do viruses cross the hydrophobic, selectively permable lipid bilayer membrane of the host?

A

By hijacking one or more receptors on the host cell

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4
Q

What receptors does HIV use to gain entry to the host cell?

A
  1. Primary receptor bound first (CD4 - TH)
  2. Secondary receptor (co-receptor)
    - Th: CXCR4
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5
Q

What receptors does HSV use to gain entry to the host cell?

A
  1. initially bind to glycosaminoglycans (GAG) sugar molecules on the cell surface
  2. bind a protein receptor (nectin-1 or HVEM) to initiate entry
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6
Q

What are some examples of viruses that can use multiple different receptors on a cell to gain entry?

A

Rabies and HSV too

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7
Q

What are the benefits of a virus having the ability to use multiple different receptors to gain entry to a host?

A

The virus will have an expanded host range because there are multiple types of receptors it can use

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8
Q

What glycoproteins does HSV have on its surface?

A

gB, gC, gD

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9
Q

How does HSV gain entry to a cell?

A
  1. gB and gC: binding to Glycosaminoglycans (GAG) which are sugars on surface of cell
  2. gD: binds to nectin-1 (primary receptor) or HVEM (also works)
  3. Virus enters cells (endocytosis or direct fusion depending on cell type)
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10
Q

What is the relationship between viruses of the same family and receptors?

A

Many viruses from the same family evolve to use similar receptors

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11
Q

What is EHV?

A

Enveloped virus w/ icosahedral capsid and large dsDNA genome

-no vaccines

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12
Q

what is the pathogenesis of EHV-1?

A
  1. Initial Respiratory Infection
    - most horses recover quickly but virus enters latent stage
  2. Abortigenic Disease
    - causes viremia and infection of endometrium
  3. Neurological Disease
    - can lead to myeloencephalopathy
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13
Q

What did Dr. Frampton’s team know about EHV before beginning their experiment?

A
  1. Glycoprotein D (gD) on surface of EHV-1 essential for entry into host cell
  2. EHV-1 entry via direct fusion w/ host plasma membrane and then endocytosis
  3. After entry EHV-1 travels along microtubules to reach host nucleus
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14
Q

How did Dr. Frampton discover Glycoprotein D (gD) was essential for entry?

A

Knock out gD from EHV-1 by going into viral genome and making deletion

  • they made a Glycoprotein D knockout virus
  • put this gD knockout virus on cells it doesn’t get in
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15
Q

What role do Glycoproteins B, C and D play in EHV-1 entry?

A

Other groups discovered:

  • gB would bind Glycosaminoglycans (GAG)
  • gC would also bind GAG

Dr. Frampton discovered:
-gD was important for entry but didn’t know what receptor it used

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16
Q

When Dr. Frampton was beginning this experiment to discover what receptors EHV-1 uses. What was his first question?

A

EHV-1 is an alphaherpesvirus, Does EHV-1 utilize any of the known alphaherpesvirus entry receptors?

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17
Q

What were the previously identfied alphaherpesvirus entry receptors?

A

HveA (HVEM) Co-receptor and HveC (nectin-1)

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18
Q

What kinds of cells did Dr. Frampton use to test EHV-1 on in his study?

A

He used Chinese Hamster Ovary (CHO-K) cells because

1) They were resistant to alphaherpesvirus infection
- HSV-1, HSV-2, BHV-1
- EHV-1 unknown?

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19
Q

CHO-K cell line is resistant to infection from HSV-1, HSV-2 and BHV-1. What did researchers do to manipulate this cell lines and allow infection?

A

Engineered this cell line to express entry receptors HveA (TNF-R) and HveC (nectin-1)

  • CHO-A: Expression of HveA allowed infection by HSV-1 & HSV-2
  • CHO-C: Expression of HveC allowed infection by HSV-1, HSV-2, and BHV-1
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20
Q

Dr. Frampton tested Whether EHV-1 is mediated by HveA or HveC by testing it on CHO-K, CHO-A, and CHO-C. What were the resulsts? What was his control?

(sequenced genome of EHV-1, engineered virus to insert reporter gene that expressed beta-galactosidase. Now they could add a substrate and if virus was present in cell then it would light up blue)

A

His control was testing HPV-1 on all three cell lines
-result: CHO-K = no infection; CHO-A/CHO-C = infection

When testing EHV-1 on all three cell lines
-CHO-K (control) , CHO-A, CHO-C all became infected

Conclusion: EHV-1 must be using a different surface receptor that HveA or HveC

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21
Q

How did Dr. Frampton go about finding the receptors that EHV-1 uses to gain entry into cells?

A

Need Resistant cells and Susceptible/Permissive cells

  1. Got cDNA libary for permissive cell line, equine macrophages
    - somewhere in library is transcript for entry receptor
  2. Got mouse melanoma cells that were resistant to infectino from EHV-1
    - don’t have receptor for virus
  3. Separate the cDNA into pools and add all of cDNA’s from macrophage line and assay for infection
    - if infection occurs then the gene that codes for that receptor is somewhere in the pool of cDNA
    - further divide that pool
  4. Amplified and sequenced the incorporated equine macrophage cDNA
  5. Equus caballus MHC class I was the receptor
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22
Q 
How did Dr. Frampton confirm Equus caballus MHC class I
was in fact the receptor used by EHV-1?
A 
Took the mouse melanoma cells that were resistant to EHV-1 and inserted Equus caballus MHC class I genes to see if susceptible to infection
-put fluroescent tag on Fc region of antibody that binds MHC I

To further prove it was MHC I he also loaded anti-MHC I antibodies on to host cell to see if it blocked EHV-1 from binding these receptors
-control: use another antibody to block cell surface receptor

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23
Q

What cell types do viruses target after gaining entry?

A
  1. Respiratory tract
  2. Gastrointestinal tract
  3. Genital tract
  4. Conjunctiva (eyes)
  5. Skin
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24
Q

What routes of entry do viruses use to get into host?

A
  1. Respiratory Tract
  2. Alimentary Tract
  3. Urogenital Tract
  4. Eyes
  5. Skin
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25
Q

What are the host barriers to infection?

A

Respiratory tract

Gastrointestinal tract

Urogenital Tract

Eyes

Skin

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26
Q

What is in the respiratory tract that blocks viral infection?

A
  • mucociliary blanket (ciliated cells, mucous-secreting goblet cells)
  • macrophages
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27
Q

What is in the Gastrointestinal tract that blocks viral infection?

A
  • mucous-lined intestinal tract
  • alkaline conditions in intestines
  • acidic conditions in stomach
  • proteases
  • phagocytic cells
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28
Q

What is in the urogenital tract that blocks viral infection?

A
  • low pH

- mucous

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29
Q

What is in the eyes that blocks viral infection?

A
  • secretions

- sclera

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30
Q

What is in the skin that blocks viral infection?

A
  • many layers

- dead skin (surface layer) cannot support virus growth

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31
Q

What is the most common route of entry for viruses? What are some examples?

A

viruses enter Repsiratory Tract as aerosolized droplets called fomites

examples: Rhinovirus and Influenza virus

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32
Q

What is a virus that enters via the Gastrointestinal tract? What kinds of symptoms does it produce?

A

Norovirus produces diarrhea, nausea, vomiting

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33
Q

How do viruses that enter via Gastrointestinal tract spread?

A

Spread via fecaloral route

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34
Q

What are the characteristics of viruses that enter via the gastrointestinal tract?

A

Viruses must be able to withstand harsh environment of intestines (alkaline) and stomach (acidic), digestive enzymes, mucous and microvilli

  • Viruses also must evade local antibody (IgA)
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35
Q

How does transmission via the oralfecal route occur?

A

Human feces spreads to water or food that is consumed by people via the following vectors:
-manure, untreated sewage, and unwashed hands

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36
Q

What are some examples of viruses that enter via the Urogenital Tract (STDs)? What are their symptoms?

A 
HIV = AIDS
HSV-2 = Herpetic lesions of cervix and urethra
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37
Q

What are viruses that enter via the Urogenital Tract?

A

They enter through skin abrasions caused during sexual intercourse

38
Q

What kinds of symptoms are caused by STDs?

A

Some enter and cause local lesions (papillomavirus – genital warts)

Some cause systemic disease (HIV and hepatitis viruses)

  • Some cause a local infection followed by a latent (quiet) period (HSV)
39
Q

What are the characteristics of eye infections?

A

Eyes are usually fairly resistant to viral infections

Infection may occur after protective layers of eye scratched providing a portal of entry for the virus

Most infections localized and result in inflammation (conjunctivitis)

40
Q

What is an example of an eye infection?

A

conjunctivitis

41
Q

What are the characteristics of viruses that enter through the skin?

A

-skin is normally a very effective barrier against viral infections

  • Viruses enter when the barrier is compromised by:
    • insect bites
    • needle puncture, sexual contact
    • animal bite
42
Q

What are some examples of viruses that enter via the skin? What are their symptoms?

A

Rabies enters via animal bite and causes acute encephalitits

West nile virus enters via mosquito bite and causes encephalitis

43
Q

What are some other rare routes of entry for viruses? What are some examples of these?

A

Transplants and blood transfusions offer a route of entry

-examples would be HIV, Hep B and Hep C

44
Q

What does latrogenic mean?

A

inadvertant exposure to a virus

45
Q

What are some examples of latrogenic viruses?

A

HIV, Hepatitis, Prions

46
Q

How are viruses classified based upon the outcome of infection?

A

Productive
- progeny (new) viruses made

Abortive
- No progeny viruses made

47
Q

What are the different patterns of disease discussed in class?

A
  1. Acute infections
  2. Chronic (persistent) infections
  3. Latent, reactivating infections
  4. Slow infections (e.g TSEs)
48
Q

What is the general pattern of infection for acute viruses?

A

(Hit+Run):

  1. cleared quickly
  2. symptoms and amount of virus in host increase quickly and decrease quickly
  3. rapid production of virus particles + transmission and then clearance
49
Q

What is the general pattern of infection for Persistent viruses?

A

Chronic Infection

  • May not see symptoms right away
  • symptoms (and even death) present late
50
Q

What is the general pattern of infection for latent infection viruses?

A
  1. initial exposure = virus production
  2. enters latent phase (“goes away”)
  3. stress event causes reactivation event
  4. symptoms not as severe usually second time around
51
Q

What is the general pattern of infection for slow infection viruses?

A
  1. might not know you’re infected b/c the symptoms are very general (flu like)
  2. good virus production initially but host immune system gets upper hand eventually
  3. enter period of clinical latency
  4. not true latency b/c the virus isn’t dormant/not replicating
    • viral load decreases but is never actually cleared
    • exhausted immune system allows for opportunistic
      pathogens => death
52
Q

What are some examples of viruses that cause acute infection?

A

Rhinovirus and influenza virus

53
Q

What are some examples of viruses that cause persistent infection?

A

Lymphocytic choriomeningitis

54
Q

What are some examples of viruses that cause latent infection?

A

Herpes Simplex Virus

55
Q

What are some examples of viruses that cause slow virus infection?

A

HIV

56
Q

What are the characteristics of acute infection?

A
  1. occurs when a virus first infects a susceptible host
    • sudden onset of symptoms
    • usually self-limiting disease of short duration
    • immune response effectively clears the virus from the host
  2. virus usually not infectious for the same host again as memory immune cells generated against the pathogen
  3. often rapidly spread from person to person during asymptomatic “prodromal” period
57
Q

What are the characteristics of chronic infection?

A
  1. continuation of infection beyond the time that the immune system should have cleared the virus
    • disease symptoms may persist or be intermittent
    • virus NOT cleared by the immune system
    • host is a reservoir for the virus (can act as a vehicle for
      transmission to other hosts)
58
Q

What is the definition of disease?

A

a harmful pathological consequence of infection

59
Q

What are the different forms viral disease can take?

A
  1. direct cell and tissue destruction
  2. induction of fever and pro-inflammatory cytokines
  3. induction of malignant tumors/cancer
60
Q

What is virulence?

A

The relative capacity of a virus to cause disease

61
Q

What are the levels of virulence a virus can be?

A

highly virulent
- cause severe disease in the host

moderately virulent
- cause less severe symptoms

weakly or non-virulent (attenuated)

 - few clinical signs of disease or inapparent infections
 - many attenuated viruses used as vaccines
62
Q

What factors influence virulence?

A

The ability of the virus to:

  1. Effectively bind to and enter susceptible cells
  2. Replicate efficiently within the host
  3. Evade the host immune response
  4. Cause cell and tissue destruction
63
Q

Viral genetics are a key determinant of virulence. What are Genes that contribute to virulence called?

A

virulence genes or virulence determinants

  • All genes that are essential for virus replication are, by their very nature, virulence genes
64
Q

How do virologists study how a virus causes

disease (pathogenesis)?

A

Animal models are critically important for viral pathogenesis studies

65
Q

What are the types of animal models used to study human diseases caused by viruses?

A

1) A human virus is directly studied in infected animals
- HSV, yellow fever, VEE, LCMV, poliovirus* in mice
- Ebola, poliovirus, variola virus in primates

2) An animal virus that is related to the human virus is studied in an animal host (SIV in chimps)

66
Q

How can a virus that doesn’t infect an animal model be studied in that animal?

A

Some viruses can be adapted to grow in non-human hosts
- continual passaging of virus in the animal until
adaptation achieved
- genetic engineering (ex. making transgenic
mice that express the poliovirus receptor*)

67
Q

How is virulence measured in an animal model?

A
  1. Clinical signs
  2. Severity of tissue pathology
  3. Death of host
  4. Growth/replication/yield of virus in infected tissues
68
Q

What are the clinical signs used to measure virulence in an animal model?

A
  • weight loss
    • ataxia - loss of full control of bodily movements
    • labored or changes in respiration
    • ruffled fur
69
Q

What are the tissue pathology signs used to measure virulence in an animal model?

A

-infect animal then dissect animal to discover which organs are targeted

70
Q

How is the death of host used to measure virulence in an animal model?

A
  • % survival of infected animals

- LD50 dose at which 50% of infected animals die

71
Q

How is the growth/replication of virus used to measure virulence in an animal model?

A
  • virus measured by plaque assays, hemagglutination assays, PCR
72
Q

What were the strains being studies in the following study, when they wanted to assess whether glycoproteins I and E (gI and gE) are virulence factors for EHV-1 (ie. Do they contribute to disease caused by EHV-1 infection?)

A

They had a virulent (RacL11) strain and attenuated (KyA) strains of EHV-1

  • KyA does not express gI and gE
  • RacL 11 expresses gI and gE
73
Q

What did they do when they assessed whether glycproteins I and E (gI and gE) are virulence factors for EHV-1?

A
  • We genetically engineered KyA to now express gI and gE (KgIgE75) or just gE (KgE75)
  • We also removed gI and gE from the virulent RacL11 strain (L11ΔgIΔgE)
74
Q

What did Dr. Frampton hypothesize when they assess whether glycoproteins What did they do when they assessed whether glycproteins I and E (gI and gE) are virulence factors for EHV-1?

A

We hypothesized that KgIgE75 and KgE75 would exhibit increased virulence compared to the parental KyA strain and RacL11ΔgIΔgE would be more attenuated than the parental RacL11 strain in a mouse model of EHV-1 pathogenesis.

75
Q

What were the results of the gI and gE experiment for RacL11 and KyA?

A

Adding gI and gE to Kya made it more virulent
-particularly mice infected w/ KgIgE75 had much more weight loss and recovered less

Regular RacL11 killed the mice infected with it but removing gI and gE caused a similar weight loss but the mice recovered

76
Q

When Assessing brain pathology in mice infected with attenuated vs pathogenic EHV-1 (KyA vs RacL11 study) what was observed?

A

Brain sections day 5 post-infection.
encephalitis observed in all cases except mock infected

Brain sections day 9 post-infection.
Encephalitis observed in KyA infected mice

77
Q

What was the survival rate for the EHV-1 (KyA vs RacL11 study)?

A

KyA had 100% survival
KgI/gE/75 had 100% survival but remember they had weight loss
KgE/75 same

RacL11 was less deadly when gI and gE were removed

78
Q

When the growth/replication of EHV-1 was assayed (KyA vs RacL11 study) what was found?

A

Many RacL11 infected mice were dying around day 8 but at day 5 no virus was found in lungs (so it was cleared at this point)
-Why were these mice still dying if the virus was cleared?

The virus caused alot of damage from encephalitis (Look at pathology in slides)
- Measured pro-inflammatory cytokines to measure
immune response
- Much more production of these cytokines in RacL11 and
KgI/gE/75 than in Kya(attenuated)
- Overaggressive immune response responsible

79
Q

What mechanism leads to changes in the virulence of a particular strain of virus?

A

Mutations are the mechanism for change in virulence

80
Q

Would you expect more changes in an RNA virus or a DNA virus or would the rate of change be about the same? Why?

A

RNA viruses make more errors and their polymerase doesn’t have proof reading capability

81
Q

How do we identify virulence genes?

A

Knockout gene and assess virulence in host. Gene sequencing and splice out the gene.

82
Q

How would you evaluate virulence?

A

Evaluate virulence using LD50 or other things listed in slide 40

83
Q

What are the possible consequences of point mutations within the coding sequence of a structural gene?

A

Silent
-no change to amino acid produced

Missense
-changes one amino acid

Nonsense
-premature stop codon (very deleterious)

Frameshift (very deleterious)
-single addition/deletion causes different reading frame

84
Q

What are the types of infections that a virus can cause?

A

Localized infections: some viruses remain at site of initial infection

Systemic infections: some viruses spread to target tissues beyond initial entry site

85
Q

What are the main ways that viruses are spread throughout a host?

A

1) hematogenous route: viremia = virus present in
the blood

2) neouronal spread: spread of virus along nerves
    (HSV, VZV)
86
Q

Walk through the progression of systemic viruses?

A
  1. Primary site of infection
    - entry
  2. Virus enters nearest draining lymph node
    - replication and infection of immune cells
  3. Primary Viremia
    - moves from lymph to blood
  4. Target organs are infected
    - commonly the spleen or liver
  5. Secondary Viremia
    - high quantity of virus in blood (most contagious)
  6. Symptoms begin showing in target organ
87
Q

What are the steps of pathogenisis for polio?

  • routes of entry
  • sites of primary/secondary replication
  • means of spread throughout the body
  • target tissues infected
  • symptoms caused by infection
  • incubation period
  • is the virus cleared from the host or not
A

routes of entry
-ingested

sites of primary/secondary replication
-small intestine and lymph node

means of spread throughout the body
-establish primary viremia

target tissues infected
-liver and spleen then secondary viremia

symptoms caused by infection
-paralysis

incubation period
-race against immune system, depends on how much virus in blood after secondary viremia ~6 days

is the virus cleared from the host or not
- cleared but may have lasting effects (CNS - motor neurons)

88
Q

Why do only a small fraction of poliovirus infections lead to paralysis?

A

The outcome of infection is a race between the virus and the immune system

  • Antibody made early enough to prevent spread to CNS = Immune System Wins
  • Virus gains access to CNS before antibody neutralizaion = Virus Wins
89
Q

What are the steps of pathogenisis for mousepox?

  • routes of entry
  • sites of primary/secondary replication
  • means of spread throughout the body
  • target tissues infected
  • symptoms caused by infection
  • incubation period
  • is the virus cleared from the host or not
A

routes of entry
-through footpad of skin (smallpox is respiratory)

sites of primary/secondary replication
-at injection site, goes to draining lymph nodes and further replicates

means of spread throughout the body
-primary viremia

target tissues infected
Liver and spleen then establish secondary viremia

symptoms caused by infection
-skin infection (rash) and lesions

incubation period
-7-8 days

is the virus cleared from the host or not
-if you survive then virus cleared

90
Q

What are the steps of pathogenisis for varicella zoster virus (chicken pox)?

  • routes of entry
  • sites of primary/secondary replication
  • means of spread throughout the body
  • target tissues infected
  • symptoms caused by infection
  • incubation period
  • is the virus cleared from the host or not
A

routes of entry
-oral or eye

sites of primary/secondary replication
-upper respiratory then draining lymph nodes

means of spread throughout the body
-primary viremia and T cells spread

target tissues infected
-liver and spleen then secondary viremia

symptoms caused by infection
-chicken pox rash

incubation period
-14 days

is the virus cleared from the host or not

  • not cleared. hides out in neurons of host
  • reactivation = shingles
91
Q

How do viruses exit/shed?

A

Usually shed through routes of entry

Mucus
Saliva
Semen
Feces
Skin abrasions
Breast milk
Cervical secretions
Urine
Viremia—blood
92
Q

You are interested in studying the pathogenesis of virus X. You know that the virus is spread from person to person via the aerosol route and can cause encephalitis.
Some researchers have shown that mice can be infected with this virus and also develop encephalitis

You want to evaluate virus X pathogenesis in mice.

1) Where does the virus go after infection? What assays could you set up to examine this?
2) In what tissues does the virus replicate?

3) What is the incubation period (time from infection to symptoms)?
- How could you examine this

4) How is the virus shed from the animal? Is it the same in mice as in the human host?
When is it shed?

5) Is the virus cleared from the host? How do you assay this.

The virus has been completely sequenced and we have many reagents available to help us study the virus including antibodies and PCR primers. Also, there is a tissue culture system that has been developed for virus X which is cytopathic (causes plaques) in cells.

A

1) Where does the virus go after infection? What assays could you set up to examine this?

Hypothesis: mice that are infected w/ virus, the virus travels to CNS
Assay: 50 mice, 25 control and 25 experimental. Every day take 5 mice and do tissue sample. Then do PCR to see which tissues contain the virus.

2) In what tissues does the virus replicate?

Can use plaque assay to see which tissues contain active viruses

3) What is the incubation period (time from infection to symptoms)?
- How could you examine this

Animal model to see how long it takes for you to see symptoms present and graph the data for analysis

4) How is the virus shed from the animal? Is it the same in mice as in the human host? When is it shed?

Cage control mice next to infected mice (not in contact) to see if virus spreads via aerosol route

5) Is the virus cleared from the host? How do you assay this.

tissue samples+PCR to see if virus is still present in host or if it’s cleared

BIO 435: Virology (18 decks)

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