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Viral pathogenesis Flashcards

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1
Q

Define pathogenesis

A

Mechanism by which disease is caused

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2
Q

Name 4 steps in the mechanism of viral infection and dissemination

A

1) Entry into host and primary replication

2) Local/ general spread in the host - cell + tissue tropism

3)Shedding in environment from host

4) Clearance of virus from host

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3
Q

What is the condition for entry into a host and what challenges appose infection?

A

Condition: Sufficient virions
Challenges:
- Debris
- Surface antibodies/ extracellular materials
- virion delivered to lysosome
- defective interfering particles: produced during faulty replication

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4
Q

How do viruses bypass the host’s defenses and attach?

A

1) Overwhelming inoculum of virus particles
2) Cuts/abrasions
3) Skin = low exposure to immune system, so virus infects there
4) After virion attaches to mucous membranes it is not affected by antibodies
5) Attachment > enveloped vs non-enveloped
6) Phagocytosis [receptor mediated] > enters cell - except those with fusion proteins on their envelopes.

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5
Q

Differentiate between the attachment mechanism of enveloped vs non-enveloped viruses

A

Enveloped - intact envelope needed to attach to cell surface receptors

Non-enveloped - Capsid proteins facilitate it

They then enter the cell via receptor mediated phagocytosis except for those with fusion proteins on their envelopes.

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6
Q

What viruses typically infect the respiratory tract? What are the host’s defence mechanism against these?

A

Rhinovirus (acid labile),
influenza, Foot and mouth
disease virus (FMD), canine
distemper virus

Defense: Mechanical barriers (muco-ciliary blanket) & cellular
and humoral immunity –
host defence mechanisms

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7
Q

What viruses typically infect the digestive tract? Why can they survive such a hostile environment?

A

Enteric viruses: Poliovirus is acid resistant and
infects the upper intestine
(rhinovirus is acid-labile).
Parvovirus, rotavirus,
coronavirus, bovine viral
diarrhoea virus (cross the
epithelial barrier).

Survival:
Hostile environment for
virions (stomach is acidic
and intestines alkaline).
Viruses are resistant to
extremes of pH, proteases*,
bile

*Some viruses facilitate infection after conversion, e.g. reoviruses
are digested by proteases in the intestinal lumen to infectious
sub-viral particles then infect epithelial cells

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8
Q

What viruses typically infect the urogenital tract? How are they usually transmitted?

A

Bovine/equine
herpesvirus,
papillomavirus and
equine arteritis virus

Transmission: Many of the viruses are
present in semen. Can also be transmitted from mother to foetus (cross placental barrier by junctions). This can lead to immune tolerance in the foetus

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9
Q

Define viremia. Differentiate between active, passive, primary and secondary viremia.

A

The presence of infectious virus in the blood.
Passive: present without replication
Active: result of replication
Primary: Virus released into the blood after initial replication
Secondary: subsequent infections of organs in much higher viruses

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10
Q

Define tropism

A

receptor population determines whether the cell can be
infected by a specific virus

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11
Q

Name the three main types of blood vessel tissue junctions that serve as routes for tissue invasion

A
  • Sinusoids – liver, spleen and bone marrow are characterised by
    Kupffer cells (liver) – route to infect hepatocyctes.
  • Fenestrated endothelium – found in villi of intestines
  • Continuous endothelium – found in the CNS, connective tissue
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12
Q

Explain what RNA interference is

A

RNA interference (RNAi) is a natural defense mechanism found in eukaryotic cells that helps regulate gene expression and defend against viral infections, especially those caused by double-stranded RNA (dsRNA) viruses.

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13
Q

What are persistent infections (PI)

A

PI occur where infectious virus is demonstrated to be in continuous circulation, cf. latent infections, virus demonstrable when reactivation occurs.

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14
Q

Why are viral PI important?

A

1) Can cause immunopathological disease: body’s immune system malfunctions leading to
disease

2) neoplasia (abnormal or excessive growth of tissue)

3) May allow viral survival in vaccinated animals

4) epidemiological importance (movement of infected animals, reintroductions)

5) Can be reactivated and cause recrudescent episodes of disease (breaking out again/reviving after a period of dormancy or abatement)

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15
Q

Discuss 4 patterns of persistent infections

A

Acute viral infection: sudden/ rapid onset of disease= fixed quickly by host’s robust innate immune responses/ kill the host.

Latent infection: specific infectious agent residing without any manifest symptoms. Reactivation has to occur e.g. herpes virus.

Chronic infection: continued presence of
infectious virus following the primary infection and may
include chronic or recurrent disease.

Slow infection: prolonged incubation
period followed by progressive disease

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16
Q

What is pathogenesis?

A

The mechanism by which disease is caused.

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17
Q

What is virulence?

A

The ability of an infectious microbe to cause disease and a measure of disease severity (e.g. LD50).

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18
Q

What are the steps of viral infection and dissemination?

A

(1) Entry & primary replication, (2) Spread & secondary replication, (3) Shedding, (4) Clearance.

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19
Q

What factors can cause failure of infection?

A

Interaction with debris, delivery to lysosome, or defective virus particles.

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20
Q

How can host defences be bypassed?

A

Through overwhelming inoculum, infection through skin, or targeting cells with low immune exposure.

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21
Q

How do viruses attach to mucous membranes?

A

Via virion attachment sites and host cell surface receptors.

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22
Q

How do enveloped viruses penetrate host cells?

A

Via fusion proteins or receptor-mediated endocytosis.

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23
Q

What is the most common route of viral entry?

A

Respiratory tract.

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24
Q

How do host defences in the respiratory tract act?

A

Mechanical barriers, immune responses, trapping particles based on size.

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25
How do enteric viruses survive the digestive system?
Resistance to pH, proteases, bile; e.g. poliovirus.
26
What is the role of Microfold cells in viral infection?
Microfold cells = specialized epithelial cells found in the gut-associated lymphoid tissue (GALT) of the Peyer's patches in the small intestine that facilitate transcytosis of virus across intestinal epithelium and delivery to underlying lymphoid tissue) Some use this mechanism to cross epithelial barrier = reovirus, (replicate in M cells and don’t spread to underlying lymphoid tissue)
27
How do viruses enter via the urogenital tract?
Through microtears, semen, or transplacental transmission.
28
How can viruses cross epithelial barriers?
Mechanical injury, iatrogenic means, bites, or vector transmission.
29
What is the difference between biological and mechanical insect vectors?
Biological vectors: The pathogen replicates or develops inside the vector before being transmitted to a new host (e.g. midges, bluetongue virus) mechanical vectors: infected when feeding on infected animal. passively carry pathogens on their bodies without the pathogen undergoing any development inside them. Transfer virus during next feeding. (e.g. biting insects and lumpy skin disease virus)
30
What are the types of viraemia?
Passive, active, primary, secondary.
31
What is viral tropism?
Restriction of infection to specific cell/tissue types.
32
What are the three types of vessel-tissue junctions?
Sinusoids, fenestrated endothelium, continuous endothelium.
33
What are examples of neurotropic viruses?
Herpesvirus, mumps, rabies.
34
How do viruses evade host defences?
Non-cytocidal infection, cell-to-cell spread, latency, immune evasion.
35
What is genetic/antigenic drift?
Continuous mutation in genes that code for surface proteins (such as hemagglutinin and neuraminidase), which are recognized by the immune system allowing immune evasion (common in RNA viruses like influenza).
36
How does RNA interference (RNAi) act as host defence?
Degrades exposed dsRNA using enzyme Dicer.
37
What are cytopathic effects?
Necrosis, apoptosis, vacuolisation, syncytia, inclusion bodies.
38
What are viral effects on the respiratory tract?
Destruction of epithelia, cilia aiding spread, blockage from necrotic debris.
39
How do viruses affect the gastrointestinal tract?
Shortening of villi (rotavirus), destruction of crypts (parvovirus), leading to diarrhea.
40
What causes persistent viral infections?
Continuous presence or latent reactivation; e.g. herpes.
41
Why are persistent infections significant?
Reactivation, immunopathology, neoplasia, epidemiological concerns.
42
What is viral tumorigenesis?
Transformation of cells by viruses causing deregulation and tumor formation.
43
What are the four steps of viral infection?
1. Entry & primary replication; 2. Local/systemic spread; 3. Shedding; 4. Clearance.
44
What are reasons a viral infection might fail?
Virus interacts with debris/antibodies, defective particles, delivery to lysosome.
45
How do viruses bypass host defenses during attachment?
Overwhelming inoculum, infection via skin breaches, receptor-mediated entry, envelope/capsid facilitates binding.
46
What are common routes of virus entry?
Respiratory, digestive, urogenital, epithelial breaches.
47
How do viruses enter via the respiratory tract?
Mucosal defenses, size-dependent trapping of particles.
48
What makes the digestive tract hostile to viruses?
Acidic stomach, alkaline intestine, enzymes, bile, mucous, antibodies.
49
How do viruses enter via the urogenital tract?
Microtears during sex, vertical transmission via placenta.
50
How can viruses cross epithelial barriers?
Injury, injections, animal/insect bites.
51
What is the difference between biological and mechanical insect vectors?
Biological: virus replicates in vector (e.g., bluetongue); Mechanical: passive transfer (e.g., LSD virus).
52
How does a virus spread locally?
Via lysis and direct cell fusion.
53
How does a virus spread systemically?
Lymphatic drainage to blood to organs.
54
What is the difference between passive and active viraemia?
Passive: no replication; Active: after replication.
55
What is primary vs secondary viraemia?
Primary: initial spread; Secondary: systemic infection of target organs.
56
What are three blood vessel types involved in organ invasion?
1. Sinusoids; 2. Fenestrated endothelium; 3. Continuous endothelium.
57
Which organs have sinusoidal endothelium?
Liver, spleen, bone marrow.
58
Where is fenestrated endothelium found?
Kidney, gut, endocrine glands.
59
Where is continuous endothelium found?
CNS, skin, muscles.
60
What does neuroinvasive mean?
Ability of virus to spread in the nervous system.
61
What does neurovirulent mean?
Ability of virus to cause CNS disease.
62
Compare neurotropism in herpes, mumps, and rabies.
Herpes: low NI, high NV; Mumps: high NI, low NV; Rabies: high both.
63
Name general mechanisms viruses use to evade host defenses.
Non-cytocidal infection, cell-to-cell spread, latency, decoy proteins, immune tolerance, immune privileged sites, genome integration, antigenic drift.
64
What is antigenic drift?
Continuous mutation allowing immune escape.
65
How do decoy proteins help viruses?
They mop up neutralizing antibodies.
66
What is the significance of infection in immunologically privileged tissues?
Reduced immune surveillance allows viral persistence (e.g., CNS, glands).
67
What is RNA interference (RNAi)?
Dicer cleaves dsRNA into fragments, initiating viral RNA degradation.
68
How does the immune system combat viruses?
Through T cells and antibodies.
69
What are key cytopathic effects of viruses?
Necrosis, apoptosis, vacuolisation, syncytial formation, inclusion bodies.
70
How does apoptosis differ from necrosis?
Apoptosis is controlled and non-inflammatory; necrosis causes inflammation.
71
How do viruses damage the respiratory tract?
Destruction of epithelial cells, mucus blockage, secondary infections.
72
How do rotaviruses affect the GI tract?
Damage villi, reduce absorption, cause diarrhea.
73
What secondary bacterial infections are facilitated by viral damage?
Pasteurella hemolytica (lungs), E. coli (intestine).
74
What is a persistent infection?
Virus detectable continuously, may not cause disease.
75
What is a latent infection?
Virus not detectable except during reactivation.
76
Why are persistent infections important?
Can cause disease recurrence, transmission, neoplasia, affect vaccinated animals.
77
How can viruses cause tumor formation?
They deregulate cell growth, causing transformation.
78
Non-cytocidal infections (arenavirus + hantaviruses)
Chronic infection without killing the cell where they replicate
79
Cell-cell spread (Canine distemper virus + herpes virus)
Causes adjacent cells to fuse so that virus can spread
80
Non-permissive cells (herpesvirus)
Certain cells don't support replication, leading to latency in those cells while productive infection occurs in others
81
Restricted gene expression (herpesvirus)
Proteins that can destroy the cell are limited; full genome transcription happens upon reactivation (stress/hormones)
82
Evasion of neutralising antibodies (Ebola virus)
Produces two surface glycoproteins: one forms capsid protein, the other is secreted extracellularly as a decoy protein that mops up neutralising antibodies
83
Induction of immune tolerance (prenatal infections)
Foetus may not recognize virus as foreign; later in life, antibodies aren’t produced in response to natural infection
84
Immunologically privileged tissues (rabies virus)
Infections in CNS confer protection to virus from immune system (T-cell suppression)
85
Integration into host genome (retroviruses)
Assures virus maintenance within host cells
86
Continuous mutation (RNA viruses e.g. influenza)
Allows virus to evade immune response via antigenic drift/shift
87
Explain how RNA interference works
1) Infection by dsRNA Virus (like AHS virus) 2) If dsRNA is exposed to the cytoplasm 3) the enzyme Dicer cleaves dsRNA molecules into short fragments 4) the RNAi pathway is triggered 5) This prevents the virus from replicating.

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