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Veterinary Virology > Virus-Host Interactions and Pathogenesis > Flashcards

Virus-Host Interactions and Pathogenesis Flashcards

1
Q

What is viral pathogenesis?

A

process by which a viral infection leads to disease

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2
Q

What 7 factors affect viral pathogenesis?

A
  1. effects of viral infections on cells
  2. entry into the host
  3. course of the infection - primary replication, systemic spread, secondary replication
  4. cell/tissue tropism
  5. cell/tissue damage
  6. host immune response
  7. virus clearance or persistence
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3
Q

What are virulent viruses? What 4 factors affect viral virulence?

A

measure of the ability of the virus to induce disease in a particular host

  1. ability of the virus to grow and multiply in a particular host
  2. ability of the virus to invade the host
  3. ability to evade the host immune response
  4. ability to cause damage in the target host
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4
Q

What viral/host-related factors affect viral virulence?

A
  • age
  • gender
  • immune status
  • virus concentration
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5
Q

What are permissive cells? Non-permissive cells?

A

PERMISSIVE: support viral replication
NON-PERMISSIVE: viral infection cannot be established

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6
Q

What are the 3 mechanisms of viral-induced diseases in the affected host?

A
  1. damaging/killing target cells
  2. induction of immuno-pathology
  3. cell transformation (tumors)
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7
Q

What are the 5 steps of viral replication in host cells?

A
  1. viral entry
  2. local/general viral spread and viral replication in target organcs (tropism)
  3. viral evasion of host immune/inflammatory responses
  4. viral shedding from host
  5. host cell damage
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8
Q

What are the 5 steps of viral replication?

A
  1. viral entry
  2. local/general spread in the host and replication in target organs (tropism)
  3. viral evasion of host immune-inflammatory responses
  4. viral shedding
  5. host cell damage
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9
Q

What must viruses do to undergo all 5 steps of viral replication?

A
  1. ENTRY: evade host’s natural protective and cleansing mechanisms
  2. SPREAD/REPLICATION: evade hosts immediate defenses and barriers to spread; take over necesary host cell functions for its own replication
  3. EVASION: evade host inflammatory, phagocytic, and immune defenses long enough to complete the transmission cycle
  4. SHEDDING: exit host at a concentration needed to ensure infection in the next host
  5. DAMAGE: pathogenicity
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10
Q

What are the 4 types of viral infections?

A
  1. PRODUCTIVE: virus introduces its genome into the cells, replicates, and produced new viral progeny
  2. LATENT: viral genome is incorporated into the host cell genome and an infectious virus is not produced immediately, rather in times of stress
  3. ABORTIVE: virus initiates infection and produces no progeny
  4. PERSISTENT: long-term viral infection when the immune system fails to clear acute infection
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11
Q

What is recrudescence?

A

new outbreak of viral infection after a period of abatement or inactivity

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12
Q

What is viral load?

A

concentration of virus in body/tissue

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13
Q

What characterizes recurrent viral infections?

A

infections occuring when several episodes of acute infection one after another due to the inability of the immune system to completely clear the infection
(AKA persistent)

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14
Q

Types of infection:

A
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15
Q

What are lytic infections? Immune complex diseases?

A

LYTIC INFECTIONS - destruction of cells by viral replication at rates greater than their replacement

IMMUNE COMPLEX DISEASE - antibodies cause immunopathologic conditions by combining with the virus and forming a complex that is deposited in glomeruli and organs, causing inflammation

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16
Q

Virus shedding and clinical signs:

A
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17
Q

What does the typical curve of acute viral infection look like?

A
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18
Q

What are the 4 main patterns of viral infection?

A
  1. acute infection followed by viral clearance
  2. acute infection causing accidental tissue infection with permanent damage despite viral clearance
  3. persistent infection: latent, slow, transforming
  4. long incubations
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19
Q

What is viral persistence? What are 5 causes?

A

inability of the immune system to clear an acute viral infection

  1. immunodeficiency (HIV infection)
  2. transplant
  3. chemotherapy
  4. genetics
  5. congenital infection
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20
Q

What are 4 possible outcomes of persistent viral infections?

A
  1. no affect
  2. chronic or progressive infections
  3. cancer
  4. clinical reactivation
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21
Q

Why is viral persistence significant?

A

maintains a virus in the animal population

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22
Q

As a viral infection persists, what must it overcome?

A
  • after incubation, it must overcome the innate immune system to cause acute infection
  • to progress to a persistent infection, the host must remain alive and it must overcome the adaptive immune system
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23
Q

What are 6 mechanisms that allow for viral persistence?

A
  1. viral evasion of the host immune response
  2. modulation of adaptive immune system
  3. induction of latency
  4. infection of tissues not readily accessible to the immune system (keratinocytes)
  5. immune response escape mutants
  6. prolonged survival of infected cell (oncogene)
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24
Q

What are 5 routes of entry for viral infection?

A
  1. RESPIRATORY: inhalation of droplet nuclei of 1-10μm causes infection; 1-3μm penetrate bronchioles
  2. SKIN: intact skin can be breached by insect bites, animal bites, and contaminated instruments
  3. GENITAL TRACT: venereal infection rare
  4. PLACENTA: viremia in pregnant female may cross the placenta and infect fetus
  5. ALIMENTARY: virus ingested with food and water or licking of contaminated objects
  6. CONJUNCTIVA
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25
Q

What must viruses overcome in the respiratory and alimentary tracts to cause infection?

A

RESP: mucociliary clearance (ciliated epithelium), phagocytosis by alveolar macrophages in the lung, mucus secretion, lower temperature

ALIMENTARY: low pH of stomach, high pH of intestine, mucous layer, peristalsis

26
Q

What are the 5 possibilities of the aftermath of a killed fetus via placenta transmission?

A
  1. infertility
  2. mummified fetus
  3. abortion
  4. stillbirth
  5. surviving fetus with congenital abnormalities
27
Q

How does Rhinovirus infection affect the trachea?

A

kills ciliated epithelium, causing it to slough off - no longer looks like a carpet

28
Q

What is the pathogenesis of Ectromelia (Mouse-pox) virus?

A
  1. skin invasion
  2. multiplication in regional lymph nodes
  3. primary viremia and multiplication in spleen and liver
  4. secondary viremia and skin multiplication
  5. primary infection - foot swelling
    - early rash = papules
    - severe rash = ulceration
29
Q

What are the major 3 ways that virsues are transmitted by the respiratory system?

A
  1. DROPLET: transmitted from one individual to another by droplets of moisture expelled from the upper respiratory tract through sneezing/coughing
    2 AEROSOL: transmitted by infectious particles or droplets through inhalation or direct contact with mucous membranes in the respiratory tract or eyes
  2. FOMITE: clinical contact surfaces such as dental units, X-ray machines, equipment knobs, or housekeeping surfaces
30
Q

Where does primary and secondary viremia occur? What are some common sites in the body for viral replication?

A

PRIMARY: in the blood after the virus has passed through the host’s natural barriers, like skin or mucous membranes
SECONDARY: in the blood after the virus has reached primarily replicated in muscle, liver, spleen, or blood vessels

  • skin, mucous membranes, lung, kidney, GI tract, brain
31
Q

What do viruses that infect via skin penetration require? What are the 4 major methods of entry?

A

the ability to breach in the physical integrity of the effective barrier - cuts, abrasion, keratin damage

  1. trauma of milking or suckling
  2. arthropod bites
  3. infected needles
  4. animal bites
32
Q

What is shingles? What is its pathogenesis?

A

viral disease caused by chicken poxvirus characterized by painful skin rash with blisters in a localized area

  • infection breaches conjunctiva and upper respiratory tract
  • replication in the primary lymph nodes
  • primary viremia
  • replication in liver, spleen, and other organs
  • secondary viremia
  • infection of the skin and appearance of skin rashes
  • infection of sensory ganglia and establishment of latent infection
33
Q

What is the incubation period? What affects its duration?

A

time between the entrance of the virus into the body of the infected host and the appearance of clinical signs

  1. respiratory virus (influenza) = few days
  2. maedi-virus, rabies = several weeks/months
34
Q

What are the general steps of systemic infection?

A
  1. virus multiplies at the site of entry and in the lymph nodes, resulting in primary viremia
  2. virus reaches the target organs through secondary viremia and multiplies, resulting in cell damage and disease development
  • virus reaches skin via bloodstream to produce skin rashes
  • virus spreads to brain via cerebellar blood vessels or peripheral nerves
  • transplacental transmission may occur in pregnant animals
35
Q

How does the route of entry affect viral shedding?

A
  • local spread from route of entry restricts viral shedding to respiratory secretions
  • viremic spread from the route of entry results in shedding from multiple mucosal surfaces
36
Q

What must viruses that cause systemic infection and spread via blood be able to do?

A

infect, replicate, and survive in lymphocytes and macrophages

37
Q

How do viruses invade the epithelium and spread via the lymphatic system?

A
  • amplifies in the epithelium or infect sub-epithelial macrophages
  • cell-free virus or infected macrophages/DC pass to regional lymph node via afferent lymphatics
  • viral progeny released into venous secretions to cause viremia that can be cell-free or cell-associated
38
Q

How does rabies able to be transmitted? How does the location of transmission affect infection?

A
  • rabies infected wild animal bites
  • inoculated virus moves in nerve tissue (retrograde)
  • virus reaches the brain and replicates
  • virus reaches salivary gland of affected animals
  • closer bite to brain = shorter incubation period
39
Q

What are the 2 possible ways that rabies and pseudorabies is able cross synaptic junctions?

A
  1. retrograde infection: spread of virus from the axon terminals to the neuronal cell body and is directionally opposite to movement of the nerve impulse
  2. anterograde infection: spread from neuron cell body toward axon terminus
40
Q

What is the purpose of virus shedding? How does this typically occur?

A

maintains the circulation of the virus in certain animal populations

same route of entry
- SKIN: direct contact with abrasions and wounds
- RESPIRATORY: coughing and sneezing (large droplets = fall on objects; small droplets = airborne)
- ALIMENTARY: feces (must be environmentally resistant)
- GENITAL: semen, genital secretions during coitus or artificial conditions
- KIDNEY: urine
- BLOOD: arthropod bites, contaminated needles, tissues from animals in slaughterhouses
- MAMMARY: milk

41
Q

What is viral tropism? What 6 things affect tropism?

A

affinity of certain viruses to certain tissues

  1. cell receptors for the virus
  2. cell transcription factors that recognize the viral promoters and enhancer sequences
  3. ability of the cell to support viral replication
  4. physical barriers
  5. local temperature, pH, oxygen levels, tension
  6. digestive enzymes, bile, etc. that inactivate viruses
42
Q

What is the mechanism of viral tropism? What are post-entry factors?

A

cellular receptors differentially expressed in certain cells limits viral entry into specific cell types

factors within the cell that make them permissive to vral cells after entry (transcription and translational machinery, innate antiviral defenses overcame by viral-encoded proteins)

43
Q

What tropism does nervous tissue, digestive system, skin, respiratory system, and various body organs/tissues have?

A

NEUROTROPIC - rabies, EEV, WNV, NDV
VISCEROTROPIC - rotavirus, BCoV, NDV
DERMOTROPIC - poxvirus, LSDV, papillomavirus
PNEUMOTROPIC - SARS-CoV, MERS-CoV, IBV, ILTV
PANTROPIC - SARS-CoV2, IBV, RPV

44
Q

What determines influenza virus tropism?

A

availability of host proteases to cleave inactive viral proteins into active ones

45
Q

What are 5 viral determinants of survival and transmission?

A
  1. viral envelope - surface protein expression and modification for the sit of infection, host receptor specificity and affinity, and formation of viral aggregates
  2. viral capsid - structure and stability
  3. internal proteins - polymerase for host-adapted replication
  4. viral genome - densely packaged for stability
  5. mutation - protects from host adaptation
46
Q

What are the 4 major outcomes of infection at the molecular and cellular levels?

A
  1. cell death (cytopathic/cytocidal) - necrosis/apoptosis with the production of daughter viral particles***
  2. persistent infection - no apparent change, constant production of virus without cell destruction
  3. transformation (hyperplasia) - alters cell morphology, but daughter virus may not be produced (tumors)
  4. abortive infection - cell may be damaged, killed, or transformed, but no daughter virus is made
47
Q

What do cytocidal viruses do? In what 5 ways do they do this?

A

ceases the cellular macromolecular synthesis of important proteins, leading to rapid destruction of the infected cells

  1. shut down cellular RNA and protein synthesis
  2. accumulates viral macromolecules during replication
  3. toxic capsid proteins
  4. accumulate ciral components at the site of multiplication forming inclusion bodies that can distort cells and increase permeability
  5. cause cellular lysosomal enzymes to leak out, resulting in autolytic digestion
48
Q

What do direct damage of the cells, edema, and immune system damage result in?

A

impairment of affected organ

inflammatory exudation and infiltration

immunodeficiency or immunosuppression

49
Q

In what 3 ways can antibodies cause cellular damage?

A

induce the formation of immune complexes (ab-ag) that can enhance infection, damage kidneys and joints, and cause persistent inflammation

50
Q

Cytopathic effects:

A

pathological effects of virus on infected cells

51
Q

What are the main 3 cytocidal viral effects

A
  1. CPE
  2. syncytia
  3. inclusion body formation
52
Q

What is syncytia? What causes it?

A

cell fusion - multinucleated giant cells

enveloped viruses with fusion proteins infect cells and cause new fusion proteins to be translated, which are transported to the cell surface and expressed on the membrane, allowing budding viruses to pick up the proteins and the fusion of the infected cells to neighboring uninfected cells

53
Q

Where are inclusion bodies found?

A

at the site of replication either in the nucleus (most DNA viruses) or cytoplasm (most RNA viruses)

  • can be large or small, eosinophilic or basophilic
54
Q

How are cytocidal viruses able to shut down cellular macromolecular synthesis?

A

code for early proteins that stop the synthesis of cellular RNA proteins

55
Q

How does the cytocidal virus’ release of enzymes by lysosomes cause cell damage?

A

increases permeability of the cell’s membrane allowing the movement of important components out of the cell

56
Q

How can cytopathic viruses affect the membrane of an infected cell? Cell chromosomes?

A
  • express their peplomers on the plasma membrane of the cell it’s infecting (hemagglutinin)
  • chromosome breaches
  • translocation
  • deletion
57
Q

Cytocidal virus effects:

A
58
Q

What is characteristic of non-cytocidal viruses?

A

non-lytic infections where the virus replicated within the cell without killing it or causing clinical pathology

59
Q

What are viral oncogenes? How are they derived? How do they affect host cells?

A

viral genes that transform a normal cell into cancer cells that can grow and multiply indefinitely

from host cell genes then incorporated into the viral genome to induce mutations

interfere with the host cell growth and multiplication genes, which causes the host cells to lose the ability to control division and multiply indefinitely

60
Q

The viral ____ play(s) a role in attaching a virion to the host cell.

a. envelope
b. capsid
c. core
d. A and B

A

D

61
Q

Which statement is true about viral shapes?

a. all have a round shape
b. cannot have a long shape
c. don’t maintain any shape
d. vary in shape

A

D

62
Q

Which statement is true of reverse transcriptase?

a. it’s a nucleic acid
b. it infects cells
c. it transcribed RNA to make DNA
d. it is a lipid

A

C

Veterinary Virology (25 decks)

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