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IVP: Veterinary Pathogenesis > Microbiology - Viruses > Flashcards

Microbiology - Viruses Flashcards

1
Q

Basic structure of a virus - how does this differ from bacteria and fungi

A

Virion - completely assembled infective virus

- protein shell (capsid) surrounds viral genome and is made up of protein subunits (capsomeres)

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2
Q

Differentiate between enveloped and non-enveloped viruses (include examples)

A

ENVELOPE - surrounds capsid and is acquired by budding through cellular membranes of the host
- contains host phospholipids and proteins + viral proteins and glycoproteins

NON-ENVELOPED - more resistant to environmental desiccation, lipid solvents or detergents

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3
Q

Basic principles of viral replication (10 steps)

A
  • Must be inside host to replicate
    1. Attachment
    2. Penetration
    3. Uncoating
    4. Transcription of early mRNA
    5. Transcription of early proteins
    6. Replication of viral DNA
    7. Transcription of late mRNA
    8. Transcription of late proteins
    9. Assembly of virions
    10. Release
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4
Q

DNA viruses

A
  • DNA is not transient or labile.
  • Replication resembles host DNA transcription and replication
  • Replicate in the nucleus (except pox viruses).
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5
Q

RNA viruses

A
  • RNA is labile and transient.
  • Genome structure determines the mechanism of transcription and replication
  • Replicate in the cytoplasm
  • More prone to mutation
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6
Q

Describe the difference between antigenic shift and antigenic drift and its implications in the outbreak of disease

A

Antigenic shift = Acquisition of a gene from a completely new Haemagglutinin or Neuraminidase (envelope proteins) from another influenza virus, resulting in new HN type
- new strains of influenza causing major flu pandemics

Antigenic drift = gradual accumulation of point mutations leading to new stereotypes
- minor change can produce a major outbreak e.g. fowl plague in Pennsylvannia

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7
Q

Types of cell interactions - Lysis of cell

A

E.g. herpesvirus
• Particles burst out of host cell into Extracellular space
• Resulting in death of host cell
• Once released enters new cell to multiply

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8
Q

Types of cell interactions - Persistent infections - Productive

A

PRODUCTIVE e.g. rabies virus

  • Cells infect productively and not killed by replication process
  • Released by budding
  • No inhibitory effect on cellular metabolism
  • Antigenic changes in infected cells
  • Insertion of glycoproteins in plasma membrane
  • Long term cellular change
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9
Q

Types of cell interactions - Persistent infections - Latent

A
  • Restricted expression of episomal or integrate virus genome
  • Few, if any, changes in the latently infected cell
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10
Q

Types of cell interactions - Persistent infections - Non-productive but transforming

A
  • May make changes that convert a normal cell into a malignant one
  • RNA: integrating own genetic material into cellular genome
  • DNA: transformation by abortive/restrictive infections
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11
Q

Effects of viral infections on cell morphology - Cytopathic

A
  • Virion infected cells release progeny virions that spread through the cell culture supernatant fluid to infect other cells
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12
Q

Effects of viral infections on cell morphology - Inclusion bodies

A
  • Changes in cells infected with certain viruses

- May form masses of viral nucleocapsids e.g. rabies virus; masses of proteins/nucleic acids

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13
Q

Effects of viral infections on cell morphology - Alteration of cell membranes

A

Changes in plasma membranes of the cell by insertion of viral glycoproteins in the membrane of the host during viral replication

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14
Q

Effects of viral infections on cell morphology - Formation of syncytia

A
  • May lead to fusion btw neighbouring infected/uninfected cells
    → fused cells allow viral nucleocapsids andnucleic acids to spread while escaping hosts defences e.g. Herpesviruses
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15
Q

Effects of viral infections on cell morphology - Haemadsoprtion

A
  • Acquire ability to absorb erythrocytes due to glycoproteins in plasma membrane
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16
Q

Mechanisms of cell damage

A
  1. Inhibition of Host Cell Nucleic Acid Synthesis
  2. Shutdown of Host Cell Protein Synthesis
  3. Cytopathic effects of toxic viral products = accumulation of toxic viral proteins
  4. Cytolysis by Immunologic Mechanisms
17
Q

Interferons

A
  • Members of family of regulatory proteins called cytokines
  • Produced and secreted transiently in response to external stimuli such as viral infections
  • Main effect in natural infections may be local, protecting cells in the immediate vicinity of the initial focus of infection, slowing down the movement of virus during crucial early stages of infection
18
Q

Outline the different routes by which viruses gain entry to the body giving examples of viruses that use this route and discuss the host defence (HD) mechanisms that viruses must overcome at each of these sites of entry

A

RESPIRATORY - trapped in mucous, then swallowed
- HD - alveolar macrophages
e.g influenza
ALIMENTARY - swallowed and reach GIT directly or infect cells in oropharynx and then be carried into intestinal tract
- HD - intestinal mucous, bile, gastric acids, intestinal enzymes
e.g. coronaviruses
SKIN - physical trauma such as cuts and abrasions, biting
- HD - keratinised outer layer
e.g. small pox
UROGENITAL - tears or abrasion in penile mucosa and lining of vagina during sexual activity
- HD -
e.g. bovine herpesvirus
Conjunctiva
- HD - constantly cleansed by flow of tears and wiped away by eyelids
e.g. adenoviruses

19
Q

Explain what is meant by viral tropism

A

Tropism = ability of a virus to selectively infect cells in particular organs

Viral tropism = a function of both host and viral factors

20
Q

Using examples, discuss how viruses spread throughout the body after entry

A

Via lymphatic (influenza) and haematogenous routes (Bluetongue virus)

21
Q

Explain the possible outcomes of viral infection of the foetus

A
  1. Abortion/still birth e.g. EHV1, parvovirus infection in pigs.
  2. Foetal malformation e.g. akabane virus infection in cattle, parvovirus in kittens
  3. Foetal tolerance e.g. bovine viral diarrhoea virus (BVDV).
  4. Recovery with no adverse effects.

Affected by stage of gestation - the earlier the more damaging

22
Q

Mechanisms by which viruses may lead to the production of disease in the animal, giving specific viral examples of each

A
  1. Viral damage to tissues and organs e.g. Herpes simplex 1
  2. Epithelial damage predisposing to secondary bacterial infection e.g Rhinoviruses
  3. Damage to the immune system e.g. in chickens bursal disease virus leads to atrophy and a severe deficiency of B lymphocytes –> increased susceptibility to other infectious agents
  4. Immune response as a cause of disease e.g. Feline infectious peritonitis
  5. Autoimmune diseases e.g. caprine arthritis-encephalitis virus in goats
23
Q

Discuss, using examples, how some viruses predispose to secondary infections with other agents of disease

A

Viral infections of the respiratory or digestive tracts often lead to bacterial infection e.g. cattle - parainfluenza virus 3

24
Q

Persistent infections

A

Able to establish infections in animals, which may persist for months or years or life - can result in late pathological manifestations of the disease.

  • development of carrier allows spread within pop
  • reactivated and cause recurrent disease
  • may lead to immunopathological disease
  • associated with neoplasia later in life

e.g. herpes simplex cold sores in people

25
Q

Latent infections

A
  • Period of latency follows recovery from a primary acute infection
  • During latency, only a few of the many genes are expressed and cannot be detected by conventional diagnostic tests.

e.g. herpes simplex virus 1

26
Q

Chronic infections

A

Continuous virus production

e.g. foot and mouth disease

27
Q

Slow infections

A
  • Very long preclinical phase
  • Virus gradually increases in number over time, leading to a slowly progressive lethal disease

e.g. HIV

IVP: Veterinary Pathogenesis (8 decks)

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