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Veterinary Virology > Prophylaxis & Therapy of Viral Infections > Flashcards

Prophylaxis & Therapy of Viral Infections Flashcards

1
Q

Who is the Father of Immunization? What observation did he make before developing the smallpox vaccine?

A

Edward Jenner

milkmaids frequently contracted cowpox, which caused lesions similar to smallpox —> those who were previously infected with cowpox almost never were infected with smallpox

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2
Q

How did Edward Jenner develop a smallpox vaccine?

A
  • collected specimen from cowpox sores
  • injected cowpox specimen into James Phipps
  • then injected James with specimen from smallpox sores
  • James never developed a smallpox infection

(vaccine comes from vaca = cow)

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3
Q

What are the 3 generations of viral vaccines?

A

FIRST GENERATION (conventional vaccines) - live anttenuated, heterologous viral, inactivated viral
SECOND GENERATION - subunit, genetic engineering
THIRD GENERATION - DNA

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4
Q

What is the purpose of vaccines? What is prophylaxis?

A

render the virus non-infectious without destroying its antigenicity/immunogenicity

when a vaccine is given to animals to protect them against some expected viral diseases

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5
Q

How are newborn animals protected from viruses before they are born?

A

pregnant animals are vaccinated to transfer the passive immunity to their offspring

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6
Q

When should vaccines be given to an animal to allow immunity to develop?

A
  • in advance before infections
  • during an outbreak with some viral infections in an attempt to protect non-infected animals at risk
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7
Q

An ideal vaccines should have the following criteria to be considered ideal:

A
  • produce some kinds of solid, long-lasting immunity
  • produce early protective immunity
  • provide protection against pathogen variants
  • produce a life-long immunity in a single dose
  • prevents infection
  • doesn’t produce any carrier state in vaccinated individuals
  • can be administered by mass immunization
  • safe and stable
  • none or minimal side effects
  • fit for long-term storage vaccine banks; thermostable
  • differentiation between infected and vaccinated individuals
  • cost effective
  • produced inexpensively and in large quantities
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8
Q

What is differentiation between infected and vaccinated individuals (DIVA)?

A

able to tell the difference between antibodies in an animal gained from vaccines or prior infection based on genetic markers and individual history

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9
Q

What are the 4 general strategies for making viral vaccines?

A
  1. ATTENUATION: make virus weak; BEST because it most closely mimics the natural wild-type virus
  2. INACTIVATION: killed, but still acts as an antigen; protein coating is present, but not viral genetic material
  3. FRACTIONATION: pieces of virus
    4 CLONING: vector vaccines, DNA vaccines, subunit vaccines
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10
Q

What are 2 examples of active immunity? Passive immunity?

A

ACTIVE
- natural infection (natural)
- vaccinations (artificial)

PASSIVE
- maternal immunity (natural)
- hyperimmune sera (artificial)

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11
Q

What are the requirements for IgG, IgA, and cytotoxic T cells to develop protective immunity against viral infection? What vaccines are used in these ways?

A

IgG: viral antigen must be processed and presented by MHC-II by APC; can be inactivated virus or viral proteins (subunit) - no need for viral replication or protein synthesis in the cell

IgA: viral antigen must be in contact with submucosal lymphocytes; virus must be alive and introduced via mucosal route

CTL: viral proteins must be synthesized in the infected cells and antigens are processed/presented at the cell surface with MHC-I; live virus, DNA

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12
Q

What immune markers for protective immunity are observed in primary protective immunity? Systemic infection immunity? Local infection immunity?

A

PRIMARY PROTECTIVE IMMUNITY: antibodies in the blood, IgA on mucosal surfaces, cell-mediated immunity (CTL)

SYSTEMIC INFECTION IMMUNITY: IgG, CTL, IgA

LOCAL INFECTION IMMUNITY: IgA, CTL, IgG

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13
Q

What are 3 important considerations in vaccine design and preparation?

A
  1. DESIGN PARAMETERS - understood pathogenesis, characteristics of virus and vaccine type/administration
  2. SAFETY AND EFFICACY - ability to use newborns, adverse reactions, safety in pregnant animals, induction of both humoral and cellular immunity, long-term memory
  3. ECONOMICAL/EASE OF HANDLING: multivalent and dose number, low cost of production, stable, needle-free
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14
Q

What are live attenuated vaccines (LAVs)? What are 4 possible side effects?

A

virus/es are weakened under laboratory conditions and will grow in the vaccinated individual, but will cause no or very mild forms of infection since they are weak

  1. possibility to revert to virulence and cause original form of disease of wild-type virus
  2. potential harms to immunocompromised
  3. contaminated cell culture vaccines
  4. not recommended in pregnant patients
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15
Q

What 2 immune responses do live attenuated vaccines (LAVs) stimulate?

A
  1. stimulates the production of excellent immune response (humoral and CMI) similar to wild-type virus
  2. stimulates the production of memory cells
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16
Q

In what 2 ways are live attenuated vaccines (LAVs) prepared?

A
  1. passage of the wild-type virus in unusual host
  2. passage of wild-type virus in unusual conditions (not optimal growth environment - pH, temp, etc)
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17
Q

How does the passage of a live virus in unnatural hosts and environments allow for the production of a vaccine?

A

UNNATURAL HOST: continued passage of the wild-type virus causes progressive adaptive mutations for the new host, causing retention of their capacity for transient growth within an inoculated natural host (lower virulence for natural host)

UNNATURAL ENVIRONMENT: growing a pathogenic virus for a prolonged period under abnormal culture conditions allows for select mutants better suited for that environment to proliferate and be unable to cause as much harm in the host with a different internal environment

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18
Q

What are 5 major advantages to using live attenuated vaccines?

A
  1. single dose is enough to induce long-lasting immunity
  2. induces the production of antibodies against surface and internal antigens of the virion
  3. stimulated cell-mediated immunity
  4. less likely to cause allergic reactions
  5. cost usually less than the killed vaccine
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19
Q

What are 5 major disadvantages of using live attenuated vaccines?

A
  1. may produce post-vaccination reactions in immunocompromised
  2. may revert to virulence
  3. may contain an agent as latent infection if prepared in cell cultures
  4. heat labile when reconstituted from lyophilized form
  5. natural spread to the contact non-vaccinated animals may occur
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20
Q

What are 3 common live attenuated vaccines used in veterinary medicine? Where are the viruses grown?

A
  1. canine parvovirus (CPV) - feline kidney cells
  2. feline herpesvirus (FHV) - feline kidney cells
  3. infectious laryngotracheitis (ILT) - chicken kidney cells, embryonated chicken eggs
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21
Q

What are live heterologous viral vaccines? How are they attenuated?

A

two viruses are antigenically related to each other, so protection can arise from the presence of the antigens cross reacting

naturally attenuated

22
Q

What are 5 examples of heterologous vaccines in veterinary medicine?

A
  1. pigeon poxvirus —> fowl poxvirus
  2. shop fibroma virus —> rabbit myxomatosis
  3. sheep pox —> lumpy skin disease virus
  4. herpes virus (turkeys) —> Marek’s disease virus
  5. rinderpest virus —> canine distemper virus
23
Q

What are inactivated (killed) viral vaccines?

A

whole virus is inactivated/killed using physical methods (formalin, heat, beta-propiolactone) or chemical methods (UV, irradiation), inactivated the nucleic acids and leaving the virus unable to replicate in the vaccinated individual

24
Q

What are 4 advantages to using inactivated (killed) viral vaccines?

A
  1. relatively stable
  2. safer than attenuated vaccines, especially for immunocompromised and pregnant animals
  3. minimal post-vaccine reactions
  4. possibility of spread is rare
25
Q

What are 4 disadvantages to using inactivated (killed) viral vaccines?

A
  1. highly expensive because it is prepared from highly concentrated viruses
  2. short-term immunity requires booster doses
  3. less efficient in the induction of cell-mediated immunity
  4. vaccinated animals require a larger antigenic mass and the use of an adjuvant to enhance the magnitude of immune response
26
Q

What are adjuvants? What are the 3 types?

A

a component that potentiates the immune response to an antigen and/or modulates it towards the desired immune response

  1. DEPOT ADJUVANT: causes a storage of the vaccine at the site of injection allowing for a prolonged immune response (mineral compounds, oil-based, liposomes)
  2. PARTICULATE ADJUVANT: acts as a delivery vehicle for the antigen to help in targeting antigens to immune cells (T lymphocytes), enhancing cell-mediated immunity
  3. IMMUNOSTIMULATORY ADJUVANT (ISCOMs): large particles made up of saponins (Quil A), lipids, cholesterol, an an antigen, help together by hydrophobic interactions, enhancing antibody productions
27
Q

Why 2 types of adjuvants did Freund use?

A
  1. Freund’s complete adjuvant (FCA) - mineral (paraffin) oil mixed with killed Mycobacteria
  2. Freund’s incomplete adjuvant (FIA) - water-in-oil emulsion without Mycobacteria
28
Q

What 8 actions can adjuvants do to “help out” vaccines?

A
  1. make vaccine more cost-effective (fewer doses)
  2. effective innate immune signals
  3. good immunomodulatory capacity
  4. high specific antibody production
  5. antigen-specific clonal expansion
  6. generation of cytotoxic T cells
  7. long-lasting adaptive immune response
  8. makes antigen more potent (less dose required)
29
Q

How does the route of administration of live vaccines affect immune response?

A

administered on mucosal surfaces (intranasal, oral, genital) = IgA, IgG, and cytotoxic T cells give protective immunity for both systemic and local infections

administered by parenteral routes (IM, SQ) = IgG, cytotoxic T cells, NO IgA gives systemic protection

30
Q

How does the route of administration of inactivated vaccines affect immune response? Why is it only given parenterally?

A

generates IgG only - giving no cellular immunity, but protective immunity for systemic infections associated with viremia and to a lesser extent local infections

has no ability to replicate

31
Q

Prime-boost vaccination approach:

A

live virus vaccine = one dose
killed virus vaccine = boosters necessary

32
Q

What are 8 common disadvantages of conventional virus vaccines?

A
  1. reversion to virulence
  2. incomplete inactivation
  3. contamination
  4. secondary effects
  5. inflammation, granuloma, fever, hypersensitivity
  6. immunosuppression
  7. inability to differentiate vaccinated from infected animals
  8. cold-chain requirement - -20 degree C is not feasible for storage in many practices
33
Q

What are the 2 types of recombinant vaccines (second generation)?

A
  1. DNA viruses - live gene-deleted replication competent, live gene-deleted replication defective, genetically engineered subunit vaccine
  2. RNA viruses - generation of viral infectious clones by bacterial artificial chromosomes (BAC) or yeast artificial chromosome (YAC)
34
Q

What are subunit vaccines?

A

split vaccine prepared from virus compounds devoid from viral nucleic acids, like capsid and envelop proteins, or other components responsible for the induction of the immune response against the virus of concern

35
Q

What are 3 advantages of using subunit vaccines?

A
  1. it is safe because it is free of viral nucleic acids
  2. it doesn’t induce febrile reactions induced by some proteins in other viruses
  3. highly immunogenic in high doses
36
Q

What are 3 common genetically engineered subunit vaccines?

A
  1. virally vectored subunit vaccine
  2. plasmid-based/vectored subunit vaccine (expressed in bacteria)
  3. expressed in yeast and mammalian cells
37
Q

What are third-generation DNA vaccines? What is the point of a plasmid in this type of vaccine?

A

vaccines based on the introduction of a DNA plasmid into the host cells (plasmid = extra, circular DNA in bacteria)

plasmid carries a protein-coding gene that transfects cells in vivo at very low efficiency and expresses an antigen that causes an immune response

38
Q

How are third-generation DNA vaccines delivered?

A
  • injection of the prepared DNA vaccine in a saline solution (IM, ID, assisted by electroporation)
  • gene gun delivery
39
Q

DNA vaccine mechanism:

A
40
Q

What are 7 advantages to DNA vaccines?

A
  1. plasmids are easily manufactured in large amounts
  2. DNA is very stable and resists temperature extremes
  3. DNA sequence can be changed easily in the lab
  4. mixtures of plasmids can be used as a broad-spectrum vaccine (multivalent)
  5. plasmid does not replicate and codes only for proteins of interest
  6. no protein component, so there is no immune response against the vector
  7. antigen is presented by both MHC-I and MHC-II, allowing for better overall protection
41
Q

What are 3 disadvantages to DNA vaccines?

A
  1. possibility for inducing antibody production against DNA plasmid
  2. may have poor immunogenicity
  3. may induce immunologic tolerance by antigens expressed inside host body
42
Q

Distribution of protective immune response in vaccinated animal population:

A

no vaccine is expected to produce 100% protection

43
Q

What is maternal immunity? What is its purpose? Why is it still important to vaccinate offspring when appropriate?

A

passive transfer of humoral immunity (antibodies) via colostrum/milk/egg yolk

protect newborn and young animals, prevent enteric infections

does not provide cellular immunity and lacks memory immune cells

44
Q

How long does maternal serum IgG persist in cattle/horses, dogs/cats/pigs, and chickens/turkeys?

A

cattle/horses: 6 months
dogs/cats/pigs: 4 months
chicken/turkeys: 1 month

45
Q

Why is it not recommended to vaccinate young animals before their maternal IgG antibodies have dispersed? How can this be overcome?

A

maternal antibodies interfere with the immunization of young animals

  • repeated vaccinations before the predicted loss of antibody
  • using the intranasal route (mucosal) when modified live vaccines are used (local immunity)
46
Q

What are 3 common causes of vaccination failure?

A
  1. wrong strain/serotype organisms
  2. method of production destroys protective epitopes in inactivated vaccines
  3. failure of an effective vaccine to stimulate protective immunity due to unsatisfactory administration, the death of a live vaccine, improper timing, or animal to animal variability
47
Q

What is the ring vaccination strategy?

A

the vaccination of all susceptible herds in a prescribed area around an outbreak of infectious disease to form a buffer zone of immune herds to prevent the spread of disease

48
Q

What is herd immunity?

A

large number of individuals become immune against circulating infectious disease by vaccinating (or recovering) 70% or more of a population to limit the chance of unvaccinated individuals coming into contact with infected individuals

49
Q

Standard human/veterinary vaccine pipelines:

A
50
Q

What are 6 common challenges in the veterinary vaccine sector?

A
  1. cost effectiveness and economy of vaccine production
  2. dangerous diseases where vaccine is most demanding are not available yet (swine fever, sheep/goat pox, bluetongue, FMD, EHV-1/4 strangles, hemorrhagic septicemia)
  3. vaccine updating: RNA viruses are highly variable, so their vaccines require frequent updating
  4. potency testing requires the administration of a vaccine to target species and lab animals
  5. viruses with genetic heterogeneity, high mutation rates, and quasi-species are difficult targets for vaccination
  6. cellular immunity and long-term memory are often difficult to achieve

Veterinary Virology (25 decks)

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