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POD > 3.8 Retroviruses and Prions > Flashcards

3.8 Retroviruses and Prions Flashcards

1
Q

what are the structural and genomic characteristics of Family Retroviridae? what type of cells do they infect?

A
  • ssRNA (2 copies of ssRNA - diploid)
  • Reverse transcriptase enzyme (RNA => DNA)
  • Enveloped, helical nucleocapsid
  • Infects lymphocytes (CD4 receptor)
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2
Q

how do retroviruses replicate?

A
  • After a retrovirus enters a host cell, reverse transcriptase converts the retroviral RNA genome into double-stranded DNA. This viral DNA then migrates to the nucleus and becomes integrated into the host genome.
  • Viral genes are transcribed and translated from the genome integrated DNA
  • New virus particles assemble, exit the cell, and can infect another cell.
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3
Q

what are the four main genes that encode the virion proteins of retroviruses? what are their functions? what other important

A

Four main genes encoding the virion proteins:
gag – (group associated gene)- structural proteins matrix, capsid and nucleocapsid
Pro – codes for a protease responsible for viral protein maturation
pol - (polymerase) reverse transcriptase and integrase
env - (envelope) codes for surface glycoprotein and transmembrane protein

Regulatory genes e.g. tat, rev, rex Oncogenes e.g. v-scr (oncogenic retroviruses)

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4
Q

the three functions of the polymerase of retroviruses?

A

The polymerase of retroviruses has 3 functions:

1) RNA dependent DNA polymerase (reverse transcriptase)
2) DNA dependent DNA polymerase
3) RNase

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5
Q

Which of the following statements is NOT CORRECT about retroviruses? a. They are enveloped viruses
b. Retroviruses can infect lymphocytes
c. They are unique in possessing a reverse transcriptase enzyme
d. A DNA copy of the viral genome is inserted into the host genome
e. Env, gag, and pol genes are important oncogenes

A

e. Env, gag, and pol genes are important oncogenes

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6
Q

what are some important retroviruses in vet med? what features do they share and have individually? which is reportable?

A
  • Reverse transcriptase enzyme (RNA to DNA)
  • Proviral DNA: integrated into the host cell genome
  • Avian leukosis virus: B cell lymphomas (slow rate)
  • Bovine leukemia virus: lymphosarcomas everywhere!
  • equine infections anemia virus: reportable
  • Feline leukemia virus: lymphosarcoma
  • Feline immunodeficiency virus: immunosuppression
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7
Q

what is lymphoma

A

Lymphoma= Lymphosarcoma any neoplastic disorder of
lymphoid tissue (lymphocytes)

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8
Q

what is leukosis?

A

Leukosis= neoplastic proliferation of leukocyte-forming tissue; the basis of leukemia (lymphocytes, macrophages, granulocytes)

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9
Q

what is leukemia?

A

Leukemia= neoplastic disease of the blood-forming organs, marked by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow

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10
Q

what are avian alpharetroviruses? what types are there?

A

Related but distinct viruses (avian leukosis/ sarcoma viruses) that can be:
1) Exogenous replication competent viruses
2) Exogenous but replication defective viruses
3) Endogenous avian leukosis viruses

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11
Q

in terms of avian alpharetroviruses, what are the characteristics of exogenous replication competent viruses?

A
  • transmitted horizontally or congenitally between birds as typical viruses
  • slow tumor development since they do not have their own oncogenes
  • tumors arise from insertional mutagenesis (e.g., Rous Sarcoma virus)
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12
Q

in terms of avian alpharetroviruses, what are the characteristics of exogenous but replication defective viruses?

A
  • Alpharetroviruses acquiring an oncogene at the expense of losing gag, pol, env, pro gene
  • Replication requires a helper virus to supply the missing gene products
  • Rapidly transforming due to the acquired oncogene
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13
Q

in terms of avian alpharetroviruses, what are the characteristics of endogenous avian leukosis viruses?

A
  • are present as proviruses in the genome due to mutations that prevent infectious virus assembly
  • Transmitted only genetically
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14
Q

what is avian leukosis virus? how does it impact the host? what is its occurence/ where is it seen? What does it cause and what the syndromes associated with it?

A

neoplastic proliferation of leukocyte-forming tissue
* Low occurrence in commercial flocks mostly seen in back yard chickens
* Slow rate of tumour development

Syndromes:
* Lymphoid leukosis: lymphoid infiltration, B cell lymphomas
* Osteopetrosis: enlarged (density) long bones of the wings and legs (virus replication in osteoblasts)
* Renal tumors: nephroblastoma

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15
Q

what does avian leukosis virus do to bones?

A

Osteopetrosis: enlarged (density) long bones of the wings and legs (virus replication in osteoblasts)
-Avian leukosis virus alters the growth and differentiation of osteoblasts

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16
Q

what will we find upon post mortem due to avian leukosis virus, in the organs?

A

Lymphoid leukosis: tumours in liver, spleen, bursa of Fabricius, kidneys

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17
Q

Diagnosis of avian alpharetroviruses - how do we do it, what is a differential disease and what are the differences?

A
  • History, clinical signs, post-mortem, histopathologic examination
  • Differential: Marek’s disease (important because it can be controlled by vaccines, but Avian leukosis cannot!
  • Avian leukosis virus: no tumours in the skin and nerves
  • Detection of viral antigen: ELISA
  • Detection of Ab in serum: ELISA
  • Detection of nucleic acid (PCR)
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18
Q

can we vaccinate for avian alpharetroviruses?

A

no!

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19
Q

Avian leukosis virus infection should be primarily differentiated from?
a. Fowlpox virus
b. Avian polyomaviruses
c. New castle disease virus
d. Marek`s disease virus

A

d. Marek`s disease virus

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20
Q

what disease does Bovine leukemia virus (BLV) cause? how is this virus related to exports?

A
  • BLV causes enzootic bovine leukosis (name of the disease)
  • OIE list 2020 Herds require to be free of BLV for exportations
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21
Q

what is the worldwide distribution of BLV? do all infected animals develop clinical disease?

A

Worldwide distribution
* 25% of dairy cattle in the USA are infected
* few animals will develop clinical disease (4-8 years)
* culling of high producing dairy cows causes economic loss

22
Q

how transmissible is BLV and how is it transmitted?

A
  • Not highly transmissible
  • mainly by blood or tissue containing lymphocytes,
  • rarely by insects as mechanical vectors, milk, colostrum, in utero
23
Q

what cells does BLV target? what is the result of this?

A
  • BLV infects primarily B lymphocytes - viral oncoprotein Tax mediates transformation
  • Causes lymphosarcoma of B cell origin in lymph nodes, abomasum, heart, spleen, kidneys, uterus, spinal meninges, brain
24
Q

how do we diagnose Enzootic bovine leukosis? how do we treat and control it? can we vaccinate?

A

Diagnosis:
* Serology: ELISA (Ab is present 4-12 wks after exposure)
* PCR

No treatment
* Control: slaughter in most cases
* There are no vaccines

25
Q

what type of virus is Feline leukemia virus (FeLV)? what determines its pathogenicity?

A
  • FeLV is an exogenous gammaretrovirus
  • Determinants of pathogenicity are located within the envelope protein giving rise to 4 antigenic types A, B, C, T
26
Q

what types of Feline leukemia virus (FeLV) are there? what are the major differentiating factors?

A
  • Determinants of pathogenicity are located within the envelope protein giving rise to 4 antigenic types A, B, C, T
  • FeLV-B: neoplasia
  • FeLV-C: erythroid hypoplasia and progressive anemia (1%, rare)
  • FeLV-T: destruction of T-lymphocytes (immunosuppression)
27
Q

what disease syndromes does Feline leukemia virus (FeLV) cause?

A
  • Causes a variety of debilitating disease syndromes including
    a. Neoplastic disorders
    b. Bone marrow suppression
    c. Neurologic disorders
    d. Immunodeficiency
    e. Immune-mediated diseases
    f. Reproductive failure in pregnant queens
28
Q

what are predisposing factors for Feline leukemia virus (FeLV)?

A
  • Predisposing factors: young kittens, shelters
29
Q

how is FeLV transmitted?

A
  • Excreted in saliva, tears (urine)
  • Transmission: close contact licking; prolonged, extensive cat-to-cat contact; congenitally, biting

“friendly cat disease”
- Spread in saliva, tears
- (maybe also feces and urine)
- Often spread to litters of kittens from their mum

30
Q

is FeLV an increasing problem?

A
  • In most countries FeLV infection and its associated disease has become much less common
31
Q

what is the pathology of FeLV? What are the clinical outcomes of infection? what are the possible disease trajectories based on?

A
  • Typically, a chronic disease course
  • Multiple disease trajectories are possible for infected cats- based on age at infection, concurrent infection with other agents, the genotype and dose of virus, genetic constitution of the cat, and other environmental factors

Progressive infection: uncontrolled and persistent viremia in infected cats. Initial infection in the oral/pharyngeal lymphoid tissue spreads to peripheral sites via lymphocytes and monocytes

Regressive infection: Viremia followed by immune-mediated clearance. Sensitive assays can detect provirus DNA in the blood

Abortive infection: FeLV replicates in the oral/pharyngeal lymphoid tissue without viremia

32
Q

How to diagnose FeLV? What should we keep in mind regarding antigen levels?

A
  • Antigen detection by ELISA
  • Nucleic acid detection by PCR

Feline leukemia provirus and antigen test results may vary depending on the cat’s immune status at the time of testing
High levels of provirus DNA and antigen: progressive infection
Low levels of provirus and antigen: regressive infection.

33
Q

prevention and control strategies for FeLV?

A
  • FeLV free catteries - test and remove

Anti-retroviral compounds
* Limited success L
* Zidovudine (AZT, Reverse transcriptase inhibitor)

CORE vaccines:
* Vaccines inactivated - clinical incidence reduced by about 70%
* Subunit vaccine (p45 from gp70) envelope protein

34
Q

what genus is Feline immunodeficiency virus (FIV) in? how long does infection last? where is the virus found and how is it shed and transmitted?

A
  • Genus Lentivirus (slow!)
  • Infected for life!
  • Endemic throughout the world
  • Shed in saliva
    >Transmission: by bites
35
Q

what demographic is at greatest risk for Feline immunodeficiency virus (FIV) infection?

A
  • At greatest risk: free-roaming, male, aged cats
    > Dual infection with FeLV is common
36
Q

what are the three stages of FIV disease? how long do they last and what are the symptoms?

A
  • Three stages (loss of CD4+ helper lymphocytes):

Acute - lymphadenopathy, fever, flu-like illness for 1-3 days

Subclinical - 1month to 10yrs

Terminal – acquired immunodeficiency opportunistic bacterial and fungal infection (mouth, periodontal tissue, cheeks, tongue); chronic respiratory disease; enteritis; urinary tract infection; dermatitis; neurologic signs (5%)

37
Q

how can you diagnose FIV? what is a limitation?

A
  • Serological assays for FIV cannot distinguish naturally infected and vaccinated cats (although the commercial vaccine is discontinued)
  • Positive serological test in kittens can detect passively transferred antibodies from the dam and not due to active infection.

FIC antibody test > if +, repeat using different test kit > if +, infected, if -, PCR test > if +, infected

38
Q

what type of diseases are Transmissible spongiform encephalopathies (TSEs)? what causes them and what is their common outcome?

A

All the diseases caused by unconventional agents are classified as transmissible spongiform encephalopathies, or shortly TSEs.

These uniformly fatal diseases are caused by PRIONS: “proteinaceous infectious particles which resist inactivation by procedures that modify nucleic acids”

Characteristic lesion is spongiform degeneration with the activation and proliferation of astrocytes and microglia in the brain and spinal cord

  • Transmissible spongiform encephalopathies (TSEs) encompass a group of neurodegenerative diseases in animals and humans which can be transmitted experimentally.
39
Q

what disease is susptected to be linked to the human Creutzfeldt- Jakob disease (vCJD)?

A

There is a suspected link of the BSE agent to variant of Creutzfeldt- Jakob disease (vCJD).

40
Q

onset of illness for Transmissible Spongiform Encephalopathy is preceded by? outcome is usually what?

A
  • The onset of clinical illness is preceded by a prolonged incubation period of months to decades and the outcome is ultimately fatal.
41
Q

how to treat Transmissible Spongiform Encephalopathy

A
  • There are no vaccines and there is no treatment.
42
Q

Transmissible Spongiform Encephalopathy pathological changes are confined to what?

A

Pathological changes are confined to the central nervous system

43
Q

what are prions?

A

Prions are highly conserved normal cellular proteins that has undergone pathological conformational change

44
Q

how does scrapie disease arise?

A

PrPc is highly expressed in neurons and may play a role in myelin maintenance

In prion-infected individual, the conformation the alpha helixes (PrPc) change to one with beta-sheets (PrPSc)
>this prion is protease resistant, insoluble, has no immune or inflammatory response, resists boiling, formaldehyde, irradiation

45
Q

Important Transmissible Spongiform Encephalopathies (TSEs) > these are reportable. what species do they effect?

A
  • Scrapie (sheep) OIE list 2020
  • Bovine spongiform encephalopathy (BSE, cattle) OIE list 2020
  • Chronic wasting disease (deer, elk)
46
Q

what is scrapie? what are the economic impacts and what is the incubation period? is it transmissible? how can we treat and prevent it?

A

“Sheep scrape off their wool”
* Fatal, neurodegenerative disease of sheep and goats
* Scrapie can have significant economic impact on the sheep industry
* Incubation period: as long as 8 years
* Highly transmissible!
* No treatment, no vaccinesL
* Best solution: humane destruction and disposal of all infected and at-risk animals

47
Q

Pathogenesis of Scrapie. what do lesions look like post mortem?

A
  • Natural route of infection is not yet proven- oral route widely accepted
  • Experimental infection- all routes of inoculation produce disease and intracerebral inoculation produces disease faster
  • Following ingestion of prions infection is initiated in the gut lymphoid tissues that move to the central nervous system (CNS)
  • At death lesions in the CNS include neuronal vacuolation and degeneration, astrocytic hypertrophy and hyperplasia.
48
Q

clinical signs of scrapie

A
  • Subtle changes in behavior or temperament
  • Pruritus, loss of coordination
  • Weight loss
49
Q

do we have scrapie in canada??

A

It is rare, but it still happens
* Two flocks positive in 2019

50
Q

what is Bovine spongiform encephalopathy (BSE)? what type of disease is it? what have the impacts been historically? where has it been found and how is it transmitted?

A

Mad cow disease
* BSE is a chronic neurodegenerative disease of cattle.
* More than 160,000 cattle died during the last decade
* BSE had a substantial impact on the British livestock industry.
* BSE confirmed in domestic cattle in Ireland, France, Portugal, and Switzerland and in cattle exported from England to Oman, the Falkland Islands, Germany, Denmark, Canada, and Italy.
* Transmission is not well understood: TSE contaminated feed?

51
Q

what does mad cow disease do to the body?

A
  • Progressive degeneration of the CNS
  • Nervousness, incoordination, decreased milk production, loss of body weight
52
Q

what type of disease is Chronic wasting disease (CWD)? what animals do we find it in and how is it transmitted? what is the incubation period? what are the symptoms? is it found in canada?

A
  • Progressive, fatal neurological disease of deer and elk
  • Highly Transmission routes: unknow, but it is highly transmitted between animals
  • Incubation period: 1.5–4 years
  • Marked weight loss (GI tract is affected), abnormal behavior
  • CWD was identified in Canada (Saskatchewan, Alberta and Quebec) and several states in the US

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