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Virology > Exam 2- Retroviral Diseases > Flashcards

Exam 2- Retroviral Diseases Flashcards

1
Q

Describe the genome of a Retrovirus

A

enveloped virus

(+) single stranded RNA genome

Only virus that is diploid

  • This virus replicates through a DNA intermediate. RNA-dependent-DNA-polymerase, or reverse transcriptase which is a pol gene product that reverse transcribes the RNA genome into DNA
  • Integrates into the host cell DNA- the Provirus form is an integrated, double stranded DNA copy of the RNA genome
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2
Q

What are proviral DNA?

A

This is a DNA copy of viral RNA that integrates into host cell genome.

LTR (long terminal repeats) comprise of U3-R-U5

U3 region in the LTR contains promoter and enhance elements for transcription of viral RNA by host cell RNA pol II

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3
Q

What protein within the Retrovirus Genome encodes for polymerase and Viral Enzymes such as RT, Integrase, and protease?

A

POL section

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4
Q

What Genera of Retroviruses encodes for Avian leukosis and sarcoma viruses

A

Alpharetrovirus- example is Raus sarcoma virus

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5
Q

What genera is associated with ovine pulmonary adenomatosis?

A

Betaretrovirus

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6
Q

What genus is associated with Feline leukemia and sarcoma viruses

A

gammaretrovirus

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7
Q

What genus is associated with Bovine leukemia virus?

A

Deltaretrovirus

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8
Q

What is cis activation

A

otherwise known as insertional activation- virus with LTR activates nearby cellular genes

seen with alpha-, beta-, and Gammaretroviruses

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9
Q

What is trans-activation

A

Virus gene product acts as transcription factor to induce cell transformation

Deltaretroviruses

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10
Q

What is a proto-oncogene

A

normal cellular gene which, when altered by mutation or transduced by a retrovirus, becomes an oncogene that can contribute to cancer. Proto-oncogenes may have many different functions in the cell- some proto-oncogenes provide signals that lead to cell division, others regulate programmed cell death

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11
Q

Oncogene

A

A gene that played a normal role in the cell as a proto-oncogene and that has been altered and now may contribute to the growth of a tumor. The growth is unregulated and can occur in the absence of normal growth signals such as those provided by growth factors.

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12
Q

What are the major mechanisms of Retroviral Oncogenesis

A
  1. Transduction of Cellular Proto-oncogenes
    • cellular proto-oncogene is inserted into the retrovirus genome
    • Oncogene has no role in the replication of the virus
    • in most cases the oncogene replaces oen or more viral genes, these are now replication defective viruses.
      • Require helper virus to complete replication
      • Ex: Rous Sarcoma virus
  2. Insertional activation
    1. Cis- activation
    2. Trans-activation
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13
Q

What method of oncogenesis takes the longest?

the shortest?

A

Insertional Trans-activation takes months to years, and has very low efficiency of transformation

Transducing takes days. and has very high efficiency of transformation

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14
Q

What are the 2 classes of avian alpharetroviruses?

A
  1. Endogenous
  2. Exogenous
    • Replication competent
      • Most often non-pathogenic
      • Serve as helper viruses for transmission of replication defective viruses
    • Replication defective
      • Depend on helper virus
      • viruses have acquired an oncogene from a cellular oncogene
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15
Q

What is the nature of disease with a Alpharetrovirus in avians?

A

Clinical outcome depends on the nature of the virus and the age of infection

  • Endogenous
    • Found in the genome of every cell and is rarely expressed, non-pathogenic
  • Exogenous- Replication competent
    • Virus can be transmitted vertically or horizontally
    • Transformation invariably occurs in the intact bursa
  • Exogneous - Replication defective
    • Virus requires a co-infection with replication competent virus for transmission. Forms of disease depend on the oncogene carried by replication defective virus,
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16
Q

Clinical Syndrome of avian Leukosis/Sarcoma

A

Lymphoid leukosis- tumors of B-lymphocytes that occurs in persistently infected chickens. They are generally multicentric and invasive

Osteopetrosis

Erythroblastosis- either proliferative or anemic

Myeloblastosis- high numbers of myeloblasts can accumulate in blood

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17
Q

Diagnosis of Avian Leukosis/Sarcoma

A

Necropsy lesions are usually adequate. Nerve lesions are absent.

histopath reveals a homogenous population of neoplastic cells

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18
Q

Pathogenesis of Avian Leukosis/sarcoma

A
  • lymphoid leukosis is a clonal malignancy of the bursal-dependent lymphoid system, with tumors composed almost entirely of B lymphocytes
  • Transformation invariably occurs in the intact bursa, often as early as 4-8 weeks after infection
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19
Q

control measures for avian leukosis/sarcoma

A

Eradication

Hygiene- all-in, all-out and through cleaning lowers the virus concenration

Genetic resistance

Vaccination- has been part of eradication program but is not an accepted method as of yet

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20
Q

What is an example of Betaretrovirus?

A

JRSV

Jaagsiekte Sheep Retrovirus

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21
Q

What is the character of disease for Betaretroviruses Agent JRSV

A

Bronchioalveolar carcinoma of sheep

Progressive weight loss, dyspnea, moist crackles

Complication from bacterial pneumonia

usually affects Adult sheep 1-4 years

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22
Q

What are methods of transmission for Betaretroviruses?

A

inhalation via infectious aerosols- close contact

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23
Q

What are methods for controling betaretroviruses

A

Prompt culling of any suspicious animal is advised

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24
Q

why is JRSV of importance

A

This is an enveloped protein , of the JSRV- related endogenous virus is required for reproduction

  • When production fo the envelope protein was blocked in early placenta (in the absence of the protein)
    • The growth of the placenta was reduced
    • Giant binucleate cells did not develop
    • Embryos could not implant
    • Sheep miscarried
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25
Q

what condition is associated with a JRSV infection?

A

Ovine Pulmonary Adenomatosis

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26
Q

what is an example of gamaretroviruses?

A

Feline Leukemia and Sarcoma Viruses

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27
Q

What are the clinical manifestations associated with Feline Leukemia and Sarcoma viruses?

A

Malignancies

Severe immunosuppression

Profound anemia

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28
Q

What are examples of exogenous gammaretroviruses?

A

Replication competent: FeLV

Replication Defective: Feline Sarcoma Virus

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29
Q

What are examples of endogenous gammaretroviruses?

A

Endogenous Feline Leukemia Virus

enFeLV

30
Q

What type of FeLV is contagious and transmitted horizontally from cat to cat

A

FeLV-A

Archetypical form of FeLV

found in all naturally infected cats

Efficient transmission

Tends to be less pathogenic

31
Q

FeLV Subgroup B

A

Arises in FeLV A infected cats as a result of recombination with enFeLV. This is found in ~50% of naturallly infected cats

Associated with neoplastic disease

32
Q

FeLV Subgroup C

A

Arises in FeLV A infected cats through recombination with an en FeLV this is distinct from FeLV B

Strong association with eruthroid hypoplasia and consequent severe anemia

33
Q

FeLV Subgroup T

A

Genetic variant of subgroup A

T-cell tropic virus

highly cytopathic

Uses two different cell receptors

immunosuppression

34
Q

FOCMA

A

Feline oncornavirus-associated cell membrane antigen

35
Q

Why is FOCMA relevant

A

it is not encoded by the virus but is expressed on cells that are transformed by FeLV

36
Q

Pathogenesis of FeLV

A
  • Transmitted predominantly via saliva
  • In absence of effective immune response, virus attaches to receptors on tonsilar lymphocytes, macrophages
  • Transient viremia- replication in thymus, lymph nodes, salivary glands
37
Q

What are potential outcomes of a FeLV infection?

A

immunity

Persistently infected

sick-neoplasia or degenerative disease/immunosuppression

Latent infection

38
Q

What are the outcomes of acute infections of FeLV?

A
  • Most common
    • cats develop effective immune response
    • transient viremia with virus shedding
    • Virus can persist in bone marrow
    • May result in latent infection
  • ~30% of cats
    • Failure of immune response to contain virus replication
    • Persistent viremia/antigenemia
    • No VN antibody or CTLs
    • Develop fatal diseases within a variable time period
39
Q

What are FeLV related disorders?

A

Neoplasia (lymphoma, myeloid leukemia)

Anemia (usually non regenerative and normochromic)

Other FeLV related disorders

  • immune complex formation associated with glomerulonephritis, polyarthritis, vasculitis
  • enteritis
  • Neuropathy- hind limb paralysis
  • Osteochondromatosis
40
Q

What are transmission methods for FeLV

A
  • Persistently viremic cats are main reservoir
    • large amount of virus shed in saliva
    • less shed in tears, urine, feces
  • Social behavior, oronasal contact
  • Age resistance- younger animals much more susceptible
  • Vertical transmission in utero or by milk
  • Incidence of infection directly related to population density
41
Q

What are methods of Prevention for FeLV

A

Management- test and remove viremic cats

Vaccination- commercial vaccines are available

42
Q

What are methods for treatment of a cat with FeLV

A

antivirals

Interferons

43
Q

Feline Sarcoma viruses

A

Do not spread horizontally from cat to cat

Replication defective (has acquired oncogene)

  • requires FeLV as a helper virus

Acutely transforming virus

  • causes solid tumors of mesenchymal origin

Polyclonal malignancy with multifocal tumors

Malignant cells express FOCMA

44
Q

give an example of a Deltaretrovirus

A

Bovine Leukemia Virus

45
Q

What is another name for Bovine Leukemia Virus?

A

enzootic bovine leukosis

46
Q

What protein plays a role in oncogenesis for BLV?

A

virus encoded Tax protein

47
Q

What is the character of disease for BLV

A

chronic disease evolving over an extended period (1-8 years)

Seropositive animals- show now clinical sings

Persistent lymphocytosis

10% of cattle develop tumors

48
Q

What is the pathogenesis for BLV?

A

infects B lymphocytes

mechanism for oncogenesis not understood

Slow developing

Tumors commonly found in the ruterus, abomausm, heart and external lymph nodes.

49
Q

Transmission for BLV

A
  • Horizontal
    • rectal palpation
    • Dehorning
    • close contact within a herd
  • Vertical transmission can occur
    • <10% calces virus positive at birth
  • pasteurization inactivates BLV
  • no evidence that BLV infects humans
50
Q

Is there a successful vaccine developed for BLV?

A

no

51
Q

Lentivirus overview

A
  • Non-oncogenic, lifelong persistent infection in infected animals.
  • Lentivirus causes chronic disease
    • Immune reactions to persistent viral antigens
    • Damage to the immune system, causing immunodeficiency
      • Opportunistic infection
      • Malignancy
  • replicate in macrophages, and a subset causing immune defficiency also replicate in T lymphocytes
52
Q

What lentiviruses have a tropism for monocytes and macrophages

A

equine infectious anemia (EIA)

bovine immunodeficinecy virus (BIV)

53
Q

What lentiviruses have a tropism for monocytes and lymphocytes

A

HIV

Feline immunodeficiency virus

54
Q

What are essential regulatory proteins for Lentiviruses?

A

Tat and Rev

55
Q

What are important features of Lentiviruses?

A
  • Genome contain a number of genes that mediate complex virus-host interactions and contribute to persistence and pathogenesis
  • High rate of genetic variation
56
Q

What are methods of transmission for Lentiviruses?

A
  • Horizontal transmission
    • transfer of blood
    • transfer of bodily fluids, secretions
  • Vertical transmission of HIV-1 (perinatal)
  • Animals infected with a lentivirus do not eliminate infection
  • Transmission efficiency can depend on virus load
57
Q

What are the non-immune deficiency Lentiviruses?

A

EIAV

OPPV

VAEV

Clinical diseases are basically the result of immune-mediated damage

inflammation cytokine, immune-mediated damage, virus antibody complexes

58
Q

What lentiviruses are classified as immunodeficiency disorder subgroup

A

HIV, SIV, FIV

initial replication in the RE system

virus then becomes lymphotrophic with destruction of CD4+ cells

Clinical disease from opportunistic infections and neoplasia

59
Q

Feline immunodeficiency virus pathogenesis

A
  • Infection of macrophages and lymphocytes
    • decreased CD4+ T cells
    • altered cytokine expression
    • Can lead to progressive immune dysfunction and opportunistic infections
  • Dissemination of virus to CNS and/or lymphoid organs
    • CNS dissemination
      • Neuronal toxicity
      • behavioral changes
    • Lymphoid organ
      • increased viremia
      • may be contained by immune response
      • lack of adequate control can lead to progressive immune dysfunction
60
Q

What is the nature of clinical disease associated with FIV

A

disease course is highly variable

Outcome of infection is the result of complex interplay among virus and host factors

FIV associated with many clinical symptoms

61
Q

What clinical signs are associated with a FIV infection

A

chronic stomatitis, severe gingivitis

chronic upper respiratory tract disease

Lymphadenopathy, mild pyrexia, depression and leukopenia

wasting, anemia, chronic skin disease, chronic diarrhea and neurological signs

62
Q

what are methods for transmission for FIV

A
  • Horizontal via paternal routes
    • mainly bite and fight wounds
    • Frequency of horizontal transmission in multicat housholds controversial
    • Higher prevalence in free-roaming cats
    • Virus present in semen
  • Vertical
    • in utero- can vary within a liter
    • Milk
63
Q

Equine Infectious Anemia Overview

A

lifeong persistent infection ofequids

Infection produces variable disease course

  • acute: high levels of virus replication, may result in death in 1-4 weeks post infection
  • Chronic: recurrent cycles of fever, viremia, and thrombocytopenia
  • Inapparent: Seropositive, no clinical sign
64
Q

What symptoms are seen with a horse infected with EIA

A

fever, thrombocytopenia associated with high levels of virus replication in macrophages

Anemia, edema, glomerulonephritis durign chronic stages

Death from anemia and wasting can ensue if cycling is frequent

Most horses eventually develop the ability to control cycles

Virus persistence is lifelong

65
Q

What are methods for transmission for EIA

A

biting flies

Blood contaminated fomites

This is reportable, USDA regulated

66
Q

Why is the development of an EIA vaccine difficult

A

Genetic mutations and Antigenic variation

67
Q

What are Ruminant Lentiviruses?

A

CAEV

OPPV

Bovine Immunodeficiency virus

68
Q

What does CAEV stand for?

A

Caprine Arthritis-Encephalitis Virus

69
Q

What symptoms do you see with CAEV?

A

Multi-organ-system disease

primary clinical sign is arthritis of the carpal joints

Encephalitis

Mastitis

Interstitial pneumonia

70
Q

What are methods of prevention and control for CAEV

A

This persists for life, so the major route of transmission is from doe to kid in colostrum and milk

Removal of kids at birth, and give them colostrum from CAEV-neg dams

71
Q

What does OPPV stand for

A

Ovine progressive pneumonia virus

72
Q

What are clinical symptoms of OPPV?

A

Progressive pneumonia

Encephalitis

Arthritis

mastitis

Visna (neurological manifestation of OPPV infection)

Virology (6 decks)

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