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Virology > Ch 11 - Retroviruses > Flashcards

Ch 11 - Retroviruses Flashcards

1
Q

basic structure of retroviruses

A

enveloped, diploid +ssRNA (RT into dsDNA)

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2
Q

retroviruses: 2 enzymes needed for production of provirus?

A

RT and integrase

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3
Q

Avian Leukosis and Sarcoma viruses: endogenous or exogenous?

A

exogenous

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4
Q

Avian Leukosis and Sarcoma virus: replication competent/incompetent

A

competent

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5
Q

mode of transmission and signalment of poultry that are at the highest risk of developing disease associated with avian leukosis virus

A

vertically (congenital infection)

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6
Q

Avian Leukosis and Sarcoma virus: most common tumor type

A

lymphoid tumors

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7
Q

Avian Leukosis and Sarcoma virus: other tumors

A

mesenchymal, myeloid/erythroid

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8
Q

Avian Leukosis and Sarcoma virus: how to distinguish from Marek’s? (histo)

A

Avian Leukosis and Sarcoma virus: B-cells. Mareks: T-cells.

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9
Q

JSRV and ENTV are gammaretroviruses, betaretroviruses, or alpharetroviruses

A

betaretroviruses

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10
Q

JSRV and ENTV: system affected

A

resp

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11
Q

JSRV and ENTV:
cell tropism

A

JSRV: pulmonary epithelial cells (sheep)
ENTV: nasal epithelial cells (goats)

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12
Q

JSRV and ENTV: tumor?

A

pulmonary/nasal adenocarcinoma

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13
Q

JSRV and ENTV: clinical signs

A

copious nasal discharge, progressive dyspnea, coughing, wt loss, anorexia

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14
Q

JSRV species affected

A

sheep

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15
Q

ENTV-1 species affected

A

sheep

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16
Q

ENTV-2 apecies affected

A

goats

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17
Q

JSRV and ENTV: transmission

A

horizontal - close contact: aerosolized resp fluid

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18
Q

JSRV and ENTV time to Dz

A

1-3 years (prolonged incubation period)

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19
Q

JSRV and ENTV incidence of tumor development

A

~30% of infected animals

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20
Q

4 common tissues in which BLV associated lymphoma tumors develop.

A

HULA!
Heart, uterus, LNs, Abomasum (+CNS)

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21
Q

BLV is an alpharetrovirus, betarestrovirus, or deltaretrovirus

A

delta

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22
Q

mechanism that BLV uses for neoplastic transformation

A

Tax (oncogenic gene) drives the cell cycle, activates NFkB, blocks apoptosis

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23
Q

BLV transmission

A

Horizontal: transfer of blood/infected lymphocytes

Vertical and congenital: < 10% of cows are + at birth. Infected milk/colostrum to calves.

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24
Q

is there a Vx for BLV?

A

No

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25
Q

Methods for control of BLV

A

periodic testing and elimiation of positives

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26
Q

FeLV is an alpharetrovirus, deltaretrovirus, or gammaretrovirus

A

gammaretrovirus

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27
Q

which FeLV subtypes are transmissible? How do they arise?

A

FeLV-A is contagious and horizontally transmitted.
the ONLY subtype that is transmitted between cats.

28
Q

How do FeLV-B and C arise?

A

de novo in FeLV-A infected cats. Arise by recombinaton of FeLV-A and enFeLV

29
Q

what is FeLV-T

A

a genetic recombinant of FeLV-A

30
Q

Which FeLV subtypes have greater virulence? (A, B, C)

A

C and B > A

31
Q

FeLV transmission

A

mainly saliva
also in milk, in utero, fighting

32
Q

which population is at highest risk of developing progressive FeLV infection

A

kittens < 16 wks of age

33
Q

Indicate the major factor that influences whether an FeLV infected cat develops a progressive or regressive infection.

List 3 other factors that can influence outcome or disease severity

A

Age

Viral dose, concurrent dose, vaccination stats

34
Q

FeLV antigen ELISA negative! Negative/regressor or transient/progressor?

what test do you run next?

A

negative or regressor. Retest with PCR. Positive = regressor. Negative = true negative

35
Q

FeLV antigen ELISA positive! Negative/regressor or transient/progressor?

what test do you run next?

A

transient viremia or regressor. Retest with ELISA in 60 days. Positive = Progressor. Negative = Regressor. Test with PCR to confirm true positive.

36
Q

outcomes of a regressive FeLV infection

A

Virus persists transiently. Can be reactivated.

37
Q

outcomes of a progressive FeLV infection

A

failure of immune response. develop fatal diseases within a variable time period (months to years)

38
Q

4 FeLV related disorders (progressor). Which is most common?

A
  1. immunosuppression (most common)
  2. bone marrow suppression and disorders
  3. immune mediated disorders/ neurologic Dz
  4. Neoplasia
39
Q

most common mechanism that FeLV induces neoplastic transformation?

A

insertional activation

40
Q

Indicate the diagnostic tests that are most appropriate for diagnosing viremia, regressive infections, and different subtypes of FeLV.

A

ELISA for capsid Ag
PCR for viral nucleic acid
Virus neutralization test for subtypes

41
Q
A
41
Q

Indicate which populations of cats should be considered to receive the FeLV vaccine and describe how the vaccine reduces FeLV associated disease

A

Vx outdoor cats! indoor cats are low risk.

Vx protects against persistent viremia.

42
Q

Three major mechanisms by which lentiviruses cause disease. Identify which mechanisms FIV utilizes.

A
  1. killing infected cells
  2. immune cell dysfunction
  3. persistent viral antigens
    (FIV uses all 3!)
43
Q

Lentivirus cell tropism

A

Monocyte, Macrophage, Lymphocytes (all 3 for immunosuppression, just mono/macro for chronic inflamm Dz)

44
Q

predominant mode of FIV transmission

A

horizontal - mainly bite/fight wound

45
Q

immunologic hallmark of FIV infection

A

progressive decline in CD4+ T-cells in the peripheral blood

46
Q

3 phases of FIV infection and clinical syndromes

A
  1. Acute phase
  2. Asymptomatic phase
  3. Terminal Phase (FAIDS)

Clinical Syndromes:
Opportunistic infections, Periodontal disease, gingivitis, stomatitis, Chronic URT, GI, urinary tract infections/disease, CNS, Weight loss

47
Q

T or F: many FIV-infected cats live a normal lifespan as uninfected cats

A

True

48
Q

difference between FeLV SNAP and FIV SNAP tests

A

FeLV SNAP measures the Ag
FIV SNAP measures that Ab response

49
Q

Positive FIV test: possible interpretation

A

infected, maternal transfer, vaccinated, or false postive

50
Q

Equine infectious Anemia Virus (EIA) and Small Ruminant Lentiviruses (SLRV): how is macrophage infection important for the disease pathogenesis?

A

they encite inflammation leading to clinical disease

51
Q

What cell is critical in the pathogenesis of EIA infection?

A

monocytes/macrophages

52
Q

EIA clinical presentations of Dz

A
  • undulating fever, anemia, thrombocytopenia –> icteric
  • vasculitis, glomerulonephritis (chronic stages)
  • death from anemia and wasting can ensue if cycling is frequent
53
Q

EIA: virus persistence is transient/life long

A

life long

54
Q

how does viral evasion of the adaptive immune response lead to the undulating nature of disease with EIA infection

A

Antigenic variation of viral proteins (Env). Periodic escape of virus from neutralizing antibody and CTL. Escape mutants break through – continued cycling

55
Q

T/F: EIA is not a reportable disease

A

F

56
Q

Implications of a positive Coggin’s Test (EIA)

A

reportable Dz in all states! Negative test required for transport across state lines. Infected horses euth/quarantined and monitored for life.

57
Q

EIA transmission

A

biting flies, blood contaminated fomites

58
Q

4 organ systems commonly affected with SRLV

A
  1. joints
  2. mammary gland
  3. brain
  4. lungs
59
Q

CAEV (a SRLV) which organ system is predominantly affected?

A

joints, brain

60
Q

OPP (a SRLV) which organ system(s) is predominantly affected?

A

Lungs

61
Q

CAEV: age of animals that typically show clinical disease?

A

Adults: arthritis
Kids (2-4 mo): neurologic Dz

62
Q

OPP: age of animals that typically show clinical disease?

A

Older sheep: progressive interstitial pneumonia

Brain: adult sheep > 2 yr

63
Q

SRLV: Identify the most common mode of transmission/source of virus.

A

mostly from doe to kid in colostrum and milk

63
Q

Testing for SRLV:

A

Serology and clinical evaluation

64
Q

What gene carried by JSRV and ENTV is oncogenic?

A

Env protein

65
Q

retroviruses integrate ? into the host cell chromosome

A

their dsDNA

Virology (6 decks)

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