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Virology > Lecture 7: Retrovirus > Flashcards

Lecture 7: Retrovirus Flashcards

0
Q

feline leukemia virus: general characteristics

A
  • naturally occurring exogenous gammaretrovirus enzootic in cats
  • infection is life long
  • prevalence is low 2% can be up to 30%
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1
Q

retrovirus properties

A
  1. diploid genome with 2 copies of ssRNA(+)
  2. RNA genome produces DNA intermediates via reverse transcriptase and RNA-dependent DNA polymerase
  3. enveloped viruses released by budding from cell membranes
  4. integrate into cell genome using integrase
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2
Q

transmission of FeLV (feline leukemia virus)

A

horizontal: infected cats shed virus in most bod fluids
vertical: transplacental

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3
Q

pathogenesis of FeLV

A
  • initial replication in oral/pharyngeal lymphoid tissue then systemic spread via lmphocytes and monoctyes
  • replicates heavily in lymphoid tissue, bone marrow, and mucosal and glandular epithelial tissue
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4
Q

virulent traits of FeLV are located where on virus?

A

on the long terminal repeats (promoter regions of provirus)

and surface glycoprotein

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5
Q

subgroups of FeLV

A

FeLV: A - minimally pathogenic
FeLV:B - linked to thymus lymphosarcoma
FeLV: C - linked to severe aplastic anemia

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6
Q

clinical signs of FeLV

A

anisocoria - unevenly sized pupils
protein deposits in anterior uvea
enlarged popliteal lymph node
chronic wounds

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7
Q

pathologies associated with FeLV infection:

A

feline lymphosarcoma or lymphoma
myeloproliferative diseases and anemia
immunopathologic disease
fibrosarcoma

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8
Q

feline lymphosarcoma or lymphoma via FeLV infection

A

multicentric: occurs in lymphoid and non-lymphoid tissue
thymic
alimentary - affects older cats lymphoid tissue of GIT (mesenteric LN)
general tumors in non-lymphoid tissue

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9
Q

myeloproliferative disease and anemia from FeLV infection

A

erythremic myelosis
granulocytic leukemia
erythroleukemia
myelofibrosis

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10
Q

immunopathologic disease

A

immune complex mediated - high levels of FeLV anitgen-antibody complexes in glomerular capillaries resulting glomerulonephritis

immunodeficiency

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11
Q

fibrosarcoma via FeLV infection

A
  • solitary tumors in old cats
  • rapid growth, frquently mets
  • induced by replication-defective feline sarcoma virus which may arise by recombination
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12
Q

dx of FeLV

A

antigen detection (SNAP tests)

  • PCR to detect FeLV provirus - confirms a positive antigen detection test
  • IF
  • vax - doesnt interfere with FeLV antigen tests
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13
Q

vaccination for FeLV protects against ______

A

progressive infection and disease but NOT against infection

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14
Q

which recombinant vaccine does not contain adjuvants? waht does this lead to?

A

canarypox vaccine (PUREVAX)

leads to the expression of “env” and “gag FeLV” antigens

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15
Q

what is the phylogeny of FeLV

A

Orthoretrovirinae: gammaretrovirus

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16
Q

phylogeny of avian leukosis and sarcoma virus

A

retroviridae –> orthoretrovirinae –> genus alpharetrovirus

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17
Q

what two diseases processes does avian leukosis and sarcoma virus cause?

A

erythroblastosis and avian lymphoid leukosis

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18
Q

what is avian lymphoid leukosis caused by?

A

exogenous RNA tumor virus (oncovirus) - of avian leukosis and sarcoma virus

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19
Q

transmission of avian lymphoid leukosis

A

vertical - hens to chicks

-horizontal - chicks infect hatch mates

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20
Q

how are endogenous viruses transmitted? is it oncogenic?

A

in the gamete genetically both rooster and hen

NOT oncogenic

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21
Q

pathogensis of avian lymphoid leukosis

A
  • tumors originate by transformation of B-cells within bursa of fabricus
  • NO nerve involvement!
  • most breeders are virtually free of exogenous lymphoid leukosis viruses (ERADICATION)
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22
Q

diagnosis of avian lymphoid leukosis

A
  • use tumor cells from BOF and react with antiserum of B lymphocytes and IgM
  • PCR
  • absence of MD MEQ gene in tumors
  • micropathology
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23
Q

control

A
  • THERE IS NO VACCINE!
  • leukosis J virus recently emerged - possible recombination btwn exogenous and endogenous virus
  • obtain chicks from LLV-free breeders
  • good sanitation and biosecurity
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24
Q

erythroblastosis signs and pathology

A

severe anemia

enlargement of spleen, liver, & kidneys - all dark red to mahogany in color

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25
Q

avian lymphoid leukosis signs and pathology

A
  • malignant lymphoblasts in tumors express B lymphocyte markers
  • malignant lmphoblasts are homogeneous in size and appearance
  • transformed lymphoblasts secrete large amounts of IgM
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26
Q

phylogeny of ovine pulmonary adenomatosis

A

retroviridae –> orthoretrovirinae –> betaretro virus

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27
Q

characteristics of ovine pulmonary adenomatosis

A

aka Jaagsiekte sheep retrovirus

  • disease of adult sheep
  • leads to wasting and severe respiratory distress
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28
Q

clinical fetures of ovine pulmonary adnenomatosis

A
  • long incubation period
  • progressive dyspnea, anorexia and cachexia
  • respiratory failure from tons of fluid in lungs produced by Type II penumocytes disseminated in neoplastic nodules
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29
Q

transmission of ovine pulmonary adenomatosis

A
  • aersolized lung fields

- virus shed in saliva, colostrum, milk any respiratory secretion

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30
Q

pathogenesis of ovine pulmonary adenomatosis

A
  • transforms type II pneumocytes located in terminal airways and alveoli
  • proviral DNA located in type II pneumocytes, lymphoid tissue, alveolar macrophages, PBLs
  • active replication restricted to bronchoalveolar epithelial cells
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31
Q

pathology of ovine pulmonary adenomatosis

A
  • nodular lesions
  • epithelial proliferation in bronchioles and alveoli
  • adenoma or adenocarcinoma
  • metastases
32
Q

dx of ovine pulmonary adenomatosis

A
  • PCR in pulmonary bronchial lavages
  • can be detected in colostrum and milk from infected ewes
  • circulating antibodies dont develop (possibly from immunological tolerance or endogenous retrovirus)
33
Q

control of ovine pulmonary adenomatosis

A
  • vaccine NOT available
    most impt –>*rear sheep in single age groups to reduce losses
  • avoid introducing new animals without quarantine
  • strict biosecurity
  • dont keep lambs of affected ewes
34
Q

phylogeny of bovine leukemia virus

A

retroviridae –> orthoretrovirinae –> deltaretrovirus

35
Q

another name for bovine leukemia virus is?

A

enzootic bovine leukosis

36
Q

disease processes of bovine leukemia virus

A

lymphoma - slow and lethal

persistent lmphocytosis: high numbers of circulating B lymphocytes in 30% infected

37
Q

clinical signs of bovine leukemia virus

A
  • most infectious are asymptomatic only revealed thru Ab testing
  • may develop multicentric lymphosarcomas in lymph nodes, abomasum, heart, spleen, kidney, uterus, brain
  • LN enlarement
  • submandibular and brisket edema
38
Q

transmission of bovine leukemia virus (BLV)

A

horizontal thru infected white blood cells (colostrum/milk)

39
Q

pathogenesis of BLV

A
  • targets B lymphocytes with IgM on surface
  • polyclonal expansion of lymphocytes
  • viral transactivating protein (Tax) enhances transcription of virus promoter (LTR)
40
Q

dx of BLV

A
  • test for specific BLV antibodies with AGP and ELISA

- PCR for proviral DNA detection

41
Q

how does BLV cause significant economic losses

A

thru culling high producing dairy cattle

- meat is condemned if cow has ONE BLV associated tumor

42
Q

prevention and control of BLV

A

could be eradicated if we tested animals every 3 months and removed all positive reactors
- separate calves from infectd dam at birth and if sero-negative, feed milk from un-infected cow

43
Q

phylogeny of caprine arthritis-encephalitis virus

A

retroviridae –> orthoretrovirinae –> lentivirus

44
Q

characteristics and syndromes of caprine arthritis-encepahlitis virus

A

its lifelong

arthritis, encephalomyelitis, pneumonia, mastitis, weight loss

45
Q

clinical signs of infection of caprine arthritis-encephalitis virus in kids

A

lameness, paralysis, paddle in bedding, depresion, circle walking, head tilt, muscle tremors

46
Q

transmission of caprine arthritis encephalitis virus

A

major route: milk/colostrum
anything that contains white blood cells bc CAE is associated with WBCS

via breeding

47
Q

clinical signs of caprine arthritis encephalitis in adults

A 
mostly asymptomatic
lameness
distension of carpal (knee) joints
weight loss, rough hair coat, labored breathing
mastitis
48
Q

dx of caprine arthritis encephalitis virus

A

serology: ELISA agar gel preciptiation test

PCR

49
Q

control of caprine arthritis encephalitis virus

A

voluntary control program

50
Q

prevention of caprine arthritis encephalitis virus

A

remove kids from infected dams as soon as they are born - this will reduce infections by more than 90%!!
- no vaccine

51
Q

phylogeny of equine infectious anemia

A

retroviridae –> orthoretrovirinae –> lentivirus

52
Q

equine infectious anemia consists of 4 syndromes:

A

acute: fever, anemia, icterus, hemmorhage in mucosa
subacute: moderate fever then recovery
life-long persistent infection: recurrent episodes of clinical signs
chronic: mild signs to cachexia, anemia and ventral edema

53
Q

pathogenesis of equine infectious anemia

A

virus infects macrophages

vasculitis and glomerulonephritis may develop from immune complex deposition

Env glycoprotein mutates - emergence of virus variants

54
Q

transmission of equine infectious anemia

A

mechanical vector via horse fly (tabanids) and stomoxys flies
iatrogenic: syringes, needles, etc
vertical: transplacental
higher in summer

55
Q

dx of equine infectious anemia

A

AGP (agar gel precip) aka coggins!!
- detects antibodies against p26

RT-PCR

56
Q

feline immunodeficiency virus occurs in which animals?

A

outdoor, unneutered, male cats that like to fight and bite

57
Q

characteristics of FIV

A
  • progressive immune suppression*
  • induces shift from T-helper-1 to T-helper 2 lymphocytes
  • cytokine dysregulation
  • anergy and apoptosis of lymphocytes in primary lymphoid tissues
  • progression of disease parallels the decline in circulating CD4+ T lymphocytes
  • incubates for years
58
Q

transmission of FIV

A

mainly thru biting

less from mating or vertically

59
Q

stages of FIV disease

A

acute: lymphadenopathy, leukopenia, fever
long sub-clinical stage: asymptomatic despite drop of CD4+ T cells
terminal: loss of immune function, infection, neoplasia, lesions in gums, recurrent fever

60
Q

clinical signs of FIV

A

non-healing infections

“feline AIDS” - poor appetite, weight loss, vomiting, diarrhea, gingivitis, stomatitis, conjunctivits, fever, swollen LN

61
Q

dx of FIV

A

antibodies persist for life

  • virus isolation is gold standard
  • PCR
62
Q

control of FIV

A

free roaming cats at greatest risk
test and removal
queens may infect kittens thru milk

63
Q

phylogeny of bovine immunodeficiency virus

A

retroviridae –> orthoviridae –> lentivirus

64
Q

pathogenesis of BIV

A

persistent leukocytosis and lymphadenopathy of subcutaneous LN

uncertain how this occurs!

65
Q

characteristic of BIV

A

as a lentivirus, it can also infect and replicate in non-dividing cells

66
Q

transmission of BIV

A

iatrogenic

67
Q

implication of BIV

A

potential for being used in gene therapy bc not infectious for humans, transduces wide range of cells, infects and replicates in nondividing cells

68
Q

phylogeny of maedi-visna

A

retroviridae –> orthoretrovirinae –> lentivirus

69
Q

maedi =

A

dyspnea

70
Q

visna =

A

wasting (neurological signs)

71
Q

maedi-visna affects what animals

A

sheep and goats

72
Q

pathogenesis of maedi-visna

A

integrates into lymphocyte DNA

73
Q

transmission of maedi-visna

A
  • infected colostrum and milk
  • direct contact - respiratory
  • both asymptomatic and symptomatic sheep and goats shed virus
  • can transmit back and forth btwn sheep and goats
74
Q

clinical signs of maedi-visna

A
  • incubation > 2 years
  • majority asymptomatic
  • maedi form = more common: progressive dyspnea, wasting, dry cough, fatal due to anoxia and bacterial pneumonia
  • visna form = progressive neurologic signs
75
Q

maedi form is seen more often in ____

A

sheep

76
Q

visna form is seen more often in _____

A

goats

77
Q

clinical diagnosis of maedi-visna:

A
  • suspected when > 2yrs
  • wasting disease signs
  • respiratory difficulties
  • neurologic signs
  • mastitis
  • arthritis
78
Q

lab diagnosis of maedi visna

A

serology: ELISA and AGP
detection of proviral DNA
virus isolation

Virology (7 decks)

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