Lecture 7: Retrovirus Flashcards
(79 cards)
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%
1
Q
retrovirus properties
A
- diploid genome with 2 copies of ssRNA(+)
- RNA genome produces DNA intermediates via reverse transcriptase and RNA-dependent DNA polymerase
- enveloped viruses released by budding from cell membranes
- integrate into cell genome using integrase
2
Q
transmission of FeLV (feline leukemia virus)
A
horizontal: infected cats shed virus in most bod fluids
vertical: transplacental
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
4
Q
virulent traits of FeLV are located where on virus?
A
on the long terminal repeats (promoter regions of provirus)
and surface glycoprotein
5
Q
subgroups of FeLV
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FeLV: A - minimally pathogenic
FeLV:B - linked to thymus lymphosarcoma
FeLV: C - linked to severe aplastic anemia
6
Q
clinical signs of FeLV
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anisocoria - unevenly sized pupils
protein deposits in anterior uvea
enlarged popliteal lymph node
chronic wounds
7
Q
pathologies associated with FeLV infection:
A
feline lymphosarcoma or lymphoma
myeloproliferative diseases and anemia
immunopathologic disease
fibrosarcoma
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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Q
myeloproliferative disease and anemia from FeLV infection
A
erythremic myelosis
granulocytic leukemia
erythroleukemia
myelofibrosis
10
Q
immunopathologic disease
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immune complex mediated - high levels of FeLV anitgen-antibody complexes in glomerular capillaries resulting glomerulonephritis
immunodeficiency
11
Q
fibrosarcoma via FeLV infection
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- solitary tumors in old cats
- rapid growth, frquently mets
- induced by replication-defective feline sarcoma virus which may arise by recombination
12
Q
dx of FeLV
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antigen detection (SNAP tests)
- PCR to detect FeLV provirus - confirms a positive antigen detection test
- IF
- vax - doesnt interfere with FeLV antigen tests
13
Q
vaccination for FeLV protects against ______
A
progressive infection and disease but NOT against infection
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
15
Q
what is the phylogeny of FeLV
A
Orthoretrovirinae: gammaretrovirus
16
Q
phylogeny of avian leukosis and sarcoma virus
A
retroviridae –> orthoretrovirinae –> genus alpharetrovirus
17
Q
what two diseases processes does avian leukosis and sarcoma virus cause?
A
erythroblastosis and avian lymphoid leukosis
18
Q
what is avian lymphoid leukosis caused by?
A
exogenous RNA tumor virus (oncovirus) - of avian leukosis and sarcoma virus
19
Q
transmission of avian lymphoid leukosis
A
vertical - hens to chicks
-horizontal - chicks infect hatch mates
20
Q
how are endogenous viruses transmitted? is it oncogenic?
A
in the gamete genetically both rooster and hen
NOT oncogenic
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)
22
Q
diagnosis of avian lymphoid leukosis
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- use tumor cells from BOF and react with antiserum of B lymphocytes and IgM
- PCR
- absence of MD MEQ gene in tumors
- micropathology
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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erythroblastosis signs and pathology
severe anemia
enlargement of spleen, liver, & kidneys - all dark red to mahogany in color
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avian lymphoid leukosis signs and pathology
- 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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phylogeny of ovine pulmonary adenomatosis
retroviridae --> orthoretrovirinae --> betaretro virus
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characteristics of ovine pulmonary adenomatosis
aka Jaagsiekte sheep retrovirus
- disease of adult sheep
- leads to wasting and severe respiratory distress
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clinical fetures of ovine pulmonary adnenomatosis
- 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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transmission of ovine pulmonary adenomatosis
- aersolized lung fields
| - virus shed in saliva, colostrum, milk any respiratory secretion
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pathogenesis of ovine pulmonary adenomatosis
- 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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pathology of ovine pulmonary adenomatosis
- nodular lesions
- epithelial proliferation in bronchioles and alveoli
- adenoma or adenocarcinoma
- metastases
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dx of ovine pulmonary adenomatosis
- 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)
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control of ovine pulmonary adenomatosis
- 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
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phylogeny of bovine leukemia virus
retroviridae --> orthoretrovirinae --> deltaretrovirus
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another name for bovine leukemia virus is?
enzootic bovine leukosis
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disease processes of bovine leukemia virus
lymphoma - slow and lethal
| persistent lmphocytosis: high numbers of circulating B lymphocytes in 30% infected
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clinical signs of bovine leukemia virus
- 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
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transmission of bovine leukemia virus (BLV)
horizontal thru infected white blood cells (colostrum/milk)
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pathogenesis of BLV
- targets B lymphocytes with IgM on surface
- polyclonal expansion of lymphocytes
- viral transactivating protein (Tax) enhances transcription of virus promoter (LTR)
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dx of BLV
- test for specific BLV antibodies with AGP and ELISA
| - PCR for proviral DNA detection
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how does BLV cause significant economic losses
thru culling high producing dairy cattle
| - meat is condemned if cow has ONE BLV associated tumor
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prevention and control of BLV
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
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phylogeny of caprine arthritis-encephalitis virus
retroviridae --> orthoretrovirinae --> lentivirus
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characteristics and syndromes of caprine arthritis-encepahlitis virus
its lifelong
| arthritis, encephalomyelitis, pneumonia, mastitis, weight loss
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clinical signs of infection of caprine arthritis-encephalitis virus in kids
lameness, paralysis, paddle in bedding, depresion, circle walking, head tilt, muscle tremors
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transmission of caprine arthritis encephalitis virus
**major route: milk/colostrum**
anything that contains white blood cells bc CAE is associated with WBCS
via breeding
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clinical signs of caprine arthritis encephalitis in adults
```
mostly asymptomatic
lameness
distension of carpal (knee) joints
weight loss, rough hair coat, labored breathing
mastitis
```
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dx of caprine arthritis encephalitis virus
serology: ELISA **agar gel preciptiation test**
| PCR
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control of caprine arthritis encephalitis virus
voluntary control program
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prevention of caprine arthritis encephalitis virus
remove kids from infected dams as soon as they are born - this will reduce infections by more than 90%!!
- no vaccine
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phylogeny of equine infectious anemia
retroviridae --> orthoretrovirinae --> lentivirus
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equine infectious anemia consists of 4 syndromes:
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
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pathogenesis of equine infectious anemia
virus infects macrophages
vasculitis and glomerulonephritis may develop from immune complex deposition
Env glycoprotein mutates - emergence of virus variants
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transmission of equine infectious anemia
mechanical vector via horse fly (tabanids) and stomoxys flies
iatrogenic: syringes, needles, etc
vertical: transplacental
higher in summer
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dx of equine infectious anemia
AGP (agar gel precip) aka coggins!!
- detects antibodies against p26
RT-PCR
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feline immunodeficiency virus occurs in which animals?
outdoor, unneutered, male cats that like to fight and bite
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characteristics of FIV
* 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
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transmission of FIV
mainly thru biting
| less from mating or vertically
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stages of FIV disease
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
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clinical signs of FIV
non-healing infections
| "feline AIDS" - poor appetite, weight loss, vomiting, diarrhea, gingivitis, stomatitis, conjunctivits, fever, swollen LN
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dx of FIV
antibodies persist for life
- virus isolation is gold standard
- PCR
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control of FIV
free roaming cats at greatest risk
test and removal
queens may infect kittens thru milk
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phylogeny of bovine immunodeficiency virus
retroviridae --> orthoviridae --> lentivirus
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pathogenesis of BIV
persistent leukocytosis and lymphadenopathy of subcutaneous LN
uncertain how this occurs!
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characteristic of BIV
as a lentivirus, it can also infect and replicate in non-dividing cells
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transmission of BIV
iatrogenic
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implication of BIV
potential for being used in gene therapy bc not infectious for humans, transduces wide range of cells, infects and replicates in nondividing cells
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phylogeny of maedi-visna
retroviridae --> orthoretrovirinae --> lentivirus
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maedi =
dyspnea
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visna =
wasting (neurological signs)
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maedi-visna affects what animals
sheep and goats
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pathogenesis of maedi-visna
integrates into lymphocyte DNA
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transmission of maedi-visna
- 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
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clinical signs of maedi-visna
- 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
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maedi form is seen more often in ____
sheep
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visna form is seen more often in _____
goats
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clinical diagnosis of maedi-visna:
- suspected when > 2yrs
- wasting disease signs
- respiratory difficulties
- neurologic signs
- mastitis
- arthritis
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lab diagnosis of maedi visna
serology: ELISA and AGP
detection of proviral DNA
virus isolation
