Lecture 15: Retroviruses 2 Flashcards
What is equine infectious anemia
contagious and potentially terminal viral disease that attacks the immune system of horses and other squid’s
what is the basic structure of EIAV that we test for antibodies for
p26 capsid protein
what cells does EIAV target/infect
monocytes and macrophages
what is the most common mode of transmission for EIAV
blood feeding insects- horseflies, deer flies and stable flies are main mechanical vectors
true or false: Part of EIAV virus life cycle is completed in the gut of a mechanical factor
false- mechanical vector just spreads no life cycle components
EIAV clinical disease is associated with active ___
viral replication
t or f: after incubation some acute EIAV infected horses with EIAV can develop severe, acute signs of disease and may die within 3-14 days
true
what are some clinical signs of acute EIA
high fever, anemia, thrombocytopenia, edema, petechial hemorrhages of MM, epistaxis, decreased appetite, weight loss, weakness
what is chronic EIA
recurring clinical disease with same or similar signs of acute EIA, interval between episodes highly variable
t or f: most equips infected with EIAV become in apparent carriers after initial illness and show no overt clinical disease
true
who serves as reservoirs for EIAV
inapparent horse carriers
t or f: horses with EIAV harbor the virus for life, carriers of the virus can have recurrent signs of disease due to stress, hard work, disease of immunosuppression
true
In EIAV there is a tight correlation between clinical disease and __
viral load
viral loads of EIAV are highest during ___ episodes of disease
febrile
clinical signs result from infection of monocytes and macrophages resulting in release of __
pro-inflammatory cytokines
what sign do inflammatory cytokines cause
fever
in EIAV antibodies bind platelets and lead to
thrombocytopenia
EIAV can bind to RBC and lead to what
lysis and anemia
what is pathogenesis of EIAV
- Virus infect macrophages and monocytes in spleen, tissue
- Viremia
- Active infection of LN, BM, lung, adrenal gland, kidney, brain
- Infection of macrophages induces upregulation of tNF-alpha, IL-1, and IL-6
- Increase in pro-inflammatory cytokines cause fever, lethargy, inappetence
- Thrombocytopenia
- Anemia
testing for infection with EIAV is required for all equids that are ___
sold, donated or traded
what is gold standard test for EIAV dx
coggins test- detection of EIAV anti-p26 antibodies
what samples are positive for EIAV
1 and 3
all animals infected with EIAV are either ___ or __
euthanized or quarantined for life
What are the main structures of avian leukosis virus
gp85 and gp37- envelope glycoprotein
P27 capsid protein
subgroups A-E and J-K of avian leukosis virus infect who. Which subtypes are most common
chickens
A and J most common
how was the first viral oncogene discovered and what was it
injected chickens with Rous Sarcoma virus- remove sarcoma and filter out all other cells—> inject chickens with filtrate—> developed sarcoma
Genome contains v-src and was first viral oncogene discovered
what did v-src trigger
uncontrolled growth an proliferation in infected cells
what does ALV cause
leukosis, lymphoid most common
what is ALV transmitted
- Horizontally- shed in saliva and feces
- Vertical- shed in hen albumen and yolk to offspring
what happens to birds that were horizontally infected with ALV
transient viremia followed by antibody production, may become carriers and intermittently shed
what happens to birds that were infected vertically with ALV
congenitally infected chickens do not produce neutralizing antibodies and remain viremia for life, neoplasms common
what is the likely reason why congenitally infected chickens lack antibodies to ALV
infection in egg leads to immune tolerance- sees virus as self- no antibodies
What is pathogenesis of ALV
- Pro viral insertion into B cells close to c-myc gene resulting in B cell transformation
- Resulting in lymphoid leukosis= clonal malignancy of B cells
what is subclinical ALV disease characterized by
depressed egg production
what are some clinical signs of ALV
loss of appetite, weakness, diarrhea, dehydration, emaciation, enlarged bursa, liver, pale wattles, osteopettrosis, diffuse or nodular tumors in liver, spleen or bursa
chicken euthanized due to decrease egg production, weakness. What do these images show and what likely wrong
osteopetrosis and tumors
Dx: ALV
how are the tumor locations different in Mareks disease vs ALV
no tumors in nervous tissue for ALV, unlike Mareks disease
what are the major structures of BLV
- Gp51 anf Gp30 envelope glycoprotein
- P24 capsid
what two important genes are present in BLV and what is function
tax and Rex- essential for oncogenesis- interact with cell cycle regulatory factors resulting in cell cycle dysregulation and eventual transformation (block checkpoints and DNA repair)
what does BLV cause
enzootic bovine leukosis= bovine lymphoma Roma
how is BLV transmitted
Horiztonally- transfer of blood containing infected lymphocytes- biting flies, tattooing, dehorning, rectal palpation, injections/blood collection
once infected with BLV cattle have life long infection, detection of ___ and ___
antibodies to BLV gp51 envelope glycoprotein and p24 capsid
what is pathogenesis of BLV
- Primary infection of B cells- flu like signs
- Persistent infection- replication of B cells due to active immune response, immune system dysregulation- overexpression of cytokines
- Persistent lymphocytosis- continued increase in lymphocytes- increase opportunistic infections
- Tumoral: transformation of B cells forming lymphosarcoma
most animals infected with BLV remain __ but have persistent ___
subclinical but persistent lymphocytosis
__-__% of cows infected with BLV develop lymphosarcoma
5-10%
what is JSRV
jaagsiekte sheep retrovirus or ovine pulmonary adenocarcinoma virus
how do you dx JSRV
no serological tests- dx on clinical and pathological findings
t or f: there are no detectable immune response to JRSV
true
how is JRSV transmitted
inhalation of aerosolized respiratory secretions
Ovine pulmonary adenocarcinoma/ JRSV cause tumors confined to ___
lungs and associated lymph tissue
what are some clinical signs of JRSV/OPAC
frothy nasal exudate (wheelbarrow test), respiratory compromise/mouth breathing
performed wheelbarrow test on goat and profuse nasal exudate came out. Euthanized and necropsy show tumors on lung and lymph tissue what dx
JRSV/ovine adenocarcinoma
what is pathogenesis of JRSV
- Virus infects lung epithelial cells as well as some lymphoid and myeloid cells
- Viral envelope glycoproteins are responsible for inducing cellular transformation
- Excess surfactant produced by cancerous cells leading to increase pulmonary fluid
- Tumors and necrosis lead to secondary infections and eventually asphyxia/death
