Lecture 15: Retroviruses 2 Flashcards by Jen McGann

What is equine infectious anemia

contagious and potentially terminal viral disease that attacks the immune system of horses and other squid’s

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what is the basic structure of EIAV that we test for antibodies for

p26 capsid protein

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what cells does EIAV target/infect

monocytes and macrophages

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what is the most common mode of transmission for EIAV

blood feeding insects- horseflies, deer flies and stable flies are main mechanical vectors

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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

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EIAV clinical disease is associated with active ___

viral replication

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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

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what are some clinical signs of acute EIA

high fever, anemia, thrombocytopenia, edema, petechial hemorrhages of MM, epistaxis, decreased appetite, weight loss, weakness

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what is chronic EIA

recurring clinical disease with same or similar signs of acute EIA, interval between episodes highly variable

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t or f: most equips infected with EIAV become in apparent carriers after initial illness and show no overt clinical disease

true

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who serves as reservoirs for EIAV

inapparent horse carriers

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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

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In EIAV there is a tight correlation between clinical disease and __

viral load

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viral loads of EIAV are highest during ___ episodes of disease

febrile

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clinical signs result from infection of monocytes and macrophages resulting in release of __

pro-inflammatory cytokines

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what sign do inflammatory cytokines cause

fever

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in EIAV antibodies bind platelets and lead to

thrombocytopenia

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EIAV can bind to RBC and lead to what

lysis and anemia

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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

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testing for infection with EIAV is required for all equids that are ___

sold, donated or traded

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what is gold standard test for EIAV dx

coggins test- detection of EIAV anti-p26 antibodies

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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

1. Horizontally- shed in saliva and feces 2. 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

1. Pro viral insertion into B cells close to c-myc gene resulting in B cell transformation 2. 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

1. Gp51 anf Gp30 envelope glycoprotein 2. 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

1. Primary infection of B cells- flu like signs 2. Persistent infection- replication of B cells due to active immune response, immune system dysregulation- overexpression of cytokines 3. Persistent lymphocytosis- continued increase in lymphocytes- increase opportunistic infections 4. 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

1. Virus infects lung epithelial cells as well as some lymphoid and myeloid cells 2. Viral envelope glycoproteins are responsible for inducing cellular transformation 3. Excess surfactant produced by cancerous cells leading to increase pulmonary fluid 4. Tumors and necrosis lead to secondary infections and eventually asphyxia/death