Oncology Flashcards Preview

BVM2 > Oncology > Flashcards

Flashcards in Oncology Deck (67)
Loading flashcards...

All retroviruses carry viral oncogenes. True or false?


Retroviruses can carry oncogenes or switch on the host's proto-oncogenes. 

Some retroviruses carry viral oncogenes, which are genes that code for proteins that can transform a host cell.

Others don't have oncogenes but integrate into the host genome NEXT TO a proto-oncogene, using the retrovirus's long terminal repeat (LTR) to switch on the proto-oncogene.

LTR is a section of the virus's genome that codes for polymerase, capsid & envelope


Name two types diseases that affect domestic animals or pets that are caused by retroviral infection.

FeLV - Feline Leukemia

Ovine Pulmonary Adenocarcinoma


Describe the pathogenesis of feline leukemia virus.

transmitted oronasally via biting, mutual grooming, sharing of feeding bowls

starts at tonsils → viraemia in bloodstream → bone marrow → GIT epithelial cells

about 60% of cats clear infection, 30% become persistently infected & develop disease


What oncogenic mechanism does FeLV use? Oncogene or LTR to switch on proto-oncogenes in host?

It switches on a proto-oncogene.

FeLV is an enveloped retrovirus with RNA oncogene that inserts into c-myc gene in host genome, leading to uncontrolled expression of myc → cell proliferation (lymphocytes)
causes tumours of lymphocytes (lymphoma)


Describe the pathogenesis of RETROVIRUSES.

Adsorption to receptor on target cell → Membrane fusion → uncoating → reverse transcription of RNA strand to DNA (RNA to RNA-DNA hybrid to DNA) → enters host nucleus → integrates into host genome → protein synthesis in cytoplasm → capsid assembly → budding → maturation, reinfection




Describe the structure of Retroviruses.

Family Retroviridae
- RNA virus
- enveloped
- carry reverse-transcriptase enzyme that transcribes RNA into DNA
- each virus gene has a long-terminal repeat section (LTR) that code for polymerase, capsid & envelope
- oncogenes (v-onc) carried by retroviruses lead to cell transformation aka tumours

- retroviruses without oncogenes use their LTR to integrate into host genome next to protooncogene, switching it on for cell proliferation



What is the pathogenesis of Ovine Pulmonary Adenocarcinoma?

- caused by Jaagsiekte sheep retrovirus with env (a structural gene) as oncogene
- malignant tumour of glandular epithelial cells in lung
transmitted via respiratory route
- Type II pneumocytes that produce surfactant proliferate and the lungs become filled with surfactant


What is Papillomavirus & how does its structure differ from Retrovirus?

Family Papillomaviridae
- dsDNA virus
- Non-enveloped
- species specific except for Bovine PV


Family Retroviridae
- RNA virus
- Enveloped
- carry reverse-transcriptase enzyme that transcribes RNA into DNA


How do Papillomaviruses & Retroviruses differ in their oncogenic mechanisms? 

Papillomaviruses use E5, a viral protein, to cause skin tumours (papillomas) & sarcoids. 

- E5 inhibits formation of gap junctions between cells, reducing communication & growth inhibitory signals

- E5 downregulates MHC Class I expression (for Killer T cells), evading host immunosurveillance

E5 binds to receptor for platelet-derived growth factor (PDGF) → cell proliferation

Retroviruses use oncogenes (v-onc) to cause cell-proliferation/transformation, or they insert themselves in the host's genome & use their long-terminal-repeats (LTRs) to switch on nearby host proto-oncogenes, causing tumours of lymphocytes (lymphomas) or glands (adenomas).



Describe the pathogenesis of Papillomaviruses.

Virus enters at base & moves up:

Enter via damaged skin or mucosa epithelium at basal layer → infect dividing basal-membrane cells → expression of “early proteins” initiates proliferation of cells → “late” or “structural genes” & virus particles are expressed in upper layers of epithelium, where epithelium finally differentiate from basal cells into keratinocytes



Which is the only papillomavirus that is not species-specific?

Bovine Papillomavirus (BPV). 

There are 10 different types & they can infect other species, including horses, in which they cause sarcoids. 


What are the clinical signs of Bovine Papillomavirus (BVP) in cattle?

Mostly affects calves & yearlings.

Usually benign tumours on head, neck ("angleberries"), shoulders & udder, as well as rumen. Secondary infection can lead to harmful infection.

Most regress spontaneously after six months.

Malignant tumours require co-factors such as mutagens & immunosuppressants from eating bracken fern - cancer in upper GIT & bladder can develop this way.


What are the clinical signs of disease caused by Canine Papillomavirus?

Usually oral papillomatosis: benign tumours on lips, tongue & palate that spontaneously regress.


What are the clinical signs of disease caused by Equine Papillomavirus?

Don't confuse this with Bovine Papillomavirus that causes usually benign sarcoids in horses.

Equine Papillomavirus causes benign skin tumours around nose and mouth, usually self-limiting.


What virus causes sarcoids in horses?

Bovine Papillomavirus

Sarcoids are locally invasive skin tumours (don't metastasize)

Sarcoids frequently reoccur after surgical removal.

Described as verrucous (covered with warts), fibroblastic (hyperplasia in connective-tissue cells), occult (early form, usually hairless area), or mixed

Transmission likely to involve biting flies that inject BPV deep into basal layer



Retroviruses carry their own RNA polymerase to transcribe DNA into mRNA. True or false?

False. Retroviruses use HOST RNA pol. 

Retroviruses carry their own reverse transcriptase, which reverse transcribes viral DNA from viral RNA (first making a DNA-RNA hybrid). The viral DNA, carrying LTRs that include envelope, capsid & reverse transcriptase, integrates into the host genome, and is then transcribed into mRNA by the host's own RNA pol. 

This mRNA is then translated in the cytoplasm on ribosomes, assembled with capsid, then buds out to mature into another retrovirus and reinfect other cells.


Feline leukemia virus (FeLV) causes tumours of lymphocytes. True or false.

True. It causes lymphoma.


How many types of FeLV are there?

Three: A, B & C. 

We are only interested in A.


FeLV can originate in any organ. True or false.


May be multicentric, involving lymphoid tissues at various sites.

It can also involve predominantly only one site, such as the thymus, alimentary tract or more rarely the skin or kidney.


What is the most common cause of death in cats with FeLV?

Secondary infections caused by immunosuppression, causd by malfunction of lymphocytes


How is FeLV diagnosed?

Detection of FeLV virus in blood by immunochromatography.

FeLV viral proteins can be detected with SNAP test that uses labelled anti-FeLV antibodies to capture virus, forming virus-antibody complexes.



What are the differences between hereditary lesions, congenital lesions & malformations?

Hereditary lesions: 

Genetically transmitted diseases
eg., viral diseases

Congenital lesions:

Disorders of growth detected at birth
NB not all congenital defects have an hereditary basis


Disorders of growth occurring during gestation
If early in gestation & sufficiently severe →  foetal death & resorption
If late in gestation → malformation limited & foetus usually survives


List some causes of hereditary lesions.

Viral diseases - some viruses cross to foetus via placenta.
Eg., Bovine Diarrhoea Virus (BVD) and Feline Panleukopenia (FPL) can result in calves & kittens, respectively, with cerebellar hypoplasia



List some examples of congenital lesions. 

Nutritional deficiencies: Copper deficiency in pregnant ewe can lead to degeneration of prenatal & neonatal lamb’s white matter & spinal cord:

Swayback - congenital form: more severe lesions in lambs affected prenatally, destruction of subcortical white matter in brain, lambs weak, ataxic, born dead

Enzootic ataxia -  delayed onset up to 6 months, demyelination of dorsolateral & ventromedial tracts in white matter of SC, varying ataxia


List some causes of malformations (occurring during gestation) that are not necessarily hereditary (can be congenital, ie., detected at birth).

Chromosomal defects - often result in early abortion or resorption
Eg. trisomy, XX true hermaphrodite

Toxins - plants, pesticides.
Eg., Veratrum californicum ingested by ewe in early pregnancy might produce cyclopia in lambs as it interferes with neural-tube development 

Drugs, hormones, antibiotics - similar to toxins, cross via placental blood supply, to cause growth defects in foetus.
Griseofulvin (ringworm treatment) given to pregnant queen can result in cleft palate in her kitten
Oestrogens & Actinomycin D (antibiotic) 

Ionising radiation - foetus very susceptible because of high rate of cell division. Eg. X-rays

Physical factors - Eg. adhesions between foetal membranes or umbilical cord, esp. around limbs, can result in amputation of skeletal segments

Anoxia - lack of O2 in gestation


What is atrophy & what are the causes?

Decrease in size of cells & organ, AFTER organ has reached normal size - Reversible if inciting cause can be corrected

- inadequate cellular nutrition eg., PSS (portosystemic shunt) in liver

- pressure: compression by nearby lesion (tumour) can compromise blood supply

- ↓ work load: eg. broken leg leads to muscle atrophy

- denervation: eg., CN V (trigeminal) damage → temporal-muscle atrophy in cat

- ↓ endocrine stimulation: eg. prolonged steroid therapy → atrophy of zona fasiculata in adrenal gland


What is the gross appearance of atrophied kidneys?

Kidneys appear smaller & paler. 



What is the appearance of adipose atrophy in skeletal muscle (skeletal muscle atrophy)?

Progressive mobilisation of fat, deposits severely depleted, clear, gelatinous material remains, occurs following severe illness & weight loss.



What is the microscopic appearance of skeletal-muscle atrophy?

- smaller cells
- inactive-looking cells
- relative ↑ in supportive connective tissue maybe



What is hypertrophy? 

↑ in SIZE of cells & ∴ organ, ↑ in organ weight

Decks in BVM2 Class (88):