Oncogenic viruses (pox not) Flashcards
General information
• Marek’s disease (MD) • Leukosis • Reticuloendotheliosis (RE) • Fowlpox • Oncogenic viruses (pox not) • Almost every cancer is virus-induced in avian species • Mostly: herpesvirus, retrovirus
Marek’s disease (MD)
Causative agent - MDV
▪ Alphaherpesvirus ✓Mardivirus genus ✓Gallid alphaherpesvirus 2 and 3; Meleagrid alphaherpesvirus 1 (=herpesvirus of turkey – HVT) ✓GaHV-2 is the prototype ▪ GaHV-2 pathotypes ✓mild (m)MDV ✓virulent (v)MDV ✓very virulent (vv)MDV ✓very virulent plus (vv+)MDV ▪ Susceptible: chicken (turkey, pheasant and quail can also be affected)
GaHV-2 Morphology
▪ 85-100 nm hexagonal nucleocapsid
▪ 150-160 nm with envelope
▪ dsDNA linear nucleic acid (latency!)
▪ 160-180 kb genome length
GaHV-2 Stability, transmission
▪ Very stable, 4-8 months on room temperature, up
to 10 years on 4°C
▪ Spread with dander, feathers, contaminated litter
(cell-free virus)
▪ Fomite transmission
▪ Hatchary hygiene to prevent early infection
▪ Spreading via inhalation – keep the newly hatched
birds separated from other age groups
▪ Vertical transmission does not occur
▪ Persistent carriers are shedding – horizontal
transmission
GaHV-2 Syndromes
▪ (m)MDV
✓„classic” fowl paralysis syndrome – sporadic, mostly
in older backyard chickens („hen paralysis” –
thickening of nerves due to lymphocytic
endoneuritis & neural edema, paralysis, no brain
lesion => spastic)
✓acute transient paralysis syndrome – also rare, but
can be surprising (whole flock paralyzed (flaccid) for a few days), then complete recovery (mostly in
unvaccinated broilers), encephalitis with histopath.
▪ (v)MDV, (vv)MDV, (vv+)MDV
✓acute neoplastic form – most frequent, in young
birds/beginning of layer season, lymphoproliferative
lesions, CD4+ T cells affected (lymphoma), high
mortality (visceral organs, peripheral nerves)
GaHV-2 Intervention
▪vaccination ✓always in breeder and layer flocks ✓attenuated GaHV-2, or GaHV-3, HVT ✓immediately after hatching (cell-associated immunity) ✓in ovo recombinant vaccines (day 18 embryo) ▪stable hygiene ▪separation of age groups ▪fomites, personnel ▪genetically more resistant strains
Leukosis
• Causative agent
▪Avian leukosis/sarcoma group – L/S
✓Retroviridae family, Alpharetrovirus genus
✓Avian leukosis virus (AVL)
✓Rous sarcoma virus also belongs here
▪10 subgroups in L/S group (A-J) based on surface glycoproteins
▪A-E and J subgroups naturally in chickens (E is endogenic)
Leukosis Morphology
▪ 35-45 nm core
▪ 80-120 nm diameter overall
▪ +ssRNA nucleic acid
▪ C-type retrovirus
Leukosis • Transmission, pathogenesis
▪ Vertical transmission (germinative)
▪ Congenitally infected chicks are
immunotolerant, and shed constantly
▪ Horizontal transmission in young age (relatively
short life of virus in environment)
▪ Maternal derived antibodies in yolk can
decrease consequences of infection
▪ Infection of bursa of Fabricius (the younger the
animal, the more successfull the neoplastic
transformation of lymphocytes)
▪ Except J subgroup (bone marrow myelocytes)
Leukosis Diseases caused by L/S group
▪ Numerous neoplastic diseases
▪ Can affect the lymphoid and hematopoietic tissues
▪ Eg. lymphoid leukosis, erythroblastosis, myeloblastosis,
fibrosarcoma, hemangioma, nephroblastoma …
▪ Economically most important: lymphoid leukosis
• L/S group can be divided ▪ Acutely transforming strains ✓few days to weeks ✓acute leukemia or solid tumours (sarcoma) ✓viral oncogenes ▪ Slowly transforming strains ✓weeks to months ✓no viral oncogenes, only promoter insertion sometimes
Leukosis • Clinical signs
▪ Non-specific
▪ Inappetence, lethargy, rarely diarrhoea, weightloss
▪ Decreased gain of bodyweight
and drop in egg production
▪ Hemangiomas in skin
▪ Sarcomas are usually visible/can be palpated
• Intervention=> Eradication
Reticuloendotheliosis (RE)
• Causative agent - REV
▪ Retroviridae family, Gammaretrovirus genus
▪ Broad host spectrum
▪ Clinical manifestation is rare, but the virus is in
many birds (mostly turkey, goose, sometimes
chicken)
• Diseases ▪Acute and chronic neoplasias ▪ Immunosuppression ▪ Runting syndrome ▪Acute death
Reticuloendotheliosis (RE) • Morphology
▪ Overall cc 100 nm diameter
▪ +ssRNS nucleic acid
▪ C-type retrovirus
Reticuloendotheliosis (RE) • Transmission, pathogenesis
▪ Primarily horizontal
▪ Litter, feces, insects
▪ Easily integrates into other viruses (herpes, pox)
– vaccine contamination!
▪ Vertical transmission is rare, but possible
(germinative route – immunotolerant chicks)
▪ Viremia after infection
✓strongly oncogenic, defective strains rapidly
transform cells of RE system, then those spread in the body making metastases everywhere
✓less virulent strains causing immunosuppression,
runting syndrome
Reticuloendotheliosis (RE) • Clinical signs
▪ Non-specific ▪ Inappetence, lethargy, mild diarrhea, weightloss ▪ Anemia ▪ If survives the acute phase: feathering disturbances ▪ In turkey: pox-like lesions on head, oropharyngeal cavity • Intervention=>Eradication
