Family: Adenoviridae Flashcards
Morphology of family Adenoviridae
Non-enveloped
Hexagonal
Icosahedral symmetry
12 vertex penton capsomers each with a fiber protruding from the surface of capsid
Genome and replication of family Adenoviridae
Non-segmented, linear double-stranded DNA
Replication takes place in the nucleus by a program of early and late transcription (before and after DNA replication)
Intranuclear inclusion bodies are formed, containing large numbers of virions, often in para-crystalline arrays
Immunosuppression achieved by Adenoviruses
Adenoviruses encode proteins hat suppress host immune and inflammatory responses
- Inhibition of class I major histocompatibility antigent transport by E3/19K
- TNF induced apoptosis is inhibited by adenoviral E3/14.7K
- Blocking of IFN produced protein kinase R-mediated inhibition of viral protein synthesis
- Modulate antiviral inflammatory responses by inhibiting nuclear factor kB transcriptional activity
Oncogenesis of Adenoviridae family
E1A and E1B gene products are associated with cell transformation
E1A - inactivate Rb protein
E1B - inactivatep53 protein
Mammalian Adenoviruses
Genus: Mastadenovirus
A single penton fiber projects from each vertex
Avian Adenoviruses
Genus: Aviadenovirus
Each penton fiber is bifurcated, appear as two fibers extending from each penton base
Canine adenovirus-1
-common names
Infectious Canine Hepatitis
Rubarth’s Disease
CAV-1 (ICH) transmission
CAV-1 is found in all secretions and excretions with acute infection
Virus is shed in urine for 6-9 months
Oro-nasal transmission
Sites of replication and target organs of CAV-1
Macrophages, Kupffer cells, hepatocytes
Vascular endothelium of different orgnans, including CNS
Parenchymal cells of organs and tissues
Liver, kidney, spleen, and lungs are main target organs
3 main pathogenesis of CAV-1 (ICH)
Hepatitis
Ocular Lesions
Disseminated intravascular coagulation
Hepatitis pathogenesis of CAV-1
Dogs with sufficient antibody titers (>500) show little clinical evidence of disease
In acute cases, sufficient Ab response by day 7 post-infection (>500 Ab by day 7) clears virus from blood and liver, and restricts hepatic damage
Persistently low Ab titer (16 but
Pathogenesis of ocular lesions of CAV-1
Corneal edema (Blue eye)
Seen in dogs during recovery or chronic cases
CAV-1 enters eye via uveal tract during viremia
CAV-1 localizes in endothelium of chorid
4-6 days post-infection, virus enters aqueous humor
Disruption of intact corneal endothelium allows aqueous to enter the cornea
Accumulation of edematous fluid within corneal stroma results in corneal edema
Pathogenesis of DIC of CAV-1
Results from damage to endothelium and inability of diseased liver to remove activated clotting factors
Clinical signs of CAV-1
Most frequent in dogs less than 1 year old
Concurrent parvoviral or distemper infection worsens the prognosis
Most infections are asymptomatic
Clinical signs in peracute cases of CAV-1 (ICH)
Severely infected dogs become moribund and die within a few hours after onset of clinical signs