Family: Adenoviridae Flashcards
Family: Adenoviridae - Morphology
Non-enveloped, hexagonal, icosahedral symmetry, capsid is 720 hexon subunits arranged as 240 trimers, 12 vertex penton capsomers each with a fiber protrude from the surface of capsid.
Family: Adenoviridae - Genome and replication
Non-segmented, linear double-stranded DNA of 35-36 kb, replication takes place in nucleus, virions released by cell lysis, intranuclear inclusion bodies, containing large number of virions.
Family: Adenoviridae - General properties
Agglutinate RBC. Hemagglutination. Tips of penton fibers bind to surface receptors on RBC. Some viruses are oncogenic in laborator animals. Relatively stable in environment, but are inactivated easily by common disinfectants, Most narrow host ranges.
Family: Adenoviridae - Pathogenesis
Many adenoviruses cause acute respiratory or gastroenteric disease. Mostly subclinical infections. Penton and fiber proteins, capsid are toxic to cell.
Family: Adenoviridae - Immunosuppression
Inhibition of class I MHC antigen transport by E3/19K. Apoptosis in inhibited by adenoviral E3/14.7K. Blocking of IFN induced protein kinase R-mediated inhibition of viral protein synthesis. Modulate antiviral inflammatory, inhibiting nuclear factor kB NF kB transcriptional activity.
Family: Adenoviridae - Long periods of latency
Virus persists in lymphoid and other tissues. Reactivated immunocompromised animals. Highly pathogenic in immunodeficient animals.
Family: Adenoviridae - oncogenesis
E1A: Inactivated Rb protein
E1B: Inactivated p53 protein
Family: Adenoviridae involve 2 genera
- Genus: Mastadenovirus
2. Genus: Aviadenovirus
Genus: Mastadenovirus
Mammalian adenoviruses. A single penton fiber projects from each vertex.
Genus: Aviadenovirus
Avian adenoviruses, penton fiber is bifurcated.
Canine Adenovirus-1
Infectious Canine Hepatitis (ICH, Rubarth’s Disease)
ICH - Transmission
All secretions and excretion. Afterwards, virus shed in urine for at least 6 to 9 months. Oronasal transmission. Contact with secretions/excretions/ fomites, and ectoparasites.
ICH - Pathogenesis
Replicates in macrophages, kupffer cells, hepatocytes and vascular endothelium
ICH - Kidney
Acute infection, glomerulonephritis. Basophilic inclusion bodies. Chronic kidney lesions may result from immune complex reactions after recovery from acute or subclinical disease.
ICH - Ocular Lesions
Corneal edema (blue eye). Occurs in about 20% of natural infections. Less than 1% of dogs after S/C MLV CAV-1 vaccination. Seen in dogs during recovery of chronic cases.
How does corneal edema develop?
- During viremia, CAV-1 enters the eye via the uveal tract.
- CAV-1 localizes in endothelium of choroid and causes mild uveitis.
- By 4-6 days post infection, virus enters the aqueous humor from the blood and replicates in corneal endothelial cells.
By day 7, Severe anterior Uveitis and Corneal Edema (Blue Eye) develop
- CAV-1 antibody production increases, and formation of viral-antibody immune complexes.
- This result in Complement activation, neutrophil chemotaxis.
- Cause extensive damage to corneal endothelium.
- Disruption of intact corneal endothelium allows aqueous to enter the cornea.
- Accumulation of edematous fluid within corneal stroma results in corneal edema.
- From days 8-21, macrophages remove the immune complexes and corneal endothelium regenerates, re-establishing the hydrostatic gradient.
- Clearing of corneal edema.