Field strains of this virus display differences in virulence, but all seem to be immunologically identical. Significant titer reduction is observed at pH 5, 6, and 10; rapid inactivation occurs at pH 3 and The virus induces vascular damage, especially in smaller blood vessels, venules, and capillaries.
This results in the development of generalized hemorrhages and progressive degenerative changes of parenchymatous organs. It has been proposed that apoptosis and necrosis of lymphocytes induced by this virus may result in lymphoid depletion and possibly immunosuppression.
An immunosuppressive state induced by DVE may also explain the presence of secondary infections by Pasteurella multocida , Riemerella anatipestifer , and Escherichia coli , which are frequently seen in natural outbreaks of DVE in ducklings.
The virus causing duck viral enteritis is mainly transmitted by direct contact from infected to susceptible ducks or by indirect contact with a contaminated environment. Water seems to be a natural route of viral transmission. Outbreaks are frequent in duck flocks with access to bodies of water cohabited with free-living waterfowl. Parenteral, intranasal, or oral administration of infected tissues can establish experimental infection. A carrier condition is suspected in wild birds.
Recovered birds become latently infected carriers and may shed the virus periodically. DVE virus may undergo latency like other herpesviruses, and the trigeminal ganglion seems to be a latency site for the virus.
Recovered birds may carry the virus in its latent form, and viral reactivation may be the cause of outbreaks in susceptible wild and domestic ducks. One study demonstrated that captive-reared and released Mallard ducks can be infected with the virus, and those latently affected may potentially transmit the virus to native waterfowl when they are released. The incubation period is 3—7 days. Sudden high and persistent mortality is often the first sign of the disease.
Adult ducks usually die in higher proportions than young ones, increasing the economic significance of the disease. Sick birds are unable to stand, and they show indication of weakness and depression. Photophobia, inappetence, extreme thirst, droopiness, ataxia, nasal discharge, soiled vents, and watery or bloody diarrhea may be seen. Adult ducks may die in good flesh. In contrast, ducklings frequently show dehydration and weight loss as well as blue beaks and blood-stained vents.
Dead males may have prolapse of the penis. In laying flocks, egg production may drop sharply. Lesions from duck viral enteritis are indicative of DIC and necrosis of the mucosa and submucosa of the GI tract and lymphoid tissues. Damage of blood vessels throughout the body induces hemorrhages in various tissues or the presence of free blood in body cavities. The spleen is an active place for DVE replication.
Journal Reference : Barber et al. Association of RIG-I with innate immunity of ducks to influenza. ScienceDaily, 9 April University of Alberta.
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Suramin inhibits in vitro infection by duck hepatitis B virus, Rous sarcoma virus, and hepatitis delta virus. Infection and uptake of duck hepatitis B virus by duck hepatocytes maintained in the presence of dimethyl sulfoxide. DNA methylation and gene function. In vitro recombinants of ground squirrel and woodchuck hepatitis viral DNAs produce infectious virus in squirrels. Hepadnavirus envelope proteins regulate covalently closed circular DNA amplification.
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