Please use this identifier to cite or link to this item:
|Title:||Update on viral accommodation, a model for host-viral interaction in shrimp and other arthropods|
|Authors:||T. W. Flegel|
|Keywords:||Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology|
|Citation:||Developmental and Comparative Immunology. Vol.31, No.3 (2007), 217-231|
|Abstract:||Comparatively little published information is available on the mechanistic response of shrimp and other arthropods to viral pathogens. Much of the literature has been focused on the use of viruses for biological control of insect pests or disease vectors and on the use of baculoviruses as a means of heterologous protein expression in insect cell lines. The situation changed dramatically with the rapid global increase in cultivation of penaeid shrimp and the massive farm losses that have occurred due to viral pathogens. Urgency to solve these problems has led to a closer examination of the shrimp response to viral pathogens in the hope of finding new methods of disease control. Field observations and results of laboratory experiments in the past decade indicate that shrimp may be capable of a specific, adaptive response to viral pathogens that cannot be explained by current knowledge and understanding of their cellular and humoral defenses. Hallmarks of this response are specific tolerance to single and multiple viral infections without gross or histological signs of disease, a phenomenon common to crustaceans and insects. The concept of viral accommodation was introduced in 1998 as a simple testable hypothesis to explain these phenomena. Key elements of the hypothesis were an unknown mechanism for specific memory of pathogens and the role of this memory in dampening viral triggered apoptosis. Recent field and research results have supported predictions of the viral accommodation hypothesis and suggest that memory may be provided by the viral pathogens themselves in persistent infections that result in reduced severity of disease. The well-known phenomenon of defective interfering viral particles may play an important role in this process, but it cannot explain cross protection that has recently been described for heterologous viral infections. The major conclusion is that homologous and heterologous reduction in disease severity resulting from persistent viral infections (i.e., accommodated viral infections) may be a key process that has evolved from host viral interaction in the arthropod line. © 2006 Elsevier Ltd. All rights reserved.|
|Appears in Collections:||Scopus 2006-2010|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.