RESUMO
Densoviruses (DVs) are parvoviruses of arthropods and causative agents of natural epizootics in insects and crustaceans populations. Structurally simple, these small DNA viruses, display a large diversity of genomic sequences, structures and organizations. Such diversity, together with the diversity of their invertebrate hosts, from shrimps to mosquitoes and recently including sea stars, suggests that DVs are largely unknown and ubiquitous in the environment. Densoviruses are considered as a model of choice to study virus-host interactions and their evolution at different scales, from individuals to populations. This review summarizes the knowledge on densovirus biology obtained through mechanistic and global approaches. Finally, the potential use of these viruses as biological control agents against insect pests and disease-vectors are exposed.
RESUMO
Densoviruses are insect parvoviruses that are orally infectious for Lepidoptera. To assess the mechanisms underlying their specificity and their virulence, we investigated the role of eight candidate residues in the densovirus capsid. We showed that the substitutions of four amino acids were associated with decreased virulence due to a decreased ability to cross the host midgut epithelium, without an effect on viral replication in other tissues.
Assuntos
Proteínas do Capsídeo/química , Proteínas do Capsídeo/metabolismo , Densovirus/fisiologia , Densovirus/patogenicidade , Spodoptera/virologia , Tropismo Viral , Motivos de Aminoácidos , Sequência de Aminoácidos , Animais , Proteínas do Capsídeo/genética , Densovirus/química , Densovirus/genética , Intestinos/virologia , Modelos Moleculares , Dados de Sequência Molecular , Virulência , Replicação ViralRESUMO
To evaluate densovirus potential against lepidopteran pests and their capacity to invade new hosts, we have characterised in vivo the infection and pathogenesis of the Junonia coenia densovirus (JcDNV) in the noctuid pest Spodoptera frugiperda. Here we show that infection starts with the ingestion of viral particles that cross the midgut epithelium without replicating. By quantitative PCR we established the kinetic and the route of infection, from virus ingestion to replication in visceral tracheae and hemocytes. JcDNV has a high particle-to-infection ratio mostly due to the barrier function of the midgut. Pathology and cytopathology suggested that infection of tracheal cells impairs oxygen delivery to demanding tissues leading to cytopathic effects in all the tissues. Finally, larval death results from several physiological shocks, including molting arrest and anoxia.