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Abstract

Defective Viral Genomes (DVGs), which are viral genomes that are defective in some way, are naturally occurring byproducts of viral replication in numerous RNA viruses, notably Orthomyxoviridae (Influenza virus), Filoviridae (Ebola and dengue), and Paramyxoviridae (Respiratory Syncytial). They have three well-defined functions: interference with regular virus replication, immunostimulation, and virus persistence. DVGs are defective viral genomes that can hijack the replication cycle of wild-type viruses, leading to partial or complete suppression of viral populations. A variety of new DVGs are created through infection of the host by one of these viruses. The researchers devised a strategy for identifying those most likely to have antiviral potential. The current study examines viruses’ inherent ability to produce defective viral genomes (DVGs) to their detriment. Even though most viruses harbor DVGs, identifying which can be used as therapeutic agents remains a challenge. Different models, such as the Zika virus as an arbovirus, were utilized to triage the DVG sequence space and discover the fittest deletions using a variety of experimental evolution and computational techniques. These experiments showed that the optimal DVGs for preventing wild-type viral infection kept the open reading frame open to maintain the translation of the insufficient evidence to conclude proteins, and that is a flavivirus genus-wide feature. Furthermore, in mammalian hosts and insect vectors, the highly fit DVG is antiviral in vivo, reducing transmission by up to 90%. The present review provides a background knowledge for defining and identifying DVGs as a promising antiviral approach for human and animal treatment and to manage vector techniques to reduce transmission of viral disease.

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