Features of the immunopathogenesis of infections caused by viroids and satellite viruses

One of the main molecular mechanisms of viroids that cause disease in plants is the blocking of ribonucleic acid functions of host cells by viroid ribonucleic acid. The variety of splicing options is due to viroid replication, which requires ribonucleic acid polymerase, ribonuclease, ligase, and deoxyribonucleic acid working on ribonucleic acid matrices. Viroids with faster replication are preferred. Identifying host proteins that interact with viroid ribonucleic acid is critical in the pathogenesis of viroid infections, which leads to gene expression changes of host plants. The study of the pathogenesis of plant infections caused by satellite viruses has shown that they have a common ancestor and that the satellite viruses suppress the reproduction of the helper virus. Satellite viruses require accessory viral proteins to encode capsid proteins for genome encapsulation and reproduction. Replication occurs in the cytoplasm and is induced by ribonucleic acid polymerase of the helper virus. Hepatitis D virus ribonucleic acid replication requires cell ribonucleic acid polymerase II. When the viral and endosomal membranes fuse, the ribonucleic acid of the hepatitis D virus moves into the nucleus, and antigenomic ribonucleic acid is produced, which is the template for the synthesis of matrix ribonucleic acids encoding delta protein. The minor delta antigen regulates ribonucleic acid editing, and the large delta antigen inhibits viral replication and induces a signal for the transport of ribonucleic acid from the cell nucleus to the cytoplasm, which ensures the assembly of new viral particles. Large and small delta antigens have been detected in the brain, liver, lungs, kidneys, and spleen of snakes by reverse transcriptase polymerase chain reaction, Western blotting, and immunohistochemical assays, indicating that all delta viruses possibly share a common ancestor that arose before the divergence of reptiles and mammals.