Effect of defective interfering RNAs on the vertical transmission of Tomato black ring virus

Viruses are thought to be the ultimate parasites, using host resources for multiplication. Interestingly, many viruses also have their own 'parasites', such as defective interfering RNAs (DI RNAs). One of the plant viruses whose infection can be accompanied by subviral RNAs is the Tomato black ring virus (TBRV). DI RNAs associated with the TBRV genome were generated de novo as a result of prolonged passages in one host. DI RNAs modulate the TBRV accumulation and the severity of the symptoms induced on the infected plants. In this study, we have addressed the question of whether DI RNAs can also affect TBRV vertical transmission through seeds. The experiments were conducted using the TBRV-Pi isolate and Chenopodium quinoa plants. C. quinoa plants were infected with TBRV-Pi with and without DI RNAs. Overall, 4 003 seeds were tested, and the analysis showed that the presence of DI RNAs made the TBRV-Pi seed transmission 44.76% more efficient. Moreover, for the first time, we showed that DI RNAs are being transferred from generation to generation.

Insight into the Contribution and Disruption of Host Processes during HDV Replication

Hepatitis delta virus (HDV) is unique among animal viruses. HDV is a satellite virus of the hepatitis B virus (HBV), however it shares no sequence similarity with its helper virus and replicates independently in infected cells. HDV is the smallest human pathogenic RNA virus and shares numerous characteristics with viroids. Like viroids, HDV has a circular RNA genome which adopts a rod-like secondary structure, possesses ribozyme domains, replicates in the nucleus of infected cells by redirecting host DNA-dependent RNA polymerases (RNAP), and relies heavily on host proteins for its replication due to its small size and limited protein coding capacity. These similarities suggest an evolutionary relationship between HDV and viroids, and information on HDV could allow a better understanding of viroids and might globally help understanding the pathogenesis and molecular biology of these subviral RNAs. In this review, we discuss the host involvement in HDV replication and its implication for HDV pathogenesis.

Defective Interfering RNAs of a Satellite Virus

ABSTRACT Panicum mosaic virus (PMV) is a recently molecularly characterized RNA virus with the unique feature of supporting the replication of two subviral RNAs in a few species of the familyGramineae. The subviral agents include a satellite RNA (satRNA) that is devoid of a coding region and the unrelated satellite panicum mosaic virus (SPMV) that encodes its own capsid protein. Here we report the association of this complex with a new entity in the RNA world, a defective-interfering RNA (DI) of a satellite virus. The specificity of interactions governing this four-component viral system is illustrated by the ability of the SPMV DIs to strongly interfere with the accumulation of the parental SPMV. The SPMV DIs do not interfere with PMV satRNA, but they do slightly enhance the rate of spread and titer of PMV. The SPMV-derived DIs provide an additional avenue by which to investigate fundamental biological questions, including the evolution and interactions of infectious RNAs.

3′-End Stem-Loops of the Subviral RNAs Associated with Turnip Crinkle Virus Are Involved in Symptom Modulation and Coat Protein Binding

ABSTRACT Many plant RNA viruses are associated with one or more subviral RNAs. Two subviral RNAs, satellite RNA C (satC) and defective interfering RNA G (diG) intensify the symptoms of their helper, turnip crinkle virus (TCV). However, when the coat protein (CP) of TCV was replaced with that of the related Cardamine chlorotic fleck virus (CCFV), both subviral RNAs attenuated symptoms of the hybrid virus TCV-CPCCFV. In contrast, when the translation initiation codon of the TCV CP was altered to ACG and reduced levels of CP were synthesized, satC attenuated symptoms while diG neither intensified nor attenuated symptoms. The determinants for this differential symptom modulation were previously localized to the 3′-terminal 100 bases of the subviral RNAs, which contain six positional differences (Q. Kong, J.-W. Oh, C. D. Carpenter, and A. E. Simon, Virology 238:478–485, 1997). In the current study, we have determined that certain sequences within the 3′-terminal stem-loop structures of satC and diG, which also serve as promoters for complementary strand synthesis, are critical for symptom modulation. Furthermore, the ability to attenuate symptoms was correlated with weakened binding of TCV CP to the hairpin structure.