Viroid Replication, Movement and Host Factors: A Comprehensive Overview

Sophie Dupont^*
*Correspondence: Sophie Dupont, Department of Epidemiology, University of Singapore, Lower Kent Ridge Rd, Singapore, Email:

Description

Viroids small, single-stranded, non-coding RNA molecules that infect plants. Unlike viruses, they lack a protein coat and rely entirely on host cellular machinery for their replication and movement. Understanding viroid replication, movement, and the host factors involved is crucial for devising effective strategies to control viroid infections in plants. Viroid replication occurs entirely within the host plant cell and involves several steps. The replication cycle of viroids is still not fully understood, but research has shed light on the key processes involved. Viroids enter host cells through wounds or natural openings such as stomata. Once inside the cell, they must overcome various barriers to establish infection. Host factors play a crucial role in recognizing viroids and initiating replication. These factors may include RNA-binding proteins, chaperones, and other cellular components [1].

Viroid RNA serves as a template for replication. The replication process involves both rolling-circle and asymmetric mechanisms, leading to the synthesis of multiple copies of viroid RNA. Host enzymes such as RNA polymerases and RNA-dependent RNA polymerases are involved in viroid replication. Additionally, viroids may interact with host proteins to facilitate their replication. Viroids induce the formation of replication complexes within the host cell. These complexes provide the necessary environment for viroid replication to occur efficiently [2]. Viroids lack the protein coat required for cellto- cell movement typical of viruses. Instead, they rely on various mechanisms to move within the host plant. Viroids can move through plasmodesmata, channels that connect adjacent plant cells. This symplastic movement allows viroids to spread locally within the plant. Viroids can also move systemically within the plant through the phloem, the vascular tissue responsible for transporting nutrients and signaling molecules [3].

This long-distance movement enables viroids to infect distant parts of the plant. Host factors such as RNA-binding proteins and transport proteins are involved in facilitating viroid movement within the plant. These factors may regulate viroid trafficking through plasmodesmata or aid in their transport through the phloem. Viroid RNA forms complex secondary structures that may facilitate movement within the plant. These structures could interact with host factors to enhance viroid mobility. Environmental conditions such as temperature, humidity, and light intensity can influence viroid movement within the plant. Optimal environmental conditions may promote viroid spread, while adverse conditions could hinder their movement [4].

Host factors play a critical role in viroid replication, movement, and pathogenesis. Understanding the interaction between viroids and host factors is essential for elucidating the molecular mechanisms underlying viroid infections. Host RNA-binding proteins interact with viroid RNA and regulate various aspects of viroid replication and movement. These proteins may stabilize viroid RNA, facilitate replication complex formation, or modulate viroid trafficking within the plant. The RNA silencing pathway is a conserved antiviral defense mechanism in plants. Viroids trigger RNA silencing responses in the host, which can inhibit viroid replication and movement. However, viroids have also evolved mechanisms to suppress RNA silencing and evade host defense.

Chaperones and heat shock proteins play a role in viroid replication by assisting in the folding and assembly of viroid RNA and replication proteins. These proteins may also facilitate the transport of viroids within the plant. Cellular signaling pathways regulate various aspects of plant development and stress responses. Viroids may manipulate these pathways to promote their replication and movement or to suppress host defense mechanisms. Host immune responses play a crucial role in restricting viroid infections. Innate immune receptors recognize viroid RNA or viroid-induced changes in host gene expression, leading to the activation of defense responses. Viroid infections can alter host metabolism to promote viroid replication and movement. Host metabolic enzymes and pathways may be hijacked by viroids to support their own replication and spread within the plant [5].

Viroid replication, movement, and the host factors involved represent complex interactions between the pathogen and its plant host. Understanding these interactions at the molecular level is essential for developing strategies to control viroid infections in agriculture. Future research efforts should focus on elucidating the specific roles of host factors in viroid replication and movement, as well as identifying potential targets for therapeutic intervention. By unraveling the intricacies of viroid-host interactions, we can better mitigate the impact of viroid diseases on crop production and global food security.

Acknowledgement

None.

Conflict of Interest

None.

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