Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Retrovirus Life Cycles01:10

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
Retroviruses02:33

Retroviruses

Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
Subviral Agents01:29

Subviral Agents

Subviral agents are infectious entities that resemble viruses but lack one or more viral components, such as a capsid or essential replication machinery. These agents include viroids, prions, and satellites, each possessing distinct structural and functional characteristics that influence their mode of infection and replication.Viroids are the simplest subviral agents, consisting of circular, single-stranded RNA molecules without a protein coat. They exclusively infect plants, relying entirely...
Viral Recombination00:57

Viral Recombination

Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
Viral Replication: Lytic Cycle01:20

Viral Replication: Lytic Cycle

Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.Attachment and DNA InjectionThe infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage...
What are Viruses?00:50

What are Viruses?

Overview

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Genomic insights into host-associated variants and transmission features of a ToBRFV isolate from Mexico.

Frontiers in plant science·2025
Same author

Dissecting the role of bHLH transcription factors in the potato spindle tuber viroid (PSTVd)-tomato pathosystem using network approaches.

PloS one·2025
Same author

Yeast Expressing a Phage Endolysin Reduces Endogenous <i>Clostridium perfringens Ex Vivo</i> in 21-Day-Old Broiler Chicken Intestinal Fluids.

Avian diseases·2024
Same author

The Remarkable Legacy of Theodor O. Diener (1921-2023): Preeminent Plant Pathologist and the Discoverer of Viroids.

Viruses·2023
Same author

Coding-complete genome sequence of an isolate of papaya virus E in tomato.

Microbiology resource announcements·2023
Same author

Mexico: A Landscape of Viroid Origin and Epidemiological Relevance of Endemic Species.

Cells·2022
Same journal

Correction: Bulatov et al. Camelpox Virus in Western Kazakhstan: Assessment of the Role of Local Fauna as Reservoirs of Infection. <i>Viruses</i> 2024, <i>16</i>, 1626.

Viruses·2026
Same journal

Correction: Franco et al. Whole Blood Volume-Based Absolute Quantification of HTLV-1 Proviral Load: A Comparative Method Evaluation Study. <i>Viruses</i> 2026, <i>18</i>, 580.

Viruses·2026
Same journal

Correction: Medkour et al. Adenovirus Infections in African Humans and Wild Non-Human Primates: Great Diversity and Cross-Species Transmission. <i>Viruses</i> 2020, <i>12</i>, 657.

Viruses·2026
Same journal

Burden of Malaria and Dengue Across Global, Asian, and Chinese Populations Based on GBD 2021 Data: A Quantitative Assessment of Importation Risks to China.

Viruses·2026
Same journal

First Report of <i>Orthonairovirus songlingense</i> in <i>Haemaphysalis concinna</i> Ticks from Russia.

Viruses·2026
Same journal

Epidemiological and Virological Characteristics of H9N2 Avian Influenza Virus in Jiangsu Province, China, 2024.

Viruses·2026
See all related articles

Related Experiment Video

Updated: May 28, 2026

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
06:02

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors

Published on: September 13, 2018

Viroid pathogenicity: one process, many faces.

Robert A Owens1, Rosemarie W Hammond

  • 1Molecular Plant Pathology Laboratory, USDA/ARS, Beltsville, MD 20705, USA;

Viruses
|October 14, 2011
PubMed
Summary
This summary is machine-generated.

Viroid infections cause plant disease symptoms similar to viruses. Viroid-derived small RNAs and host RNA silencing pathways are key to pathogenicity, highlighting complex host responses.

Keywords:
RNA silencingdisease inductionviroid pathogenicity

More Related Videos

Protocols for Investigating the Host-tissue Distribution, Transmission-mode, and Effect on the Host Fitness of a Densovirus in the Cotton Bollworm
11:12

Protocols for Investigating the Host-tissue Distribution, Transmission-mode, and Effect on the Host Fitness of a Densovirus in the Cotton Bollworm

Published on: April 12, 2017

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes
10:11

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes

Published on: September 27, 2014

Related Experiment Videos

Last Updated: May 28, 2026

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
06:02

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors

Published on: September 13, 2018

Protocols for Investigating the Host-tissue Distribution, Transmission-mode, and Effect on the Host Fitness of a Densovirus in the Cotton Bollworm
11:12

Protocols for Investigating the Host-tissue Distribution, Transmission-mode, and Effect on the Host Fitness of a Densovirus in the Cotton Bollworm

Published on: April 12, 2017

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes
10:11

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes

Published on: September 27, 2014

Area of Science:

  • Plant pathology
  • Molecular biology
  • Virology

Background:

  • Viroids, though non-coding, induce symptoms mimicking plant viruses.
  • Viroid pathogenicity is increasingly linked to small RNAs and host RNA silencing.

Purpose of the Study:

  • To explore the role of viroid-derived small RNAs in pathogenicity.
  • To understand the complex host responses, including signaling pathways, to viroid infection.

Main Methods:

  • Analysis of viroid-derived small RNAs.
  • Investigation of host RNA silencing pathways.
  • Examination of host signaling cascades and hormonal crosstalk.

Main Results:

  • Viroid-derived small RNAs are crucial effectors in viroid pathogenicity.
  • Host responses involve intricate signaling networks with protein kinases.
  • Crosstalk between hormonal and defense pathways is evident during infection.

Conclusions:

  • Viroid pathogenicity relies on small RNAs interacting with host silencing machinery.
  • Host responses are complex, involving multiple signaling layers.
  • Further research is needed to fully elucidate viroid-host interactions within biochemical pathways.