Principles Of Virus Taxonomy PDF

 PRINCIPLES OF VIRUS TAXONOMY The International Committee on Taxonomy of Viruses (ICTV) has established four principles for viral taxonomy: Evolutionary relationships: Viruses should be classified based on their evolutionary history. Monophyletic...

 PRINCIPLES OF VIRUS TAXONOMY The International Committee on Taxonomy of Viruses (ICTV) has established four principles for viral taxonomy: Evolutionary relationships: Viruses should be classified based on their evolutionary history. Monophyletic taxa: Viruses should be assigned to taxa that are monophyletic, meaning that all members of a rank share a most recent common ancestor. Phenotypic and ecological properties: These properties can be used to inform the placement of ranks, but not override evolutionary relatedness. Taxon names: All taxon names should be capitalized, italicized, and never abbreviated Reproduction in animal viruses Animal viruses replicate by infecting a host cell and hijacking its machinery to produce new viruses: Attachment: The virus binds to the host cell using glycoproteins that interact with specific receptors on the cell membrane. Penetration: The virus enters the host cell. Uncoating: The virus's coating is removed. Gene expression and replication: The virus's genes are expressed and the host cell's machinery is used to manufacture the virus's components. Assembly: The new virus particles, called virions, assemble. Release: The virions are released into the environment.  Viroids are infectious pathogens that affect only plants, therefore are also called plant pathogens. Structurally, viroids are smaller than viruses and possess circular strands of ribonucleic acids (RNAs) with no protein coating. These entities hijack the cellular machinery present in plant cells to replicate new copies of themselves. It primarily affects all forms of higher plants. A second type of pathogenic RNA that can infect commercially important agricultural crops are the virusoids, which are subviral particles best described as non–self- replicating ssRNAs. RNA replication of virusoids is similar to that of viroids but, unlike viroids, virusoids require that the cell also be infected with a specific “helper” virus. There are currently only five described types of virusoids and their associated helper viruses. The helper viruses are all from the family of Sobemoviruses. An example of a helper virus is the subterranean clover mottle virus, which has an associated virusoid packaged inside the viral capsid. Once the helper virus enters the host cell, the virusoids are released and can be found free in plant cell cytoplasm where they possess ribozyme activity. The helper virus undergoes typical viral replication independent of the activity of the virusoid. The virusoid genomes are small, only 220 to 388 nucleotides long. A virusoid genome does not code for any proteins, but instead serves only to replicate virusoid RNA PRION At one time, scientists believed that any infectious particle must contain DNA or RNA. Then, in 1982, Stanley Prusiner, a medical doctor studying scrapie (a fatal, degenerative disease in sheep) discovered that the disease was caused by proteinaceous infectious particles, or prions. Because proteins are acellular and do not contain DNA or RNA, Prusiner’s findings were originally met with resistance and skepticism; however, his research was eventually validated, and he received the Nobel Prize in Physiology or Medicine in 1997.  A prion is a misfolded rogue form of a normal protein (PrPc) found in the cell. This rogue prion protein (PrPsc), which may be caused by a genetic mutation or occur spontaneously, can be infectious, stimulating other endogenous normal proteins to become misfolded, forming plaques.  Today, prions are known to cause various forms of transmissible spongiform encephalopathy (TSE) in human and animals. TSE is a rare degenerative disorder that affects the brain and nervous system. The accumulation of rogue proteins causes the brain tissue to become sponge-like, killing brain cells and forming holes in the tissue, leading to brain damage, loss of motor coordination, and dementia (see Figure 6.4.3 ). Infected individuals are mentally impaired and become unable to move or speak. There is no cure, and the disease progresses rapidly, eventually leading to death within a few months or years. Creutzfeldt-Jakob disease (CJD) is a fatal disease that causes degeneration of neural tissue. (a) These brain scans compare a normal brain to one with CJD. (b) Compared to a normal brain, the brain tissue of a CJD patient is full of sponge-like lesions, which result from abnormal formations of prion protein. (credit a (right): modification of work by Dr. Laughlin Dawes; credit b (top): modification of work by Suzanne Wakim; credit b (bottom): modification of work by Centers for Disease Control and Prevention) Replication and transcription in DNA viruses-influenza virus, reteroviruses-HIV https://www.youtube.com/watch?v=hCoZTYr62RE https://www.youtube.com/watch? app=desktop&v=tB5FQZi4HKY