TABLE OF CONTENT

• PLANT VIRUSES

• Plant viruses are also known as "PHYTOPHAGINAE". They are usually rod shaped. They contain nucleic acid in the form of RNA. They attack only plants. They are harmless to all other organisms. The plant viruses multiply within living cells but some may be able to reside within the bodies of aphides and nematodes. Some of the examples are:- TMV, CaMV etc.

  Plant viruses enters cells through wounds made mechanically or by vectors or by deposition on to an ovule by an infected pollen grain.

  ROUTE OF INFECTION

  1) VEGETATIVE PROPAGATION: Whenever plants are propagated vegetatively by budding or grafting, any virus present in the mother plant from which these organs are taken almost always will be transmitted to the progeny. such transmission is common in almost all fruit, many ornamental trees and shrubs, field crops like potatoes etc. 2) THROUGH SAP: It implies direct transfer of sap by contact of an wounded plant with a healthy one. Such process occurs during agricultural practices by tools, hands, or by animal feeding on the plant. generally TMV, potato viruses and cucumber mosaic viruses are transmitted via sap.

  3) TRANSMISSION THROUGH SEED: More than 110 viruses are transmitted via seeds. Infected seeds are produced by the fertilization of healthy ovule by infected pollen. The viruses then reside in the integument of seed

  and infects seedling as they germinate. viruses transmitted by pollen results in reduction of fruit yield.

  4) TRANSMISSION THROUGH INSECTS: The most common means of viral transmission is by insect vectors. These include the members of order-Homoptera (Aphides, leaf hoppers, white flies, plant hoppers, tree hoppers.), Order- Hemiptera( tree bugs) & Order- Coleoptera( bettles).

  
  ANIMAL VIRUSES

• The animal viruses are also called as Zoophaginae. They are generally poly hedral or spherical in shape. They contain nucleic acid in the form of either DNA or RNA.

  There are at present 20 recognized families of viruses that contain viruses of humans or animals.

  Pappiloma Virus

  Herpes Virus

  Historically, properties used most often in classification derive from electron microscopic examination e.g. virion morphology, structure and dimensions, and presence or absence of an envelope.

  Additional characterization is supplied by the type and nature of the genomic nucleic acid.

  Examples- rabbies, dog distemper virus, HIV etc
  

  GENERAL CHARACTERISTICS:

  • Attachment sites are plasma membrane proteins and glycoproteins.
  • Capsid enters by endocytosis or fusion.
  • Uncoating-Enzymatic removal of capsid proteins.
  • Biosynthesis (Eclipse)-In nucleus (DNA viruses) or cytoplasm (R.NA viruses).
  • Chronic infection-Latency; slow viral infections; cancer.
  • Release-Enveloped viruses bud out; non-enveloped viruses rupture plasma membrane.
  • 
    
  BACTERIOPHAGES

• Bacteriophages (phages) are viruses that infect bacteria. Typical phages have hollow heads (where the phage DNA or RNA is stored) and tunnel tails, the tips of which have the ability to bind to specific molecules on the surface of their target bacteria.

  Several bacteriophages are used as cloning vectors, the most commonly used E.coli phages being lambda & M13 phages. plasmid vectors have to be introduced into the bacterial cells, which are then cloned and selected for the recovery of recombinant DNA.In contrast, the phage vectors are directly tested on an appropriate bacterial lawn.( a continuous bacterial growth on an agar plate) where each phage particle forms a plaque.( a clear bacteria free zone in the bacterial lawn).

  The viral DNA is then injected through the tail into the host cell, where it directs the production of progeny phages often over a hundred in half an hour. These "young" phages burst from the host cell (killing it) and infect more bacteria.

• 
  
  VIROIDS
• Structure:
  Viroids are infectious agents composed exclusively of a single piece of circular single stranded RNA which has some double-stranded regions.
  Because of their simplified structures both prions and viroids are sometimes called subviral particles. Viroids mainly cause plant diseases but have recently been reported to cause a human disease.

  Catalytic RNAs are those that have the intrinsic ability to break and form covalent bonds; Viroids are catalytic RNA's (ribozymes) that cleave RNA to produce fragments containing a 5'-hydroxyl and a 2', 3'-cyclic phosphate.

  This is a nonhydrolytic reaction in which the same number of phosphodiester bonds are maintained and the transesterification reaction is theoretically reversible. This reaction is considered to play an essential role in the replication of these RNAs in vivo. Such reactions are all intramolecular and hence quasi-catalytic with single turnover. These RNAs can be manipulated, however, to provide true catalytic cleavage in trans-reactions.
  
  
  Replication:

  Circular, pathogenic RNAs are replicated by a rolling circle mechanism in vivo. There are two variations of this rolling circle mechanism:

  In the first variation (A), the circular plus strand is copied by viroid RNA-dependent RNA polymerase to form a concatameric minus strand (step 2). Site-specific cleavage (arrows) of this strand produces a monomer that is circularized by a host RNA ligase (step 3) and then copied by the RNA polymerase to produce a concatameric plus strand. Cleavage of this strand (step 5) produces monomers which, on circularization, produces the progeny circular, plus RNA, the dominant form in vivo.

  In the other variation (B), the concatameric minus strand of step 1 is not cleaved but is copied directly to give a concatameric plus strand (step 3), which is cleared specifically to monomers for ligation to the circular progeny. Those RNAs that self-cleave only in the plus strand in vitro are considered to follow this route.

  The hepatitis D viroid genome is a minus strand that gives rise to two RNA species. One of these is a mRNA for the delta antigen and the other is a complete complimentary copy (plus strand or anti-genome). The anti-genome acts as a template to make more minus strands. The minus strand self-cleaves and self-ligates. HDV replication takes place in the nucleus but delta antigen is made in the cytoplasm. The delta antigen is the only protein made by the HDV mRNA. It has a +12 charge at physiologic pH, accumulates in the nucleus and binds to minus strand RNA as a dimer. The delta antigen is necessary for viroid assembly but its exact mode of action is unknown.

  Human pathologies induced by viroids:

  The only human disease known to be caused by a viroid is hepatitis D. This disease was previously ascribed to a defective virus called the delta agent. However, it now is known that the delta agent is a viroid enclosed in a hepatitis B virus capsid. For hepatitis D to occur there must be simultaneous infection of a cell with both the hepatitis B virus and the hepatitis D viroid. There is extensive sequence complementarity between the hepatitis D viroid RNA and human liver cell 7S RNA, a small cytoplasmic RNA that is a component of the signal recognition particle, the structure involved in the translocation of secretory and membrane-associated particles. The hepatitis D viroid causes liver cell death via sequestering this 7S RNA and/or cleaving it.

  Transmission:
  The hepatitis D viroid can only enter a human liver cell if it is enclosed in a capsid that contains a binding protein. It obtains this from the hepatitis B virus. The delta agent then enters the blood stream and can be transmitted via blood or serum transfusions.

  
  PRIONS

• A prion — short for proteinaceous infectious particle that lacks nucleic acid (by analogy to virion) — is a type of infectious agent made only of protein. Prions are believed to infect and propagate by refolding abnormally into a structure which is able to convert normal molecules of the protein into the abnormally structured form. However, the term in itself does not preclude other mechanisms of transmission.

  Prions are generally quite resistant to denaturation by protease, heat, radiation, and formalin treatments,although potency or infectivity can be reduced. Ozone sterilization is currently being studied as a potential method for prion deactivation.
  Although genetic research may shed light on prions, and there is a genetic component to many prion diseases, prion diseases are not exclusively genetic diseases and are grouped as transmissible spongiform encephalopathies.

  Diseases as varied as fatal familial insomnia and kuru (translated as "to tremble with fear") are believed to be associated with prions. Other prion diseases include scrapie (a disease of sheep), chronic wasting disease, (in deer and elk), variant Creutzfeldt-Jakob disease (vCJD), and bovine spongiform encephalopathy (BSE or mad cow disease), all caused by similar proteins in different species It should be noted that the same gene is responsible for spongiform encephalopathies which are not known to be transmissible, as well as some non-neurological diseases.
  

  Some require a mutation for transmission to occur, and there are respective mutations which can prevent transmission for most of the TSEs. Whether or not the prion gene has a non-disease function is an area of considerable active research. All of these diseases affect the structure of the brain or other neural tissue, and all are untreatable and fatal. However, a vaccine has been developed in mice that may provide insight into providing a vaccine in humans to resist prion infections.
  Proteins showing prion behaviour are also found in some fungi. Some fungal prions may not be associated with any disease; it is unknown whether these prions represent an evolutionary advantage for their hosts. All known prions are believed to infect and propagate by formation of an amyloid fold, in which the protein polymerizes into a fiber with a core consisting of tightly packed beta sheets. Other mechanisms may exist in yet undiscovered infectious protein particles.

  Prions in human disease:
  There are four principal disease syndromes associated with prions in humans:

  Creutzfeldt-Jakob Disease (CJD),

  Creutzfeldt-Jakob Disease (vCJD),

  Kuru and

  Fatal Familial Insomnia.

  Genetic engineering research:

  On 31 December 2006, Hematech, a biotechnology company based in Sioux Falls, South Dakota, announced that it had genetically engineered cattle lacking a necessary gene for prion production - thus theoretically making them immune to BSE.Research with mice had previously indicated that animals lacking endogenous prion protein are resistant to infection by scrapie prion protein.
  

GENERAL
CHARACTERISTICS

• They
  are ultramicroscopic in size
• they
  do not have a cell wall
• they
  do not have cellular organization
• they
  cannot survive or reproduce outside the host cell
• they
  are obligatory intracellular parasites
• they
  contain either DNA or RNA but never both
• there
  is no protein synthesis machinery

• they do not grow
  but replicate
• they can pass
  through bacterial filters
• they can be
  crystallized

LIVING CHARACTERS

• They contain either DNA or RNA as genetic material.
• They undergo mutations
• they are capable of multiplication.
• they are parasites and show very high host specificity
• they can be transmitted from one host to another.
• they react to heat, radiation and chemicals.
• they are ultramicroscopic disease producing entities.

NON LIVING CHARACTERS

• They can be crystallized
• They are inert outside the host.
• They do not posses cell wall
• They do not posses cellular machinery
• They are unaffected by antimicrobial antibiotics.
• They do not have energy producing enzyme systems