VIRUS VIROID PRION. Ms.Tanyaratana Dumkua Biology Department, Mahidolwittayanusorn School

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1 VIRUS VIROID PRION Ms.Tanyaratana Dumkua Biology Department, Mahidolwittayanusorn School

2 What is virus? Living? Need food? Reproduction? Cell? Cytoplasm? Cell membrane? Metabolism? Size? Component?

3 Adenovirus Herpesvirus Tobacco mosaic virus Rabies virus

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6 David Baltimore s viral classification

7 Multiplication of DNA Virus Virion attaches to host cell Multiplication of DNA Virus 7 Virions are released Capsid DNA 1 6 Virions mature Papovavirus DNA Cytoplasm 2 Virion penetrates cell and its DNA is uncoated Capsid proteins Host cell mrna 5 Late translation; capsid proteins are synthesized 4 Late transcription; DNA is replicated 3 Early transcription and translation; enzymes are synthesized

8 Multiplication of RNA Virus

9 Multiplication of Retro Virus Reverse transcriptase Capsid DNA Virus Two identical + stands of RNA Identical strands of RNA Viral proteins RNA 4 5 Mature retrovirus leaves host cell, acquiring an envelope as it buds out. Transcription of the provirus may also occur, producing RNA for new retrovirus genomes and RNA that codes for the retrovirus capsid and envelope proteins. Provirus Host cell Reverse transcriptase Viral RNA 3 1 DNA of one of the host cell s chromosomes Retrovirus penetrates host cell. 2 Virion penetrates cell and its DNA is uncoated The new viral DNA is tranported into the host cell s nucleus and integrated as a provirus. The provirus may divide indefinitely with the host cell DNA.

10 Multiplication of Bacteriophage

11 Group Discussion Attachment / Adsorption Penetration & Uncoating How many Biosynthesis steps of the viral multiplication? Maturation /Assembly Release

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13 Zika virus is ssrna(+) Rotavirus is dbrna jpg

14 What should we do to fight the virus?

15 Shall we use antibiotic to kill virus?

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17 SUBVIRAL AGENTS Viroid : Plant pathogen key/communityserver-wikis-components-files/ /f107_2d00_01_2d00_ png

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19 Thai Agricultural Research Jounal. Vol 31 No 1 (2013): January - April The New Strain of Columnea latent viroid (CLVd) Causes Severe Symptoms on Bolo Maka (Solanum stramonifolium Jacq.) Columnea latent viroid (CLVd), one of the smallest plant pathogens consisting of nucleotides, is an important plant pathogen in tomato causing stunting, necrosis of leaf veins, petioles, and stem, leaf discoloration, flower dropping, small fruits, as well as death of the whole plant, Nevertheless, it can cause high yield loss in tomato, potato, and pepper crop productions, but cut causes symptomless on some species of Solanum such as eggplant (Solanum melongena), and bolo maka (S. stramonifolium). ln 2011, a new strain of CLVd was found inducing severe symptoms in bolo maka such as stunting, apical stunt, rugosity and mosaic of leaves, small lateral leaves, necrosis of leaf veins and petioles, By nucleotide sequence analysis of the new strain and the previously reported CLVds in GenBank, 7-9 different changed gases were shown In these bases, only two bases at position 83 and 292 that varied by the symptom on bolo maka. Both positions were part of pathogenic domain (P domain) on the new strain which base A was added at the position 83 (base insertion) and A or T was changed to G (base substitution) at the position 292. Since, the pathogenic domain sequences (nucleotide position at upper P- domain and at lower P-domain) have been known as the domain that controls the disease symptoms and virulence on host plants of most viroids. Base on this work, it is possible to assess whether the two positions play the role in the pathogenicity and severity controller of this viroid. This is the first report for CLVd. However, to prove this hypothesis, further study is needed to confirm the assumption.

20 SUBVIRAL AGENTS Prion : Animal pathogen : Proteinaceous infectious particle

21 CJD Kuru kuru Mad cow disease

22 Bovine Spongiform Encephalopathy situation in Thailand Abstract Bovine Spongiform Encephalopathy (BSE) in an extremely serious and deadly epizootic disease, mainly spread throughout the United Kingdom. It has caused a tremendous economic loss and up to million cattle have been slaughtered in order to eradicate BSE. Moreover, extensive studies show, BSE could pose a risk to human health and possibly life also. Bovine spongiform encephalopathy is one of the transmissible spongiform encephalopathies (TSEs) with prion protein as the proteinaceous infectious particle, causing damage to the central nervous system (CNS) and death in the final stage. Vacuolation of cerebrum and cerebellum are evident, coupled with plaques and scrapie associated fibrils (SAF). Epidemiological studies point to contamination in cattle feed. Changes in the manufacturing procedure of meat and bone meal for bovine consumption has worsened the transmission risk factor. Prion protein may accumulate in blood, nerve fibers or lymphoreticular organs of the BSE cow before invading the CNS. Originally, only brain, spinal cord and retina were identified as possible prion sources. At the time, the Spongiform Encephalopathy Advisory Committee (SEAC) is waiting for the results of inoculation of BSE infected meat, milk and lymphoreticular organs in calves, which is experimentally tested to be 1000 times more sensitive than mice. Our report also includes BSE chronological events and control measures in some countries. Diagnostic techniques and the possible treatment ideas are also mentioned. Creutzfeldt-Jakob s Disease (CJD) is one of the fatal human diseases involving the CNS. Lately, a new variant of CJD (nvcjd) has been reported and has been found to have different in clinical signs and neuropathological lesions than the known CJD. Western blotting technique has proved that the causative agent of nvcjd is similar to BSE, not the sporadic CJD. Exposure of nvcjd individuals with BSE prion protein is postulated. Organ, dura matter and retinal transplantation including brain surgery with contaminated equipment can transmit CJD, especially to those groups of people with homozygous gene at codon 129. Apart from this, there are 90 ( ) and 54 ( ) CJD cases treated with growth hormone and gonadotropin (human-deriverd) reported. Also the World Health Organization concluded early in 1997 evidence of a CJD causative agent in plasma of the experimental mice. Precautions should be taken in procedures involving blood transfusion, organ donation from individuals with a history of hereditary nervous disorders and those who have been treated with growth hormones or gonadotropin.