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UCR / Biology / BIOL 123 / How do plants control viral diseases?

How do plants control viral diseases?

How do plants control viral diseases?

Description

School: University of California Riverside
Department: Biology
Course: Virology
Professor: Rao
Term: Spring 2016
Tags: UCR, Bio, 123, Virology, Rao, final, study, and guide
Cost: 50
Name: Final Study Guide
Description: This study guide covers material since the second midterm
Uploaded: 06/08/2016
19 Pages 38 Views 8 Unlocks
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June 2016


How do plants control viral diseases?



[Comparative Virology] [Dr. Rao]  [Study Guide – Final Exam]

Highlight = Extremely Important Concept Highlight = Important Concept Highlight = Key Term

**This Final Exam Study Guide covers all material since the  second midterm. The study guides for Midterm 1 and Midterm 2  will not be repeated here **

 [Lecture – Viral Pathogens of Plants]

∙ Plant viruses can be RNA or DNA, single or double stranded o Use host machinery to replicate  

∙ Remember that viroids use host machinery to TRANSLATE ∙ Bromoviridae viruses are (+)ssRNA 

∙ (+)ssRNA viruses vary greatly in size

∙ Have nucleic acids and a capsid protein, but no envelope 


What are the example of mosaic?



o Plant viruses have no envelopes and no surface  receptors because entry into host occurs through a  wound on plant or injection into plant  

∙ TMV – rod shaped virus/helical

∙ CMV – spherical shape

June 2016

∙ Can survive in insects, nematodes, fungi, or humans o Plant viruses may have many or few hosts

∙ A single species may have many strains If you want to learn more check out What is the definition of consumer culture?
We also discuss several other topics like What is ischiopubic ramus?
Don't forget about the age old question of What is the second largest reservoir in the hydrosphere, and where is it located?

∙ Naming Plant Viruses:

o The name of a plant virus does not mean that is the  only plant the virus can infect, but that it was the first  plant the virus was isolated from

o Example: Alfalfa mosaic virus does not only infect  alfalfa plants, but also peppers  


What are the different types of plant diseases?



Don't forget about the age old question of What is octet rule?

∙ Types of symptoms of plant viruses:

o Mosaic/mottle

o Ringspots/Line patterns

o Flower break

o Leaf deformation

o Fruit deformation

o Stunting  

o No symptoms/ asymptomatic  

∙ Types of Mosaics:

o Rose mosaic 

 Results from multiple viruses:

∙ Rose mosaic virus

∙ Apple mosaic virus

June 2016

∙ Prunus necrotic ringspot irus

∙ Arabis mosaic virus

o Cucumber mosaic virus / Nandina mosaic virus o Wisteria mosaic virus  

o Mosaic of fig

o Tomato mosaic virus (doesn’t just affect tomatoes!) ∙ Coleus (type of plant)

o Can be infected by Tobacco etch virus  member of  Potyvirus group  Don't forget about the age old question of Define octet rule.

∙ Hydrangea (type of plant)

o Can be infected by chlorotic mottling

o Hydrangea chlorotic mottle virus (Carlavirus)

∙ Camellia (type of plant) and Carrotwood trees o Experiencing possible new virus emergence  

∙ Steps of infection:

o Entry into plant via wound or vector

o Replicate using host machinery  

o Package new virus particles and infect plant cells

 First: Localized movement (rapid)  within a single  leaf

 Second: Cell to cell movement (slow)

June 2016

∙ Virus moves from cell to cell via  

plasmodesmata

∙ Viral nucleic acids and virions cannot pass  

through plasmodesmata channels without  

movement protein  If you want to learn more check out Is cost a function of age?

∙ Movement protein: 30k Protein (for TMV,CMV, TRV)

∙ Movement protein binds to viral RNA,  

transfers it to new cell, then releases it  

∙ Vascular system invaded (virus travels to  

roots)  then travels to upper young parts of  

plant  then to entire plant 

o Infect other plants via vectors  

∙ Meristem of plant is often not infected  

∙ Some viruses only infect phloem  

∙ Virus usually modifies a membrane bound structure for its  replication, replication can occur in:

o Endoplasmic reticulum  

o Chloroplast outer membrane

o Vacuolar membrane

o Peroxisome

o Mitochondria

o Nucleus  

∙ Plant RNA viruses encode movement protein, capsid protein,  and RNA dependent RNA Pol

June 2016

o Animal and human viruses don’t need a movement  protein  

∙ TMV structure

o Rod-shaped / helical

o Hollow core surrounded by identical coat protein  subunits  

∙ Within 22hrs from first exposure to viral TMV RNA, infection  of third group of cells occurs

o Within 4-10 days, infection spreads from epidermis to  mesophyll cells

∙ Self-defense: RNA silencing mechanism 

o HR genes – Hypersensitive Response  

∙ Cross protection induces resistance in plants  

o Natural infection – infect plant intentionally with a mild  strain to prevent subsequent infection  

o Transgenic plants – plants that are able to produce a  certain capsid protein that confers resistance  

 TMV coat protein accumulation protects plants  from TMV infection  

 For potyviruses like TEV – resistance was achieved  without TEV coat protein accumulation  

 Papaya ringspot virus (PRSV) – stunting, mosaic,  defoliation, crop loss  inoculated cross protection  not successful, CP accumulation/transgenic  

papaya was successful

June 2016

∙ CTV

o Natural inoculation used in some locations

o Many fields maintain resistance for 20yrs

o New strains continually selected  

[Lecture – Multicomponent RNA Viruses] ∙ Focus on Bromoviridae  

∙ Multicomponent viruses may have helical symmetry or  icosahedral symmetry 

o May be two-component, three-component, or four component  

∙ Remember that for viruses like TMV only one particle is  needed to infect a host – only one RNA needed

o This is not true for multi-component viruses  

∙ Family: Bromoviridae 

o Genus: Bromovirus  

 BMV (Brome mosaic virus), BBMV (Braod bean  

mottle virus), CCMV (Cowpea chlorotic mottle  

virus)

 All are icosahedral and have identical sized  

capsids 

∙ They have different weights however because

they each contain different genomes/ RNA

 Transmitted by beetles and nematodes

June 2016

 BMV  

∙ No envelope 

∙ Genome includes THREE (+)ssRNA --  tripartite virus – four proteins expressed from  3 genomic RNAs 

o RNA 1 in a single capsid – encodes  

helicase 

o RNA 2 in a single capsid – encodes  

polymerase 

o RNA 3 and 4, together in a single capsid  – encodes MP and CP 

∙ A genome divided into separate capsids  allows RNA segment re-assortment and  

simplifies gene regulation 

∙ RNA 4 is NOT required for infection 

∙ No drastic symptoms that would affect crop

∙ All of the RNAs have a 5’Cap, but instead of a 3’PolyAtail they have a tRNA-like structure  which functions as a (-) strand promoter 

∙ Replicase 1 and 2 (from RNA 1 and 2) must  combine to be functional

∙ RNA 3 encodes the movement and capsid  protein  

o RNA 3 must first be replicated into (-)  sense, then from the (-) sense strand it  

can form the RNA4 (+) strand  the RNA

June 2016

4 strand is not the full RNA 3 but only a  

portion of it (just the CP portion) 

o On the RNA3 (-) strand there is an  

internal promoter that ribosomes can  

bind to, they cannot bind to this point on

the RNA3 (+)strand

o Advantage is that the virus can control  

when the genes get expressed  

Replicase proteins are made at very low  

levels and capsid proteins are made at  

highest concentration 

∙ First virus that showed how the genomes are  distributed, first virus used to make cDNA 

∙ Can replicate to very high levels

∙ Life cycle:

o Entry via wound or insect  

o Translation of (+)ssRNA occurs  

immediately upon entry  

o Translation occurs in vesicles (in ER) 

gives the virus an advantage to hide  

from the plant’s defense mechanisms  

o MP moves virus particle from cell to cell

o Capsid proteins encase virions and are  

picked up by insects and transmitted to  

other plants

o Nucleus is not involved

o Genus: Cucumovirus

June 2016

 Includes satellite viruses

 CMV

∙ Translation occurs in vacuolar membrane 

 All are icosahedral and have identical sized  capsids 

 They have different weights however because they each contain different genomes/ RNA

 RNA 4 is NOT required for infection  need only 3  particles to be infectious 

o Genus: Alfamovirus

 AMV

 Four-component

 Rod shaped, different sizes 

 RNA4 CP required for replication  need all 4  particles to be infectious 

 Translation occurs in Chloroplast membrane  Mosaic, stunted growth 

 Transmitted by aphids 

 Infects peppers as well  peppers and alfalfa often  grown side-by-side  

o Genus: Ilarvirus

 TSV (tobacco streak virus)

 Four component

June 2016

 Icosahedral shape, Different sized capsids 

o Genus: Oleavirus

 Olive Latent virus

∙ Five component virus – Ourmiavirus

o Different sizes  

∙ Studying Virus replication

o Intact plants: plants used b/c they are the natural host   inoculate leaf and look for local symptoms or systemic accumulation

 Infections not synchronous

 Replication and movement signifies accumulation

o Viral reporter systems: cloned viral genomes allow  reporter molecules to be expressed within viral genome

 Allows real time measure of virus in plants

o Protoplasts: lack cell wall (degraded using enzymes)  Infection is synchronous

 Allows measurement of viral replication usually  measured by Northern analysis  

o Yeast: BMV replicates in yeast

 Promoters and replication of RNA3 studied  

∙ Advantages 

o Having multiple components – Each gene can be  efficiently manipulated whenever it is needed

June 2016

o Recombinants can develop  

∙ Disadvantages 

o Need more virions to initiate life cycle/for infection

 If you just have RNA 1 and RNA 2 transmitted  

then the virus cannot move because RNA 3  

encodes movement protein  

[Lecture – Subviral Pathogens]

∙ Satellite viruses – depend on helper viruses for replication  only 

∙ Satellite RNAs – depend on helper viruses for replication,  encapsidation, AND transmission  b/c satellite RNAs do not  encode proteins 

o They are completely dependent on helper viruses for  infection 

∙ Helper virus Pol replicates satellite RNAs and satellite viruses 

∙ Hepatitis delta agent – depends on helper virus for some  encapsidation and transmission, does NOT need helper for  replication 

∙ Defective interfering RNAs – composed of helper virus  sequences

∙ The above (^) all depend on helper viruses  

∙ VIROIDS do NOT depend on helper viruses

June 2016

o Small, circular ssRNAs 

o Replicate independently  

∙ Most satellites associated with plants

o Some satellites dependent on animal viruses  

∙ Satellites interfere with helper virus replication 

∙ Satellites may accelerate symptoms of helper virus, or may  lessen symptoms

∙ Satellite RNAs fold into secondary structures  

∙ Helper viruses do NOT depend on satellites for replication  

∙ Little or no nucleotide sequence similarity between satellites  and helper virus genome  

∙ Satellite viruses

o Encode their own capsid protein (only require helper  virus for replication) but no replicase 

o Icosahedral capsid  

o Do not need to share natural vector with helper virus  o Genome = 1200 bases

o Linear ssRNA 

o Satellite tobacco necrosis virus

o Satellite tobacco mosaic virus (STMV)

 Helper is rod-shaped  

 The only satellite virus with a helper shaped  

differently from itself

June 2016

o Keep in mind that TMV is rod shaped, the satellite TMV  is icosahedral

∙ Satellite RNAs

o Requires capsid protein of helper virus to make virions  (dependent on helper for encapsidation), and therefore  also dependent for transmission 

o In (ss)satRNAs there is a high degree of base pairing  o Large satellite RNAs = 1400 nt

o Small linear satellite RNAs = 200-400 nt

o Small circular satellite RNAs = 200 -400 nt, rolling-circle replication like viroids (but not independent like  viroids!)

o Chimeric molecules = Defective interfering RNAs and  satellite hybrid

∙ Satellites are often parasitic to the HELPER viruses because  they often reduce disease symptoms and interfere with the  helper virus replication (because they hijack the helper virus  replication machinery)

∙ Satellite genomes are extremely small compared to their  helper viruses 

∙ Viroids and satellite RNAs both form secondary structures,  but the difference is that viroids can replicate by themselves  and sat. RNAs cannot

∙ Satellite viruses are slightly larger than satellite RNAs ∙ Most satellite RNAs are NOT related to their helper virus

June 2016

∙ Dependoviruses

o Aka AAV (Adeno-associated virus)

o A satellite virus that is only infectious if the host cell is  also infected by Adenovirus or Herpesvirus  

o ssDNA genome 

∙ Hepatitus delta virus (Hepatitis D)

o Viroid-like properties, but the Hep. Delta Virus has a  larger RNA, is encapsidated, and encodes a virion associated protein

o Can replicate independently  

o Makes HBV infection worse  

o Usually if you get Hepatitis B you also get Hepatitis D  because they are both encased in the same capsid  (because HDV requires HBV as a helper virus)

 HDV therefore has satellite-like properties

o Replicates in nucleus

o Replicates via host DNA-dependent RNA Pol II

o Found worldwide  

[Lecture – Viruses and Cancer]

∙ Cancer = uncontrolled growth of a single cell

∙ Link found between viruses and cancer

o Cancer also linked to carcinogens – 80% of cancers  caused by carcinogens (tobacco, asbestos, radiation)

June 2016

o 20% of cancers due to viruses

 Hepatitis B – liver cancer 

 Hepatitis C – liver cancer 

 HPV – Cervical cancer 

 Epstein- Barr 

 Kaposi’s herpesvirus  

 Human T-lymphotropic virus types I and II 

∙ We already have oncogenes present in our genomes

o Viruses activate the cancer-inducing gene in place of  the healthy gene  

∙ History

o Hippocrates – carcinomas

o Chimney sweeps – scrotal cancer

o Reims, France – first cancer hospital

∙ Early Cancer Research

o Bishop and Varmus – found cancerous genes (src gene  of RSV) in normal DNA of chickens  

 Oncogenes are healthy cellular genes, after viral  infection they are hijacked

 The genes are originally healthy genes, and  

become cancerous AFTER viral infection  leads to  uncontrollable cell growth

o Ellerman and Bang – showed that “filterable agents”  could produce tumors in chickens

June 2016

o Rous – showed that a bacteria-free filtrate caused  sarcomas in chickens  

 The agent became known as Rous Sarcoma Virus  (retrovirus)

∙ Oncogene – a gene that is already present in the host and  has the potential to convert a normal cell to a cancerous cell

∙ Viral oncogene – the gene within the virus that is responsible for turning the host oncogene into a cancerous gene  

∙ Proto-oncogene – host genes that promote NORMAL  GROWTH and division of cells  

∙ Tumor suppressor genes – suppress conversion of normal cell to cancer cell  viruses turn these genes off

∙ Cell transformation -- change of morphological, biochemical, or growth properties of a cell

∙ Cancer cells can spread through the bloodstream and  lymphatic system to other parts of the body

∙ Metastasis – when cancerous cell spread  

∙ Benign tumor – highly unlikely that the cells will grow and  spread  

∙ Cancer cells in vitro (lab)

o Cancer cells require less serum in medium to grow  

o Genetic changes – polyploidy, high levels of  

telomerases  

o Metabolic changes – grow rapidly

∙ DNA Tumor viruses

June 2016

o Shope discovered first DNA tumor virus – rabbit  fibromas  

o Differ from RNA tumor viruses in structure, genome  organization, and replication strategies

o Viral oncogenes are essential for viral replication 

o Oncogenes of small DNA tumor viruses do not have  cellular homologs

o HBV

 Causes chronic hepatitis, progresses to liver  

cancer

 Infects hepatocytes of liver

 HBV vaccine was FIRST vaccine to prevent a  

“cancer” 

o HCV

o Adenovirus

∙ EBV 

o Aka Human Herpes Virus 4

o Causes mononucleosis  teens usually infected o Named after 2 people, Epstein and Barr

o Was isolated from lymphoma samples collected by  Burkitt

 Lymphoma called Burkitt’s lymphoma  

∙ Most odten infects children in central Africa

June 2016

∙ Weakens immune system (infects B  

Lymphocytes)

o 95% of the population in US between 35-40 are  persistently infected with EBV

∙ Kaposi’s Sarcoma

o Aka Human Herpesvirus 8

o Causes skin cancer

o Virus is the cause  

o Most often in elderly men of Mediterranean, Middle  Eastern, or Eastern European descent, or AIDS patients

∙ HPV

o Often infects sexually active individuals

o Over 100 types  

o High-risk types cause cervical cancers, and other types  of cancers  

o HPV vaccine: second vaccine available to prevent  cancer 

 Merck GARDASIL

∙ Adenoviruses

o Animal DNA tumor viruses

o Isolated from human adenoids

o 47 types

o Some can cause malignant tumors in baby rodents

June 2016

o E1A and E1B genes transform rodent cell lines ∙ SV-40 (Simian Vacuolating Virus)  

o Isolated from primary African green monkey kidney  cells

o Isolated accidentally by Sweet and Hilleman during  testing of poliovirus vaccine

o Did not cause CPE (cytopathic effects)  NO cell  changes  

o dsDNA, icosahedral 

o Frequently contaminated rhesus monkey kidney cell  culture

o Is a polyomavirus  

∙ Polyomaviruses found in humans

o Jamestown Canyon Virus (JCV)

o BK virus (BKV)

o Cause tumors in animals and AIDS patients  

∙ Mouth Cancer and Oral Sex

o Can be caused by chewing tobacco  

∙ Link found between cancer and obesity

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