Final Study Guide
Final Study Guide BIOL 123 001
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BIOL 123 001
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This 19 page Study Guide was uploaded by Anastassia Erudaitius on Wednesday June 8, 2016. The Study Guide belongs to BIOL 123 001 at University of California Riverside taught by Dr. Rao in Spring 2016. Since its upload, it has received 87 views. For similar materials see Virology in Biology at University of California Riverside.
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Date Created: 06/08/16
June 2016 [Comparative Virology] [Dr. Rao] [Study Guide – Final Exam] Highlight = Extremely Important ConcHighlight = 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 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 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 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 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 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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