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The Genetics of Viruses
Background Structure Life Cycles
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Viral infections, past & present
Viral infection have been one of the major infectious challenges of the human species, for as far back as we can tell.
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Polio Viral infection have been one of the major infectious challenges of the human species, for as far back as we can tell. If one looks as far back as the Egyptian hieroglyphics, one can find evidence there of polio infection.
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Ebola Virus
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Herpes Virus
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Severe acute respiratory syndrome (SARS)
Figure A, B (a) Young ballet students in Hong Kong wear face masks to protect themselves from the virus causing SARS. (b) The SARS-causing agent is a coronavirus like this one (colorized TEM), so named for the “corona” of glycoprotein spikes protruding from the envelope.
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Let’s size them up…
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Compare the size of: eukaryotic cell, bacterial cell and a virus
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I. Background Everyone is at risk for infection! Size 20nm-250nm
Bacteriophages infect bacteria only All eukaryotes (animals, plants, fungi, protist) all vulnerable Size 20nm-250nm 0.5 m Ghost phage 100 to 1000 times smaller than the cells they infect Can pass through filters To put viral size into perspective, a medium sized virion next to a flea is roughly equivalent to a human next to a mountain twice the size of Mount Everest.
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Viral Diseases in Plants
More than 2,000 types of viral diseases of plants are known. Spots on leaves and fruits, stunted growth, and damaged flowers or roots
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Tobacco Mosaic Virus
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I. Background Virus Discovery: Tobacco mosaic disease (1930’s)
Stunts growth produces the speckled coloration
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I. Background Viral Evolution proposal: Fragments of cellular nucleic acid Reproduce within host cells only (non-living) Obligate intracellular parasites Host range
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II. Structure of viruses
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II. Structure of Viruses
1. Nucleic acid Enclosed in a protein coat Genomes may be ds/ss DNA ds/ss RNA
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II. Structure of Viruses
2. Capsids Protein Various shapes & structures Capsids are produced by host 18 250 mm 70–90 nm (diameter) 20 nm 50 nm (a) Tobacco mosaic virus (b) Adenoviruses RNA DNA Capsomere Glycoprotein Capsomere of capsid
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Viral structure
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II. Structure of Viruses
3. Envelopes Found in many animal viruses Glycoprotein and lipids Derived by host “Spikes” fuse with membrane or receptor mediated entry 80–200 nm (diameter) 50 nm (c) Influenza viruses RNA Glycoprotein Membranous envelope Capsid
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Receptor mediated model
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Fusion Model
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Basic Infection: Just Genome and Capsid
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Bacteria and Eukaryotic Models
III. Life Cycles Bacteria and Eukaryotic Models
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III. Life Cycles: 1. Bacteriophages complete two reproductive mechanisms: lytic cycle lysogenic cycle Figure 18.4d 80 225 nm 50 nm (d) Bacteriophage T4 DNA Head Tail fiber Tail sheath
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III. Life Cycles A. Lytic Cycle:
Digests the host’s cell wall, releasing the progeny viruses Kills host Virulent phage
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Phage assembly 1 2 5 4 3 Head Tails Tail fibers
Attachment. The T4 phage uses its tail fibers to bind to specific receptor sites on the outer surface of an E. coli cell. 1 Entry of phage DNA and degradation of host DNA. The sheath of the tail contracts, injecting the phage DNA into the cell and leaving an empty capsid outside. The cell’s DNA is hydrolyzed. 2 Release. The phage directs production of an enzyme that damages the bacterial cell wall, allowing fluid to enter. The cell swells and finally bursts, releasing 100 to 200 phage particles. 5 Assembly. Three separate sets of proteins self-assemble to form phage heads, tails, and tail fibers. The phage genome is packaged inside the capsid as the head forms. 4 Synthesis of viral genomes and proteins. The phage DNA directs production of phage proteins and copies of the phage genome by host enzymes, using components within the cell. 3
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Life Cycles B. Lysogenic cycle
Incorporate viral DNA into bacteria genome (propahge) Phage genome is replicated (for free!) w/o destroying the host Temperate phages capable of using both cycles
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The lytic and lysogenic cycles of phage , a temperate phage
Many cell divisions produce a large population of bacteria infected with the prophage. The bacterium reproduces normally, copying the prophage and transmitting it to daughter cells. Phage DNA integrates into the bacterial chromosome, becoming a prophage. New phage DNA and proteins are synthesized and assembled into phages. Occasionally, a prophage exits the bacterial chromosome, initiating a lytic cycle. Certain factors determine whether The phage attaches to a host cell and injects its DNA. Phage DNA circularizes The cell lyses, releasing phages. Lytic cycle is induced Lysogenic cycle is entered or Prophage Bacterial chromosome Phage DNA Figure 18.7
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III: Life Cycles 2. RNA viruses typically infect animals
Retroviruses (HIV), use reverse transcriptase to make cDNA Integrated into genome, provirus
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The reproductive cycle of HIV, a retrovirus
Figure 18.10 mRNA RNA genome for the next viral generation Viral RNA RNA-DNA hybrid DNA Chromosomal DNA NUCLEUS Provirus HOST CELL Reverse transcriptase New HIV leaving a cell HIV entering a cell 0.25 µm HIV Membrane of white blood cell The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. 1 Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. 2 catalyzes the synthesis of a second DNA strand complementary to the first. 3 The double-stranded DNA is incorporated as a provirus into the cell’s DNA. 4 Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. 5 The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). 6 Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. 7 Capsids are assembled around viral genomes and reverse transcriptase molecules. 8 New viruses bud off from the host cell. 9
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III: Life Cycles Life after infection Viruses may damage or kill cells
Tissue damage Toxins that lead to disease symptoms may be produced Asymptomatic
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Sources http://www.aapsj.org/
Campbell Reece Mitchell. Biology, Prentice Hall 1999, 2001 Sherris. Medical Microbiology: An introduction to infectious disease, Appleton and Lange,1990
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