Chapter 13 The Genetics of Viruses and Prokaryotes

1. Chapter 13The Genetics of Viruses and Prokaryotes Biology 101 Tri-County Technical College Pendleton, SC

3. Viral Components • Are obligate intracellular parasites • Outside living host cell exist as individual particles called VIRIONS • Have central core of either DNA or RNA but never both • Surrounded by CAPSID composed of capsomeres (one or more proteins)

4. Components, cont. • Animal viruses may have ENVELOPE derived from host cell’s plasma membrane • Virions lack cell wall and ribosomes of bacteria • Therefore, they are unaffected by antibiotics • VIROIDS are infectious genetic material

5. Describing Viruses • Can be described by whether the genome is DNA or RNA • Whether the nucleic acid is single-stranded or double-stranded • Whether the shape of the virion is simple or complex crystal • Whether the virion is surrounded by a membrane (envelope)

6. Obligate Intracellular Parasites • Viruses NOT classified as “living” • Whole viruses NEVER arise directly from preexisting viruses • Develop and reproduce ONLY within cells of specific hosts • Cells of animals, plants, fungi, protists, and prokaryotes (both bacteria and archaea) serve as hosts

7. Parasite, cont. • Use host’s synthetic machinery to reproduce themselves • Usually destroy host cell in process • How quickly is extremely variable depending on replication cycle utilized • Host cell releases progeny viruses which then infect new hosts

8. Replication Cycles • Virus that infects bacteria called bacteriophage (phage for short) • Virus that reproduces only via LYTIC cycle is called a VIRULENT virus • Once phage has injected its nucleic acid into host, that nucleic acid takes over host cell’s machinery • Viral genome contains promoter sequence that attracts host RNA polymerase

9. Cycles, cont. • EARLY GENES code for proteins that shut down host transcription, stimulate viral genome replication, and stimulate LATE GENE transcription • Nuclease enzymes digest host’s chromosomes, providing nucleotides for synthesis of viral genomes • In late stage, viral late genes code for proteins of viral capsid and for those that lyse host cell to release new viriions

10. Lytic Cycle Visual

11. Cycles, III • LYSOGENIC virus called TEMPERATE virus • Lysogenic bacteria contain noninfective entity called a PROPHAGE • Prophage can remain inactive within host genome through many cell divisions • Cell becomes stressed or damaged, prophage released from inactive state and lytic cycle proceeds

12. Enveloped Cycle(s) • **Influenza virus’s glycoproteins (on capsid) bind to receptors on host cell’s plasma membrane • Virus enters cells by endocytosis • Viral and vesicle membranes fuse, capsid breaks down, and viral RNA is released • Viral RNA makes mRNA via viral RNA-dependent polymerase

13. Enveloped cycles, cont. • Viral mRNA is translated into viral proteins (capsid and envelope) • Virion is assembled • Envelope glycoproteins made on host ER and transported to cell membrane via Golgi apparatus • New viruses assemble by budding and are released from cell

14. Influenza Visual

15. Enveloped III • HIV is a retrovirus (reverse transcriptase) • Attaches to host cell at membrane protein CD4 • Viral envelope fuses with host’s plasma membrane, capdis breaks down, and viral RNA released into cell • Viral RNA uses reverse transcriptase to make complementary DNA (cDNA)

16. Enveloped IV • Viral RNA degrades • Second DNA strand is synthesized • cDNA enters nucleus and is integrated into host chromosome forming PROVIRUS • Upon activation, proviral DNA transcribed into viral RNA which is exported to cytoplasm • In cytoplasm, viral RNA translated into proteins using host ribosomes

17. Enveloped V • Viral proteins, new capsids, RNA, and envelopes are assembled • Assembled virus buds from plasma membrane • Spend some quality time on Overheads 13. 4 (influenza) and 13.5 (HIV) • Enough said

18. HIV Visual

19. Lytic vs Lysogenic • In animal cells, lytic and lysogenic cycles cause differing pathologies • lytic infections of plasma cells by the Epstein-Barr virus (EBV) occur in mononucleosis • latent infections of B cells by EBV predispose the person to lymphoma • lytic infections by human papilloma virus (HPV) cause genital warts • latent infections by some strains of HPV lead to cervical cancer

20. Vectors and more… • VECTOR is an agent like an insect that carries a pathogen affecting another species • Can also refer to plasmid or virus that carries an inserted piece of DNA into bacterium for cloning purposes in recombinant DNA technology • Viruses that infect plants must pass through cell wall as well as PM

21. Vectors, cont. • Insect vector penetrates cell wall with its proboscis allowing virions to move from insect to plant • HORIZONTAL transmission refers to spread from plant to plant • VERTICAL transmission refers to spread from parent to offspring • Can be either vegetative or sexual reproduction

22. The good and the bad… • Phages using lytic cycle destroy their hosts so might be useful in treating bacterial infections • D’Herelle used phages to control infection of chickens by Salmonella gallinarium • Phage protected group did not get the bacterial disease • Also used phage treatment successfully with plague-causing bacteria and with infectious cholera

23. Prions • “Proteinaceious infective particle” • Are simply abnormal proteins • Transmissible spongiform encephalopathies (TSEs) • Include scrapie, mad cow disease, and kuru

24. Prions • molecules of a normal body protein that have changed their three-dimensional configuration • PrPC • The normal protein • is called PrPc (for cellular) • is a glycoprotein normally found at the cell surface inserted in the plasma membrane • has its secondary structure dominated by alpha helices • is easily soluble • is easily digested by proteases • is encoded by a gene designated (in humans) PRNP located on our chromosome 20

25. Prions, cont. • PrPSC • The abnormal, disease-producing protein • is called PrPSC (for scrapie) • has the same amino acid sequence as the normal protein; that is, their primary structures are identical but • its secondary structure is dominated by beta conformation • is insoluble in all but the strongest solvents • is highly resistant to digestion by proteases • When PrPSC comes in contact with PrPC, it converts the PrPC into more of itself (even in the test tube). • These molecules bind to each other forming aggregates • It is not yet clear if these aggregates are themselves the cause of the cell damage or are simply a side effect of the underlying disease process