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Assigned readings

Assigned readings. Chapter 1 of Zimmer and Emlen text--The virus and the whale: how scientists study evolution. Biological evolution. Any change in the inherited traits (genetic structure) of a population that occurs from one generation to the next.

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Assigned readings

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  1. Assigned readings • Chapter 1 of Zimmer and Emlen text--The virus and the whale: how scientists study evolution.

  2. Biological evolution • Any change in the inherited traits (genetic structure) of a population that occurs from one generation to the next. • Note that evolution is a populationprocess that occurs from generation to generation. • The above definition is a definition of Microevolution.

  3. Biological evolution • The microevolutionary changes in genetic structure of a population over time can lead to substantial changes in the morphology of organisms over time and the origin of new species. • Such changes are referred to as Macroevolution.

  4. Why study evolution? • Evolution explains the diversity of life. All living things are related to each other and are the products of millions of years of evolution. • Understanding evolution allows us to understand why the living world is the way it is. We can understand e.g., the similarities and differences between species, as well as their adaptations and their distributions.

  5. Why study evolution? • There are also practical reasons to study evolution. • Evolution allows us to understand the evolution of disease organisms such as viruses and bacteria and combat them.

  6. Why study evolution? • Evolution also gives us insight into such “big” questions as: • “How did we get here?” and • “How did thought and language evolve?”

  7. Evolution case studies • Whales: mammals gone to sea • Viruses: the deadly escape artists

  8. How do we know whales are mammals? • Whales share synapomorphies(shared derived characters) with mammals • Mammary glands • Three middle ear bones • Single jaw bone (dentary) • Hair (in developing embryos) • Similarities with fish [streamlining, fins] arose through convergent evolution

  9. Whale evolution • Whales are aquatic mammals that evolved from terrestrial ancestors through the process of natural selection by which individuals that possessed traits that best fitted them to life in water left behind the most offspring.

  10. Fossil whales • The evolution of whales is well documented by fossil discoveries. • Modern whales have peg-like teeth or baleen for feeding. Early fossil whales such as Dorudon (40 mya) however had more complex teeth that were similar to those of contemporary terrestrial mammals.

  11. Dorudon

  12. Dorudon and modern whales share numerous features of the skull in common, including a distinctively thick-walled ectotympanic bone. • The same distinctive bone is found in Pakicetusa terrestrial wolf-like animal from 50 mya.

  13. Pakicetus • Pakicetus also possesses a distinctive ankle bone called the astragalus. In Pakicetus it has a double-pulley like morphology and this structure is found only in artiodactyls (hoofed mammals such as cows, pigs and deer).

  14. Fossils reveal links to land mammals • Shape of astragalus connects to artiodactyls

  15. These and other fossil discoveries have enabled biologists to construct a phylogentic tree (a tree of branching relationships) that depicts the evolutionary history of the group.

  16. Evolution case studies • Whales: mammals gone to sea • Viruses: the deadly escape artists

  17. Viruses • Your text has a nice discussion of the evolution of the flu virus. You need to read it and be familiar with it. • We will discuss a different example in class– the HIV virus to illustrate the process of natural selection.

  18. Natural History of HIV/AIDS • Acquired immune deficiency syndrome (AIDS) caused by Human Immunodeficiency Virus (HIV). • Disease first described in 1981. • Transmitted through transfer of bodily fluids. • Immune system attacked. Victim dies of secondary infections.

  19. Scale of problem • More than 60 million people so far infected. • Mortality so far about 20 million. • Projected mortality by 2020 --90 million lives • Responsible for about 5% of all deaths worldwide. • Approx. 8,000 deaths per day.

  20. The Human Immunodeficiency Virus • HIV, like all viruses, is an intracellular parasite • Parasitizes macrophages and T-cells of immune system • Uses cells enzymatic machinery to copy itself. Kills host cell in process.

  21. HIV binds to two protein receptors on cell’s surface : CD4 and a coreceptor, usually CCR5. • Host cell membrane and viral coat fuse and virus contents enter cell.

  22. What the virus inserts • RNA genome • Reverse transcriptase: transcribes viral RNA into DNA • Integrase: this enzyme splices DNA into host DNA • Protease: this enzyme involved in production of viral proteins

  23. Viral DNA inserted in host DNA produces HIV mRNA and all components of virus • Viral particles self assemble and bud from host cell.

  24. HIV budding from human immune cell

  25. HIV hard to treat • Because HIV hijacks the host’s own enzymatic machinery: ribosomes, transfer RNAs, polymerases, etc. it is hard to treat. • Drugs that targeted these would target every cell in the hosts body

  26. Progress of an HIV infection • Three stages • Acute • Chronic • AIDS

  27. Acute • Viral load increases rapidly • CD4 helper T cell level declines • Immune system mobilizes • Viral load declines, CD4 T cell level increases

  28. Chronic • HIV not eliminated • Viral load increases slowly • CD4 helper T cell levels slowly decline

  29. AIDS • CD4 helper T cell level drops so low immune system fails. • Patient vulnerable to all infections • Life expectancy of only 2-3 years

  30. How HIV causes AIDS • Human body responds to infection with HIV by mobilizing the immune system. • The immune system destroys virus particles floating in bloodstream and also destroys cells infected with virus. • Unfortunately, the cells that HIV infects are critical to immune system function.

  31. How HIV causes AIDS • HIV invades immune system cells especially helper T cells. • These helper T cells have a vital role in the immune system. • When a helper T cell is activated (by having an antigen [a piece of foreign protein] presented to it, it begins to divide into memory T cells and effector T cells.

  32. Memory T cells • Memory T cells do not engage in current fight against the virus. • Instead they are long-lived and can generate an immune response quickly if the same foreign protein is encountered again.

  33. Effector T cells • Effector T cells engage in attacking the virus. They produce signaling molecules called chemokines that stimulate B cells to produce antibodies to the virus. • Effector T cells also stimulate macrophages to ingest cells infected with the virus. • In addition effector T cells stimulate killer T cells to destroy infected cells displaying viral proteins.

  34. Why is HIV hard to treat?Viral disguise • First round of infection with HIV reduces the pool of CD4 Helper T cells (those that can recognize and attack HIV). • Loss of CD4 cells costly, but immune system now primed to recognize viral protein. • What’s the problem?

  35. Why is HIV hard to treat?Viral disguise • Virus mutates and the proteins on its outer surface (gp120 and gp41) change. • These surface proteins are not recognized by the immune systems memory cells. • Mutants survive immune system onslaught and begin new round of infection

  36. Why is HIV hard to treat?Viral disguise • Each round of infection reduces the numbers of helper T cells because they are infected by virus and destroyed. • Furthermore, because each lineage of T cells has a limited capacity for replication after a finite number of rounds of replication the body’s supply of helper T cells becomes exhausted and the immune system eventually is overwhelmed and collapses.

  37. Why is HIV hard to treat?Drug resistance. • AZT (azidothymidine) was the first HIV wonder drug • It works by interfering with HIV’s reverse transcriptase, which is the enzyme the virus uses to convert its RNA into DNA so it can be inserted in the host’s geneome.

  38. Why is HIV hard to treat?Drug resistance. • AZT is similar to thymidine (one of 4 bases of DNA nucleotides) but it has an azide group (N3) in place of hydroxyl group (OH). • An AZT molecule added to DNA strand prevents the strand from growing. The azide blocks the attachment of next nucleotide in the DNA chain.

  39. Why is HIV hard to treat?Drug resistance. • AZT successful in tests although with serious side effects. • But patients quickly stopped responding to treatment. • Evolution of AZT-resistant HIV in patients usually took only about 6 months.

  40. How does resistant virus differ? • The reverse transcriptase gene in resistant strains differs genetically from non-resistant strains. • Mutations are located in active site of reverse transcriptase. • These changes selectively block the binding of AZT to DNA but allow other nucleotides to be added.

  41. How did resistance develop? • HIV reverse transcriptase very error prone. • About half of all DNA transcripts produced contain an error (mutation). • HIV highest mutation rate known. • There is thus VARIATION in the HIV population in a patient.

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