4/28/2013. The Ever-Evolving Flu p The 1918 Flu p. 617

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1 The Ever-Evolving Flu p Influenza (Fig 18.10) rapidly evolves each year, and processes such as reassortment give rise to new genotypes. 2. Flu virus evolves rapidly to evade our immune system (Fig 18.12) 3. Viral reassortment leads to rapid evolution (Fig 18.13) The 1918 Flu p Wartime conditions facilitated the rapid spread of a deadly flu strain 2. Worldwide travel may alter the selective environment of pathogens, favoring high virulence 3. About 50 million people died from a massive flu pandemic in Evolutionary biology helps explain why it was so virulent and helps scientists prepare for new pandemics. Ewald s transmission rate hypothesis 1. Pathogens spread by social contact require the host to be socially active to spread (low virulence). 2. Malaria and cholera, don't fit this model because they can spread from inactive hosts (mosquitoes; water) 3. Ewald argues that the 1918 flu was likewise an exception, A. trenches in Western Europe and the open sick wards of hospitals allowed the virus to spread effectively from incapacitated hosts to many new ones. 4. Crowded conditions drive flu outbreaks (Fig 18.14) 3 1

2 Resurrecting a Monster p Understanding the path to virulence is the key to some epidemics, and it may be locked in their evolutionary history. 2. Tumpey et al. reverse engineered viral DNA from the preserved tissues of people who died in 1918 and The virus began with bird flu genes but then mutated to become infectious to humans. 4. The replicated 1918 strain replicated 50 x faster than contemporary strains 18.3 Molded by Parasites Pathogens evolve to adapt to their hosts, and their hosts, in turn, adapt to the pathogens. 2. Humans have evolved defenses against many diseases. A. The immune systems coevolves with pathogens B. Measures of strength of selection on immune-system genes consistently turn up near the top of the list 5 Malaria, Mutation, and Selection 1. Plasmodium that causes the most harm today evolved in Africa within the past 6,000 years as farmers began to clear forests. 2. Malaria-spreading mosquitoes breed in the standing water in their fields, and infected farmers as they slept in their villages 3. Humans have evolved a number of defenses to malaria in just the past few thousand years. Sickle-cell anemia is the byproduct of one of those defenses. 4. Without coevolutionary history, hosts may be defenseless (Fig ) 2

3 18.4 Evolution s Drug War p The invention of antibiotics has given rise to strong selection for resistant bacteria. 2. Silver Bullets 623 A. The rapid evolution of resistance to antibiotics raises concerns about whether new drugs will be effective for long 7 Evolution of antibiotic resistance within a single patient (Fig ) 1. In 2000 a patient developed an infection of Staphylococcus aureus 2. Doctors took a series of blood samples and identified the new mutations that arose in the bacteria over the course of the infection. 3. Mutations that conferred more resistance to antibiotics were favored by natural selection 1. Resistance increases with frequency of antibiotic use (Fig ) 2. The effectiveness of most antibiotics is short-lived (Fig ) 3. Antimicrobials are locked in antagonistic coevolutionary relationships with pathogens 4. Antibiotic resistance evolves rapidly because bacteria can acquire mutations through vertical and horizontal transfer (plasmids) 3

4 18.5 Human Variation and Medicine p The variation in human populations resulting from drift and natural selection may be crucial to treatment of diseases and genetic disorders. 2. Achromatopsia A. a recessive genetic disorder causing colorblindness, extreme sensitivity to light and reduced visual acuity B. In most populations affects less than 1 20,000 C. Affects 1 in 20 of the 3000 Pingalapese 10 Sampling Processes and the Founder Effect Ellis-van Creveld Syndrome (Fig ) 1. an autosomal recessive disorder characterized by polydactyly (six fingers), short stature, and shortening of the forearms and lower legs. 2. All 50 EvC cases can be traced back to a single couple who immigrated to Eastern Pennsylvania in 1744, thus demonstrating founder effect and a recessive pattern of inheritance. Old Age: Evolution s Side Effect p Medical researchers seeking to slow the effects of old age are investigating the evolution of senescence in humans and other species. 2. Aging can be explained by evolutionary trade-offs 3. The maximum speed for the 100 meter run starts dropping in the third decade of life (Fig ). 12 4

5 JBS Haldane recognized an important feature of natural selection 1. It acts weakly on mutations with effects in old age 2. it acts strongly on mutations with effects in childhood and the prime reproductive years. 13 Huntington s disease 1. It is unusually common for a devastating genetic disorder: about one in 18,000 people suffers from the disease. 2. If it resulted only from germ cell mutations, it should be much rarer 3. Its effects usually begin in the forties, past prime reproductive years, after passing on the disease-triggering alleles to the next generation before they died George Williams proposed that a mutation that benefits an organism while it s young will be favored by natural selection, even if it becomes harmful in old age. 15 5

6 1. Organisms face a trade-off between reproduction and repairing their cells. 2. If they put all their energy into repairing their cells, they will slow down the aging process, but they won t be able to produce as many offspring as other organisms. 3. Fast breeding individuals pass down more of their genes, and as a result the population cannot repair its cells very well. 4. They get old. 16 p53 tumor-suppressor protein. 1. p53 responds to stress inside cells, particularly to damaged DNA. 2. It can cause a cell to die or to stop dividing and prevent the cell from growing into a tumor. 3. Over time, p53 can kill or stunt so many cells that tissues can no longer renew themselves. 4. By forcing cells into early retirement, p53 may prevent them from becoming tumors, but the cells may damage surrounding tissue and release abnormal proteins that stimulate the growth of cancer cells. 5. p53 helps keep young people relatively cancer free. But it also damages the body 17 Aging is a pleiotropic byproduct of selection on other age classes 1. The damage accumulates slowly, over the course of many years. 2. By the time it has an impact on us, we re so old that natural selection cannot alter it 18 6

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