BIO 115
Human evolution
Human evolution
Kartei Details
| Karten | 288 |
|---|---|
| Sprache | English |
| Kategorie | Biologie |
| Stufe | Universität |
| Erstellt / Aktualisiert | 23.01.2021 / 24.01.2021 |
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Five stages of pathogens (pyramid)
- Stage 1: agent only in animals
- Stage 2: primary infection (anthrax, rabies, West Nile virus)
- Stage 3: limited outbreak (Ebola, Marburg, monkeypox viruses)
- Stage 4: long outbreak
- Stage 5: exclusive human agent (measles, mumps, malaria, smallpox, syphilis)
Steps to emerging infectious diseases
Step 1: Ecological factors that increase exposure -> jump rates e.g. land use, agricultural practices, livestock practices, trading, bush meat use, water supply, climate change
Step 2: Increased transmission bewtween humans
ecological factors: urbanization, living conditions, hygiene practices, travel and migration
evolutionary factors: genetic change in pathogen in the reservoirs, genetic change in pathogens during human infection
Reproduction number
R0 is the average number of secondary cases generated by a single primary case into a large population
When does a disease transition from stage 2 to 3 to 4?
If R0 is larger than 1.
Example: Eco-evolutionary changes have huge historical consequences
Conquest of the New World -> small pox from Europe to LATAM -> indigenous people are not immune and die from small pox
HIV
- two sources (HIV1 and HIV2) -> from chimpanzees and sooty mangabeys -> common ancestor
- HIV1 has three subtypes with two having R0 > 1
- HIV1 2 subtypes R0 > 1 -> large exposure to reservoirs, migration of virus, evolutionary change in the virus
Definition: Virulent
More virulent -> show strong symptoms; patients easier to isloate look SARS outbreak 2003
Three categories of emerging infectious diseases
- Diseases caused by newly evolved pathogen (SARS-COV2)
- Novel variants of existing pathogen (H1N1 influenza virus)
- Previously rare diseases are now on the increase (Lyme disease)
Definition: Co-evolution
Evolutionary changes that occur within two or more organsims as a response to interaction between them e.g.Humming bird plant interactions
Antagonistic co-evolution
Evolutionary change in one partner -> decreases fitness for the opponent -> counter adpations necessary (low evolutionary potential might lead to extinction)
Red-queen hypothesis
based on Alice in the Wonderland
running an evolutionary race -> selection pressure leads to constant adaption to be able to survive
Potential targets of selection - Example host and pathogen
Host: host resistance, pathogen avoidcance, clearance of the infection
Pathogen: pathogen infectivity, host seeking, evading host defenses
What are the two population dynamics co-evolution can lead to?
1. Selective sweeps -> evolutionar arms race, accumulated improvements in both populations
2. Dynamic polymorphism -> fluctuation in allele frequencies, stochastic fixation of allele possbile
What can be taken as evidence for antagonistic co-evolution?
Local adaption
Example: two patches with each one host and pathogen -> host and pathogen are adapted to each other -> if they switch places -> they are maladapted -> antagonistic co-evolution
Definition: Gene x Environment interaction (GxE)
Two different genotypes respond to environmental variation in different ways.
“A good allele in one time and place may be a bad allele in another time and place”
Definition: Evolvability
Ability of a biological system to produce phenotypic variation that is both heritable and adaptive
Definition: Antigenic drift
Small variation in antigenic properties from year to year e.g. seasonal flu
Definition: Antigenic shift
Radical change in antigens, change of serotype e.g. Spanish influenza 1918-1919
How can humans keep up with rapid evolution of pathogens?
They cannot.
Definiton: Adaptive immunity
Protection of a host organism from a pathogen and is characterized by immunological memory
Why is HbS (sickle cell allele) maintained in certain populations?
Co-occurence with malaria -> there is selective advantage for individuals with heterozygous HbA/HbS -> are fitter (have reduced malaria prevalence and disease intensity)
Do mutations arise frequently enough to explain the co-occurence of malaria with sickle cell (HbS)?
No. Mutation rate is way too low to explain the high prevalence of HbS.
How does the major histocompatibility complex (MHC) in humans work?
0. Cell has HLA markers
1. Virus invades a cell
2. Exposure of non-self structures on the cell surface
3. Attracts killer cells that kill the invaded cell
Definition: HLA
Human leukocyte antigens
Definition: Life history traits
A species' or population's strategies related to reproduction
How do pathogens affect evolution of human life-history traits?
High pathogen diversity -> increased infant mortality -> higher number of offspring -> infant survival depends on body conditions -> higher birth weight (evidence for adaption to pathogens)
How can large HLA diversity be explained?
As response to pathogen diversity and is maintained by balancing selection.
What are important pathogen traits?
- Finding a host
- Infectivity
- Growth within host
- Virulence factors
- Transmission
Definition: Virulence
Pathogen-mediated morbidity and mortality
Pathogen traits trade-offs
High transmission rate -> low host survival -> high virulence -> low pathogen growth e.g. Ebola
High pathogen growth -> high host survival -> low virulence -> low transmisision e.g. Heliobacter pylori
Evolution of virulence
1. accidental infections -> pathogen not adapted to host -> virulence depends on host (stochastic)
2. succesful invasion -> pathogen starts to transmiss between hosts -> virulence maladapted but transmission ensured -> leads to epidemic
3. evolution of optimal virulence
Vaccination (Immunization)
1. Injection of pathogen antigens or toxins
2. Immune system produces antibodies
3. Individual is immune against infections
Examples: Pathogen evolution to vaccination
1. Diphteria -> response to vaccination -> lose its phage-inserted DNA -> becomes a avirulent strain
2. Marek's disease (MDV) -> cancer-causing herpes in chickens -> virus develops -> chickens need several vaccines to keep up with the evolution of the viruses
For what diseases are vaccines very useful?
Childhood diseases e.g. Smallpox, polio, measles, pertussis, diphteria, mumps
-> acute infections
For what diseases are vaccines not as succesful?
Diseases such as the flu, malaria, pneumonia, HIV, tuberculosis
-> chronic infections and recurring infections with high antigen variation
What is the key factor in finding a vaccine against SARS-CoV-2?
Antigene evolvability/mutability -> if SARS-CoV-2 can change very fast and how often it can potentially escape vaccination
What evolutionary process is behind antibiotic resistance?
Selective sweeps
1. growing population -> random genetic mutation -> antibiotic treatment -> growth and spread of adapted survivors
Who invented the first antibiotic treatment?
Alexander Fleming (1929)
What are the five common mechanisms of antibiotic resistance?
1. Prevention of drug entry -> cell channels can close these entry points
2. Increase of drug reflux -> pumps drug out of the cell
3. Enzymatic inactivation -> enzymes that cleave the antibiotic
4. Bypassing -> the cellular process that is inhibited by the antibiotic is bypassed through an alternative pathway
5. Target alteration -> Modificiations of the antibiotic target inhibits the antibiotic to perform its action
What genetic changes leads to the 5 mechanisms of antibiotic resistance?
SNPs -> Prevention of drug entry and target alterations
Insertions/Deletions -> Increase of drug reflux and bypassing
Horizontal gene transfer -> Enzymatic inactivation
