Unit 4 Revision Notes.

These notes do not cover absolutely everything, but they do cover those major topics and the wording you seem to have the greatest difficulty with.

Check the Specification and the ‘Check Your Notes’ summary.

TOPIC 5

Topic 5 summary

Make sure your notes cover the following points. The points are listed in the approximate order they appear within the topic. All the points are covered in the textbook but where there is supporting information within the activities this is indicated.

There are suggestions on making notes and on revision in the Exam/coursework support.

You should be able to:

o Explain that the numbers and distribution of organisms in a habitat are controlled by biotic and abiotic factors. (Activity 5.1 and 5.2) (Checkpoint question 5.4)

o Explain how the concept of niche accounts for distribution and abundance of organisms in a habitat. (Activity 5.1 and 5.2) (Checkpoint question 5.1)

o Describe how to carry out a study on the ecology of a habitat to produce valid and reliable data (including the use of quadrats and transects to assess abundance and distribution of organisms and the measurement of abiotic factors, e.g. solar energy input, climate, topography, oxygen availability and edaphic factors). (Activity 5.2)

o Describe the concept of succession to a climax community. (Activity 5.3) (Checkpoint question 5.2)

o Describe the overall reaction of photosynthesis as requiring energy from light to split apart the strong bonds in water molecules, storing the hydrogen in a fuel (glucose) by combining it with carbon dioxide and releasing oxygen into the atmosphere. (Activity 5.4 and 5.5) (Checkpoint question 5.3)

o Describe how phosphorylation of ADP requires energy and how hydrolysis of ATP provides an immediate supply of energy for biological processes. (Activity 5.4 and 5.5)

o Describe the light-dependent reactions of photosynthesis including how light energy is trapped by exciting electrons in chlorophyll and the role of these electrons in generating ATP and reducing NADP in photophosphorylation and producing oxygen through photolysis of water. (Activity 5.4 and 5.5)

o Describe the light-independent reactions as reduction of carbon dioxide using the products of the light-dependent reactions (carbon fixation in the Calvin cycle, the role of GP, GALP, RuBP and RUBISCO) and describe the products as simple sugars that are used by plants, animals and other organisms in respiration and the synthesis of new biological molecules (including polysaccharides, amino acids, lipids and nucleic acids). (Activity 5.4, 5.5 and 5.6)

o Describe the structure of chloroplasts in relation to their role in photosynthesis. (Activity 5.4)

o Carry out calculations of net primary productivity and explain the relationship between gross primary productivity, net primary productivity and plant respiration. (Activity 5.8)

o Calculate the efficiency of energy transfers between trophic levels. (Activity 5.8)

o Analyse and interpret different types of evidence for global warming and its causes (including records of carbon dioxide levels, temperature records, pollen in peat bogs and dendrochronology) recognising correlations and causal relationships. (Activity 5.9, 5.10 and 5.11)

o Outline the causes of global warming – including the role of greenhouse gases (carbon dioxide and methane, CH4) in the greenhouse effect. (Activity 5.12 and 5.13)

o Discuss the way in which scientific conclusions about controversial issues, such as what actions should be taken to reduce global warming or the degree to which humans are affecting global warming, can sometimes depend on who is reaching the conclusions. (Activity 5.14 and 5.15)

o Describe how data can be extrapolated to make predictions, that these are used in models of future global warming, and that these models have limitations. (Activity 5.16)

o Describe the effects of global warming (rising temperature, changing rainfall patterns and changes in seasonal cycles) on plants and animals (distribution of species, development and life cycles). (Activity 5.17 and 5.21) (Checkpoint question 5.5)

o Explain the effect of increasing temperature on the rate of enzyme activity in plants, animals and micro-organisms. (Activity 5.18)

o Describe how to investigate the effects of temperature on the development of organisms (e.g. seedling growth rate, brine shrimp hatch rates). (Activity 5.19 and 5.20)

o Describe how evolution (a change in the allele frequency) can come about through gene mutation and natural selection. (Checkpoint question 5.6)

o Describe the role of the scientific community in validating new evidence (including molecular biology, e.g. DNA, proteomics) supporting the accepted scientific theory of evolution (scientific journals, the peer review process, scientific conferences). (Activity 5.22 and 5.23)

o Explain how reproductive isolation can lead to speciation. (Activity 5.24)

o Discuss how understanding the carbon cycle can lead to methods to reduce atmospheric levels of carbon dioxide (including the use of biofuels and reforestation). (Activity 5.25) (Checkpoint question 5.7)

Demonstrate knowledge and understanding of the How Science Works areas listed in the table on page 13 of the specification

Topic 5

Biotic and abiotic factors affect the distribution and abundance of species in a habitat

Learn the definitions:

Environment: the conditions in which an organism lives. Biotic factors: environmental factors due to other living organisms e.g. predationAbiotic factors: environmental factors due to the physical conditions e.g. soil pHHabitat: the particular place where a community of organisms livesPopulation: a group of individuals of the same species living and breeding together in the same place at the same timeCommunity: all the organisms of the different species living and interacting together in the same habitat.Ecosystem: a stable unit consisting of a community of organisms in the same place, which interact with each other and with the environment (biotic and abiotic factors) in which they live.

Niche: the particular combination of abiotic and biotic factors within a habitat that an organism is adapted to, e.g. where it lives, how it feeds, what else it does etc

The distribution and abundance of any species can be explained by the niche concept, and the way the organism is adapted to survive and exploit its niche. The distribution and abundance of any organism varies because of

the abiotic factors e.g. amount of light or temperature etc. and the biotic factors e.g. where its food is found, predators, parasites,

competition for food etc.

When these factors are favourable organisms survive, grow and reproduce successfully. When these conditions are unfavourable, organisms don’t survive, grow or reproduce as successfully.

Be prepared to answer questions on organisms and habitats you have not seen before; the question and any data should give you sufficient information to be able to interpret the factors, both biotic and abiotic, affecting the distribution (i.e. where the species lives in the habitat) or abundance (how many there are per unit area) of the organisms in question. Do not be afraid to think and come up with biologically sensible ideas!

The distribution and abundance of any species varies because of the abiotic factors e.g. amount of light or temperature, and the biotic factors e.g. preadators, parasites, competition for food. When these factors are favourable organisms survive, grow and reproduce successfully. When these conditions are unfavourable, organisms don’t survive, grow or reproduce as successfully.

Sampling methods to determine the distribution and abundance of organisms in a habitat.

In any habitat it is clearly impossible to count all the organisms so we need to take a representative sample i.e. a sample within which the numbers of the different organisms or species is representative of the whole area i.e. in the same proportions.

Sampling strategies

This produces a valid representative sample.This allows us to estimate the abundance (i.e. how many) of species in a particular area.

In a non-uniform environment where conditions change across a habitat (e.g. on the sea shore between the low and high water marks) random sampling is not always appropriate. In this case quadrats are placed systematically (i.e. in a sequence

This is used to determine the abundance of particular species and the pattern of distribution of particular species.

Investigation of the biotic and abiotic factors affect the distribution and abundance of species in a habitate.g. Investigation of the distribution and abundance of heathers on the heathlandLine transect top to bottom of slope/sample every 5 m/ 3 random samples chosen using dice – avoids bias – 0.25m2 quadrat, count number of each of 3 species of heather in the 100 small squares to estimate frequency/soil samples to determine % moisture/plot data on kite diagram.Erica cinerea only found in dry soil, Erica tetralix found only where soil is wet

Succession

Succession is the progressive change in the composition and diversity of the species in a community in one place over a period of time

Primary succession: Starts in new habitats with no soil and no previous community; extreme environmental conditions: Secondary succession: Starts on bare soil where there had previously been a community; extreme environmental conditions

Characteristics of all successions

The initial environment is hostile and extreme. First colonisers are called pioneer species

Pioneer plants are highly adapted to withstand hostile conditions The abiotic factors in this environment mainly determine what species are

present since few species can tolerate such conditions so in the initial stages the biodiversity will be low

The initial colonisers modify the environment to make it less extreme pioneer plants die à organic matter incorporated into developing soil/nitrate

content of soil increases existing plants provide increasing dead organic matter and nitrates so soil

develops, they provide shade and shelter, reduce wind speed to reduce transpiration etc so improve the environment so more plants now able to establish and grow so early colonisers are outcompeted by later colonisers (e.g. grasses shade out mosses, trees shade out grasses) so community changes so more plants can grow so biodiversity increases

As number of different species present increases so there will be more microhabitats for organisms to exploit/greater variety of food plants for associated organisms/greater variety of feeding niches so biodiversity of associated animal community will change too

In the latter stages biotic factors largely determine which organisms can survive, e.g. predation, grazing, competition etc

The stable end point community is characteristic and is called the climax community usually dominated by trees. It is in equilibrium with the environment so undergoes little it any further change

Photosynthesis

Light dependent stage

Chlorophyll in thylakoid membranes in chloroplasts absorbs light energy and releases

‘excited’ electrons excited electrons pass along a series of electron carriers in the membranes

of the thylakoids of the chloroplast As electrons pass down the electron carrier chain there is a series of

oxidation-reduction reactions which release energy The energy is released and is used to generate ATP (chemical energy) from

ADP + Pi ‘excited’ electrons then combine with the protons from the photolysis of

water together with NADP to produce reduced NADP Photolysis of water

electrons from water are used to replace the electrons lost from the chlorophyll

these are then excited when the chlorophyll absorbs light to be used to make more ATP as before

oxygen is the valuable waste product of photolysis

Light independent stage

Ribulose bisphosphate RuBP combines with CO2 to produce 2 molecules of GP (glycerate-3-phosphate)

GP is reduced to GALP usingo the H atoms from reduced NADPo the energy from the hydrolysis ATP

Some GALP is converted into glucose which is stored as starch, as well as being used in the synthesis of amino acids, lipids etc.

More GALP is also used to regenerate RuBP in the Calvin cycle so more CO2 can be taken in to produce more sugar etc; this also uses ATP to transfer a phosphate group.

NB: The short-term source of chemical energy (ATP) has been converted into a long term store of chemical potential energy (starch).

Use of the products of the light dependent stage.

Reduced NADP is used • to reduce GP to GALP (provides the H atoms)

ATP is used• to provide energy to reduce GP to GALP (energy released by hydrolysis)• to provide a phosphate group to make RuBP (phosphorylation)

Energy transfer in ecosystems

Primary producers

Primary consumers (herbivores)

Primary producers are autotrophic i.e. synthesise their own complex organic compounds

Consumers are heterotrophic ie. obtain their organic compounds ‘ready made’ from the environment as ‘food’

Secondary consumers (carnivores)

Trophic levels

A trophic level is a feeding level in a food chain

Efficiency of energy transfer

Energy transfer: sunlight à producers

Not all the visible light energy coming in from the sun ever reaches a plant Some is reflected by clouds and dust Some will miss the leaves altogether Some is not of the right wavelength to be absorbed by the photosynthetic

pigments which absorb blue and red but not green Some of this is then lost as heat by the reactions of p/s

What is left is fixed in the organic molecules which are the products of p/s; this

the gross primary productivity

Gross primary productivity = the amount of energy fixed in the sugars etc. produced by the chloroplasts by p/s

Much of the sugars produced are immediately broken down in respiration to provide the energy for the metabolic reactions of the cells. The remaining sugars are converted into starch, cellulose, etc in the cells of the plant becoming new biomass.

The energy incorporated into biomass = net primary productivity NPPi.e. NPP = GPP – respirationThe energy in the biomass is what is available to the primary consumers.

Energy transfer: producers à 1o consumers

Not all the biomass gets eaten! Not all the biomass is digestible and capable of being assimilated, Metabolism of some of the organic material leads to the formation of

excretory products e.g. urea which are lost Much of the organic material absorbed and assimilated are respiratory

substrates so used in respiration to provide energy for metabolism, e.g. movement, growth etc

much of the energy is lost as heatThis leads to a loss of a lot of energy. What is left over is incorporated into the biomass and so is available to the secondary consumers

In general less than 10% of the energy in the food taken in ends up in the biomass

As a consequence of the use of energy and losses of energy at each trophic level, less energy is transferred to each successive level so the amount of energy in each successive level decreases.

This ultimately limits the number of trophic levels. So much energy is lost between levels that final level contains so little energy that, if only 10% of this is transferred there simply isn’t enough to support any further biomass.

The amount of energy available decreases in successive trophic levels so the amount of biomass which can be supported also decreases and this is ultimately reflected in a general reduction in numbers in successive trophic levels. (this is shown in pyramids of energy, biomass and numbers)

Natural selection.

Learn the wording – it can be applied to any example.

In a population of organisms random mutations produce new alleles (versions of genes) so are the cause of new variation (which adds new alleles to gene pool of population) so individuals in populations have different genotypes and show genetic variation

If there is a change in the environment some genotypes may make organisms more likely to survive long enough to reproduce to pass their particular alleles on to their offspring i.e. they are better adapted to their environment.

Others less well adapted will die from predation, competition for food, disease etc.

Those that reproduce will have offspring, some of which will inherit the favourable alleles in their genotypes and so themselves are more likely to survive to breed to pass their alleles on

Over time the proportion of individuals with favourable genotypes will increase in the population.

Formation of new species (speciation)

A group of individuals from a population somehow get separated and reproductively isolated from the rest of the population so they cannot breed with them.

Each population accumulates different random mutations so the different genes pools may contain different alleles.

The variation in a small isolated population may be reduced because some alleles may be lost by genetic drift and genetic diversity may be reduced by inbreeding, so that the isolated and the original population may now show significant differences.

Each population may be subject to different selection pressures in their habitats so only those individuals with genotypes that enable them to survive to breed will pass their alleles on to the next generation; this changes the frequencies of particular alleles* in the gene pools.

Over time this results in individuals in each population becoming specifically adapted to their new environments and genetically different from each other over many generations.

If individuals in each population have changed so much that they can no longer interbreed successfully – e.g. changes in breeding behaviour, timing of breeding etc. - by definition they have become separate species.

Modern evidence for evolution

All organisms contain DNA which is ‘read’ in the same way, providing evidence of evolution from a common ancestor.DNA and proteins contain a record of genetic changes resulting from random mutations over time, indicating gradual change within and between species. Studying DNA and proteins allows these changes to be identified.

Genomics (the study of DNA); look at the sequence of bases in genes; the more distantly related two species are the more differences there will be due to the accumulation of mutations over time.

Analysed by DNA hybridisation, DNA profiling, DNA molecular clocks

Proteomics (the study of proteins). mutations in DNA change the base sequence in a gene which changes the sequence of amino acids that are incorporated into the protein product. The more different amino acids there are in a particular protein, the more distantly related two species are (the fact that they have the same protein is evidence in itself for evolution from common ancestors!)

In order for new evidence to be accepted as support (or rejection) for the theory of evolution (or any other theory for that matter) it needs to be regarded as VALID.

The process of validation of evidence involves:

Peer review. Before a scientific paper is published is would be sent to a few eminent experts in the field for a peer review; they would examine the paper critically to check the validity of the method,(e.g. use of the right controls) the proper use of statistics to analyse the data and the validity of the conclusions, especially in the light of what other scientists have found and published.

Publishing the research and its conclusions. The scientific paper is then published in a reputable scientific journal so the rest of the scientific community are made aware of the findings. Many of these are now on-line so that important information is so much more accessible and available faster to a wider audience.

o One of the big problems with use of the Internet is that the peer review process can be circumvented and poorly conducted research or invalid conclusions could get into the public domain.

Presentation of papers at scientific conferences Many new findings are also brought to the attention of other scientists in the field by the presentation of papers at scientific conferences. Here perceptive questions ensures the author can justify his findings and also spark new interpretations, new ideas and new lines of research.

Climate Change/Global warming

The evidence

1: Temperature records show temperature has risen by over 1˚C

How reliable is the data? Records only go back to mid C16 Early records not reliable Inaccurate equipment (only mercury thermometers) Records only collected in a few places Modern records more reliable: accurate equipment;

data-logging/computers allows vast numbers of readings to be collected and processed

Records taken from many parts of the world

So now lots of reliable data

2: Evidence from pollen analysis from peat bog cores

Provides information back possibly as far as the last Ice Age (circa 12 000 years ago).Peat formed when plant material dies but does not decomposeThe peat accumulates in successive layers; lowest layers are the oldest: pollen trapped in peat layersUse of carbon dating techniques can establish the age of the layers

Use of pollen records from peat

Each types of plant produces a characteristic and recognisable type of pollen.

The more pollen there is of a particular species in particular layers of a peat core the more common it was at the time the peat was laid down

Using knowledge of the present day distribution of species and climate we know that particular species of plants survive in particular climatic conditions.

From this we can infer what the climatic conditions were likely to be when the pollen was deposited.

3: Evidence from tree ring analysis

Trees produce a ring of new xylem each year = growth ring. Xylem vessels produced in spring are wider than those produced in the summer and the difference in vessel size from summer to the next spring is what demarcates the ring.

Outer ring is current year; each ring can be dated by counting inwards Width of ring reflects amount of xylem produced which reflects amount of

growth Wide ring = lots of growth so by inference climatic conditions favoured

growth e.g. warm/wet So, age of rings and widths provide clues about past climatic conditions

So, what does all this combined evidence show?

The Earth appears to have been warmer since 1980 than at any time in the last 18 centuries.The Earth has warmed by 0.5oC over the last century and at least 0.2oC in the last 20 years or so - the greatest amount by which it has warmed or cooled over the space of a century in the past.

Causes of global warming?

Temperature and other data shows mean global temperature is rising. Fact.What is causing it? Several possible explanations (i.e. theories)

Greenhouse effect

light energy from the Sun reaches the Earth’s surface and is absorbed so the Earth warms up

some of this energy is radiated back into space as longer wavelength infrared radiation.

the atmosphere contains gases, including carbon dioxide, water vapour and methane, which absorb some of this infrared radiation so stopping it leaving. These are called greenhouse gases.

this causes the atmosphere to warm up which in turn warms up the Earth’s surface.

Greenhouse gases absorb infra red radiation: the main greenhouse gases are:

water vapour carbon dioxide methane

Enhanced greenhouse effect; increased levels of greenhouse gases, especially CO2 and methane, result in more heat trapped in the atmosphere leading to global warming

The consensus view. The evidence shows a positive correlation between CO2 levels and

temperature. But is does not prove the cause i.e. it does not prove that the high CO2

levels cause the observed rise in global temperature But there is now a great deal of other evidence supporting the theory

that global warming is caused by rising CO2 levels Theory and fact; cause and effect.

The enhanced greenhouse effect, due to raised CO2 levels, is a theory to possibly explain the fact that global warming is occurringi.e. the enhanced greenhouse effect is a possible cause and global warming is the effect

Sources of carbon dioxide.

Review the carbon cycle.

Sources of carbon dioxide; processes which add CO2 to the air Respiration Decomposition Volcanic activity Combustion

Processes which remove CO2 from the air Photosynthesis

o carbon atoms become incorporated into organic substances o some used as respiratory substrates and so lost againo others used in growth and incorporated into biomass e.g. wood o wood in trees acts as a ‘carbon sink’ because carbon atoms that

were in CO2 accumulate in the biomass (so effectively lock out of the cycle)

Fossil fuelso fossil fuels e.g. coal reserves are carbon sinkso carbon locked away in undecomposed organic remains that have

become fossil fuels was once CO2 in the atmosphere that was taken up by photosynthesis but not released by respiration, so this carbon has been ‘taken out of the cycle’

Causes of the increase in CO2 in the atmosphere

Under normal circumstances the CO2 level will remain constant because the processes which add CO2 are balanced by the processes that remove CO2 from the atmosphere, i.e. in equilibriumBut the CO2 level will increase if the processes of the carbon cycle become unbalanced.

Extra CO2 comes from human activities:

Combustion o burning fossil fuels e.g. coal. oil, petrol, natural gas o burning of trees and tree debris (from felling operations) releases CO2:

trees contain a lot of biomass and are important ‘carbon sinks’ (i.e. CO2 used by p/s as the tree grows and the carbon atoms are removed from the carbon cycle and ‘locked away’ in the cellulose and lignin of the wood biomass so a lot of extra carbon will be released by burning)

Deforestation:o Loss of trees will result in loss of CO2 uptake by photosynthesis in the

short term so CO2 level will riseo Increase in decomposition of dead organic matter in soil

loss of forest cover exposes soil to the sun so it warms up so the rate of activity of the decomposers will increase so releasing more CO2.

Other possible causes of global warming

Increase in levels of methane fromo anaerobic decay in paddy fields and of domestic refuse in landfill siteso flatus from herds of beef and dairy cattleo melting Siberian permafrost

Increase in water vapour warming increases evaporation so more water vapour in the atmosphere –

which is a greenhouse gas so absorbs more heat

Predicting the changes

1. Extrapolation of existing data into the future ‘looks forward’ based on previous data;Extrapolation is involved extending the line of best fit through existing data into the future. Assumes: there is enough data to establish the trend accurately/present trends continue, e.g. in fossil fuel use, no changes in control of emissions

2. Use of computer models to predict possible future changes ‘looks forward’ and makes predictions based on current knowledgeModels are tested by using previous data and seeing if they match the current reality – allows for ‘tweaking’ but never will be perfect, but they make the best predictions of trends based on all the data available.

Predictions may be incorrect because of: (don’t learn all of these – be selective!) Limited data –accurate records do not go back far enough to produce a

reliable trend line - but bigger datasets are becoming increasingly available e.g. accurate CO2 data only from 1950s, early temperature measurements inaccurate using mercury or alcohol thermometers

Models assume existing trends will continue (by extrapolation of a trend line which has lots of fluctuations in it – these are limitations in themselves!)

Limited knowledge of how the global climatic system works so models are only approximations – but knowledge is increasing all the time; e.g. impact of changing ocean currents on weather systems

Not all factors included; e.g. effects of increasing cloud cover, decreasing snow cover; unforeseen factors (e.g. major volcanic events,

changes in solar radiation levels) could upset models too. Future changes in future changes is usage of fossil fuels or emission controls Limitations of computing resources – but computer technology is improving

all the time

Climate change; what to do about it.

If we accept the CO2 levels are rising and are probably linked to rising global temperatures, what can be done about it? How could we restore the CO2 balance?

1: Reduce CO2 release (cut the emissions of greenhouse gases) by reducing use of fossil fuels

2: Move towards alternative sources of energy e.g. nuclear power, wind, wave power

3: Use of biofuels (= biomass)o biofuels are any source of energy produced, directly in plants or

indirectly in animals, by recent photosynthesis]o they can be any kind of fuel made from living things e.g. wood (e.g.

willow biomass), or from the waste they produce e.g. straw, chicken waste,

o or ethanol (from fermentation of plant biomass ) or methane, (from fermentation of animal waste, sewage waste), or biofuel oils from plants

o biofuels such as wood are o ‘carbon neutral’ i.e. they fix CO2 from the atmosphere by p/s to

grow, so burning simply releases this CO2 back into the atmosphere again to be re-used in photosynthesis by more growing crops.

o since burning a biofuel replaces the CO2 used in its growth there is no net increase in CO2 levels in the atmosphere.

o In theory at least, using biofuels means less fossil fuels are burned so reducing CO2 emissions.

Unlike fossil fuels, biofuels are renewable and sustainable o i.e. can regrow to replace what has been harvested so more is

producedo unlike fossil fuels which are not renewable (i.e. once burned, they

have gone)

4: Increasing CO2 uptake by photosynthesis by new forests

Reafforestation:

o Replaces treeso Young forests grow rapidly – take up CO2 by p/s rapidly (especially

if climate is warmer!) and turn it into biomass (growing new wood) faster than respiration occurs, so net CO2 absorption occurs

o As trees get bigger carbon taken up and ‘locked away’ in biomass of wood of tree so forests act as a carbon sink to keep carbon out of the atmosphere (so there is less CO2 contributing to global warming)

o May slow down further increase in atmospheric CO2 so long as reafforestation is a continuous process on a large scale worldwide > deforestation

Limitations to reforestation:o Mature forest has trees which are not growing so becomes carbon

neutral [CO2 uptake by p/s = CO2 release by respiration] so benefit only lasts whilst forest grows

o Only a limited amount of land which can be used to grow forests (land needed to live on, grow food on etc, plus trees don’t grow above the tree line)

Effects of global warming

Changing rainfall patterns some areas will get increased rainfall, including torrential rainstorms à

flooding other areas will get less rain

Changes is seasonal cycles warmer winters/warmer earlier spring dry seasons may last longer warmer autumns/shorter winters

Rising sea levels Increased temperatures can lead to higher sea-levels (+ 30 cm) through

several o mechanisms melting of ice pack and glacierso thermal expansion of sea water.

Why is global warming potentially a problem to living organisms?

A typical question:. Why might relatively small increases in temperature have a large effect on the survival of particular animals and plants in particular places?

Enzyme activity is temperature-sensitive; increases in temperature increase rate of reactions

Rate of photosynthesis could increase so more energy fixed so increasing growth; this may give competitors an advantage so one species may increase and another decrease

This may mean more food for some species of primary consumer and less for others, with the consequent changes in prey abundance/choice for predators so altering the dynamics of food webs

Means rate of photosynthesis may be sufficient to support growth further north because it is now warmer. But temperature may be too high in the southern limits so enzyme rates increase differently and metabolic sequences become chaotic; increased temperature may increase respiration >p/s so less growth possible; high temps reduce amount of water so p/s decreases, so a plants distribution may shift northwards, and increased p/s there may mean these plants now grow better and outcompete other species

May alter the synchronisation between life cycles in the environment e.g. flowers may be produced before their insect pollinators have hatched, so flowers don’t get pollinated which will reduced their numbers, and the insects don’t get their food so their numbers decrease too

Or food plants have grown earlier and so died off before caterpillars appear from eggs laid by butterflies so numbers of butterflies could decrease, and birds that depend on caterpillars have less food with which to raise their young…or insect life cycles speed up so that larvae or adults are produced before the food plants

Seeds may not germinate if don’t get the cold stimulus from a cold winter; over-wintering stages of insect pests won’t get killed leading to pest epidemics in the following year

But natural selection will operate too so that, in any population with some individuals with the combinations of genes to enable them to survive long enough to breed will do so, so more of the offspring inherit the genes so the population becomes adapted to the changing conditions e.g. insects hatch earlier too so they remain in synchronisation with their food plants

Global warming and decomposition

As temperatures of soils increase enzyme activity of decomposers increases so more decomposition of dead organic matter in soil occurs. products of decomposition are used by the decomposers for respiration which itself increases as a result of the warmer temperatures so more CO2 (and methane) is released

TOPIC 6Topic 6 summary

Make sure your notes cover the following points. The points are listed in the approximate order they appear within the topic. All the points are covered in the textbook but where there is supporting information within the activities this is indicated.

There are suggestions on making notes and on revision in the Exam/coursework support.

You should be able to:

1) Describe how DNA can be amplified using the polymerase chain reaction (PCR). (Activity 6.4)

2) Describe how gel electrophoresis can be used to separate DNA fragments of different length. (Activities 6.1 and 6.2)

3) Describe how DNA profiling is used for identification and determining genetic relationships between organisms (plants and animals). (Activities 6.3 and 6.5) (Checkpoint question 6.1)

4) Describe how to determine the time of death of a mammal by examining the extent of decomposition, stage of succession, forensic entomology, body temperature and degree of muscle contraction. (Activity 6.5) (Checkpoint question 6.2)

5) Describe the role of microorganisms in the decomposition of organic matter and the recycling of carbon. (Checkpoint question 6.2)

6) Distinguish between the structure of bacteria and viruses. (Activity 6.6) (Checkpoint question 6.3)

7) Describe the non-specific responses of the body to infection, including inflammation, lysozyme action, interferon, and phagocytosis. (Activity 6.7) (Checkpoint question 6.4)

8) Explain the roles of antigens and antibodies in the body’s immune response including the involvement of plasma cells, macrophages and antigen-presenting cells. (Activity 6.8) (Checkpoint question 6.5)

9) Distinguish between the roles of B cells (including B memory and B effector cells) and T cells (T helper, T killer and T memory cells) in the body’s immune response. (Activity 6.8) (Checkpoint question 6.5)

10) Explain how bacterial and viral infectious diseases have a sequence of symptoms that may result in death, including the diseases caused by Mycobacterium tuberculosis (TB) and Human Immunodeficiency Virus (HIV). (Activities 6.9, 6.11 and 6.17) (Checkpoint question 6.6)

11) Explain the process of protein synthesis (transcription, translation, messenger RNA, transfer RNA, ribosomes and the role of start and stop codons) and explain the roles of the template (antisense) DNA strand in transcription, codons on messenger RNA, anticodons on transfer RNA. (Activities 6.12 and 6.13)

12) Explain the nature of the genetic code (triplet code, non-overlapping and degenerate). (Activity 6.12)

13) Explain how one gene can give rise to more than one protein through post-transcriptional changes to messenger RNA. (Activity 6.13)

14) Describe the major routes pathogens may take when entering the body and explain the role of barriers in protecting the body from infection, including the roles of skin, stomach acid, gut and skin flora. (Activity 6.14)

15) Explain how individuals may develop immunity (natural, artificial, active, passive). (Checkpoint question 6.7)

16) Describe how to investigate the effect of different antibiotics on bacteria. (Activity 6.15)

17) Distinguish between bacteriostatic and bactericidal antibiotics. (Activity 6.16)

18) Discuss how the theory of an ‘evolutionary race’ between pathogens and their hosts is supported by the evasion mechanisms as shown by Human Immunodeficiency Virus (HIV) and Mycobacterium tuberculosis (TB). (Activity 6.17)

19) Describe how an understanding of the contributory causes of hospital acquired infections have led to codes of practice relating to antibiotic prescription and hospital practice relating to infection prevention and control. (Activity 6.17)

Demonstrate knowledge and understanding of the How Science Works areas listed in the table on page 13 of the specification.

Table of ContentsPolymerase chain reaction..................................................................................18Producing a DNA profile......................................................................................18Determination of the time of death....................................................................19Causes of decomposition....................................................................................20Forensic entomology...........................................................................................20

Non-specific responses to infection...................................................................22TB........................................................................................................................24

Antibiotics........................................................................................................... 25HIV................................................................................................................... 27

Nature of genetic code........................................................................................27HIV Infection and AIDS.................................................................................................................29

Topic 6

How to identify a dead body

Identification by Physical resemblance Physical appearance checked against photographic i.d. e.g. driving

licence, Identification by colleagues, friends, relatives, house-to-house inquiries

etc., Use of specific identifying features e.g. birth marks, scars

Identification by Dental Records Teeth, fillings, crowns etc only decay slowly and are more resistant to

fire. Each person’s dental records are fairly unique so they can be as reliable

as fingerprints

Identification by DNA profilingWorks on the premise that everyone’s DNA is unique

Polymerase chain reactionUse of the polymerase chain reaction [PCR] can increase the amount of DNA accurately and quickly to produced sufficient amounts to subsequently use to produce an accurate DNA profile. DNA mixture heated to 95oC; H bonds break so DNA strands separate Mixture cooled to 55oC; primers bind to the complimentary bases on the

DNA strands Mixture warmed to 75oC; DNA polymerase attaches to primers,

nucleotides attach to DNA bases (base complimentarity rules apply )and are joined by the enzyme so two new sample DNA strands are made.

The amount of DNA doubles for each cycle

Producing a DNA profile DNA sample from cells (collect cheek cells, extract DNA); amount can be

increased by polymerase chain reaction DNA cut into fragments by restriction enzymes Fragments separated by gel electrophoresis; small fragments travel

furthest Fragments removed from gel by Southern blotting Gene probe (complimentary base sequence) for short tandem repeats

used (STRs are particular bits of the non-coding DNA with regular repeats of particular nucleotide sequences unique to an individual but inherited from both parents)

Binds to DNA of STRs by base complimentarity Gene probe located by e.g. by UV light. Produces a DNA profile; a pattern of bands similar in appearance to a bar

code. o Use of at least 10 different STRs increases the chances of making a

positive identification.o The chance of two unrelated people’s DNA profiles being identical,

is about one in ten trillion.

DNA profile from body could be matched to: Existing police records

DNA database DNA profiles produced from samples of hair/cells/blood taken from the

homes of known missing persons

Determination of the time of death

Use of body temperatureBody temp = deep core temp, measured deep inside the body (often using a long thermoprobe pushed into the liver

Mean body temperature = 36.8oC Due the heat released by metabolic reactions e.g. respiration. On death these metabolic reactions stop so no heat is produced So cooling will occur

Estimate of time of death influenced by factors affecting rate of cooling e.g. Environmental temperature Body size (SA/vol relationship) Body position e.g. surface area exposed to cooling Clothing

Degree of muscle contractionOn death

Muscles initially relaxed Once oxygen supply depleted respiration ceases so ATP production stops. Lack of ATP results in cross-links between muscle contractile proteins

becoming fixed Muscles become stiff = rigor mortis so limbs remain fixed in position Most bodies have complete rigor mortis 6 – 9 hrs after death

Extent of decomposition

Causes of decompositionAutodigestion or autolysis due to action of hydrolytic enzymes (= self-digestion!) begins about 4 mins after death!

In gut from lysosomes in cellsCauses breakdown of body tissues

Action of bacteria From gut especially, later those from outside which invade through

natural openings or wounds, Initially aerobic bacteria but these use up oxygen so replaced by

anaerobic bacteria which cause putrefaction

Extent of decomposition depends on time and temperature

Forensic entomologThis is especially useful when the body has been dead for more than a few days, because the features that are normally used to determine the time of death, like temperature or rigor mortis, are no longer helpful

Many types of fly will lay their eggs in a dead body because it is a source of food for the larvae (maggots). Eggs can be laid on the skin, in body openings, e.g. nose, ears, mouth or in wounds

How maggots are useful Identification of the stage of development at the ambient temperature

can give an estimate of age and hence time since the eggs were laid and hence the time of death

The time taken for eggs to hatch can also give an indication of when the eggs were laid and hence the time of death.

The age of the maggot, and hence when the eggs were laid can be determined by measuring the fully extended length of the maggot and the ambient temperature

Assumptions made to make this method useful: Temp has been fairly constant Flies found the body to lay eggs soon after death

Insect succession used to date a body:

As the body decomposers it undergoes changes which may make it more attractive to other species.

The flies etc which feed on the body also bring about changes in it that also make attractive to other species.

Decomposition follows a predictable sequence, so do the insect species found over time.

Cause of death: structure of bacteria and viruses

Structure of a bacterium

Comparison of bacteria and viruses

Bacteria Viruses• Prokaryotic cells• Cell wall, cell membrane,

cytoplasm, no organelles, DNA not in a membrane-bound nucleus. May have mucilage capsule

• Typically 10 mm in size(x 25 times bigger)

• Genetic material is DNA• Reproduce by binary fission

(asexual)

• No cellular structure• Protein coat surrounding nucleic

acid molecule. May have outer envelope derived form host cell

• Typically up to 400 nm in size, so very much smaller

• Genetic material is DNA or RNA• Reproduce by inserting nucleic

acid into host cell which ‘reads’ the genes to synthesise new virus particles which are released

Defence against disease.

Non-specific responses to infection

Lysozyme• Enzyme found in tears, nasal secretions, saliva• first line of defence against bacteria entering body through eyes, nose or

mouth• breaks down bacterial cell wall

Inflammation• Damage/infection causes damaged mast cells (cells found in connective

tissue) to release hisamine • causes vasodilation of the arterioles nearby so more blood flows to area

of infection • also increases permeability of capillaries so more tissue fluid forced out -

> localised swelling• Phagocytes can squeeze out of capillaries into the tissues to destroy the

bacteria to limit infection.

Phagocytosis• Non-specific first line of defence mechanism if any pathogens have got

into the blood or tissues• phagocytes recognise antigens on surface of pathogen as foreign; engulf

pathogens (phagocytosis – a form of endocytosis); killed by hydrogen peroxide produced and digested by enzymes from lysosomes

Interferon• Cells infected with virus secrete a protein called interferon (a type of

cytokine)• attaches to membranes of surrounding cells.• this triggers the cells to make their own antiviral proteins which inhibit

synthesis of viral proteins so no new viruses can be produced, so limiting infection.

• Also stimulates virus-infected cells to ‘self-destructSignificance• Interferon system reacts very quickly to viral infection• This limits the infection until the slower acting specific immune response

kicks in to take over.

Specific Immune reponse .

Involves B and T lymphocytes in the blood and lymphatic system responding to a specific pathogen once it has got passed the non-specific lines of defenceBoth type of cell respond to specific antigens associated with the pathogen (or foreign tissue) and this specificity is what makes them part of the specific immune response.

Antigens are molecules which trigger an immune response e.g. production of antibodies They are usually proteins e.g. membrane proteins, toxins

The significant thing is that they are large molecules with a specific molecular shape.

The B and T cells have membrane receptor proteins with antigen-binding sites with a specific shape complimentary to the shape of its specific antigen.

Specific immune response; production of antibodies by B cells.

Primary Immune response:

• Infection by bacterium with specific antigens on surface• Phagocytosis by macrophage• Antigen from bacterium inserted in membrane on MHC proteins (these

become antigen presenting cells) • T helper cells (which have complimentary receptors [called CD4]) bind to

the antigen then divide to become a clone of active T helper cells + memory cells

• At the same time B cells with complimentary receptor engulf bacterium • Antigen inserted in membrane• T helper cells bind to B cells displaying the same antigen and release

cytokines • Cytokines stimulate activated B effector cells to divide to produce clone

of plasma cells + memory cells • Plasma cells produce antibodies which destroys bacterium (after approx

10-17 days)• Memory cells produce antibody quickly on subsequent infection

Antibodies do a variety of jobs, including clumping bacterial cells together so they can be taken in by phagocytes.

Specific immune response; production of T cells.

• Infected cell has pathogen’s antigens on surface• T killer cells with complimentary receptors binds to these antigens• T cells becomes active T killer cells• Cytokines from T helper cells stimulate these cells to divide to produce a

clone of active T killer cells which increases the number of cells to fight the infection

• These T killer cells bind to the antigens on the surface of the infected cell and release chemicals which either cause the infected cell to ‘self-destruct’ or swell and burst

B and T memory cells Ensure immune system can deal with any reinfection by the same pathogen

Secondary immune response

• Memory cells from the first infection (primary immune response) enable a much faster response to occur to a subsequent infection by the same pathogen with the same antigens.

• Exposure to the antigen results in the B memory cells differentiating into plasma cells;

• Response occurs in 2-7 days (since all the initial activation steps don’t need to happen)

• more cells are produced much faster than in 1o response because the initial antibody presentation/B cell multiplication phases to produce the memory cells in the first place has already happened (so the sequence is further along)

Characteristics of the 2o immune response

• Antibody is produced sooner and faster• More antibody is produced (more cells) over a longer time period• Effect lasts longer•

Often the pathogen is destroyed before if has had a chance to proliferate enough to cause symptoms of infection.

This is immunity.

Active immunity• the body produces antibodies in response to an antigen following infection• artificially acquired by injection of vaccines containing dead or weakened

forms of a pathogen

Passive immunity• Ready-made antibodies pass from mother across placenta and in milk• Artificially acquired by injection of serum containing antibodies e.g. anti-

venom.

Herd immunity• Achieved when enough people in a community are immunized against

certain diseases so it is more difficult for that disease to get passed between those who aren't immunized.

TB

Tuberculosis is caused by the bacterium Mycobacterium tuberculosis. Course of the disease.

Some M. tuberculosis bacteria may survive inside macrophages. The bacteria have very thick waxy cell walls, making destruction inside the macrophages very

difficult. The bacteria can lie dormant for years.

After 3–8 weeks, the infection is controlled and the infected region of the lung heals.

Anaerobic tissue masses known as a granuloma or tubercules form in response to infection. They contain dead bacteria and

macrophages at their centre.

An inflammatory response by the host’s immune system occurs. Macrophages engulf the bacteria.

The first phase (primary infection) can last for several months; it may have no symptoms.

Infection may occur when M. tuberculosis bacteria are inhaled and lodge in the lungs. Here they start to multiply.

Tuberculosis (TB) is a contagious disease caused by the bacterium Mycobacterium tuberculosis. Respiratory or

pulmonary TB is the most common form.

Active TB

the number of bacteria increases producing more tubercules and severely damaging the lung tissue leading to break down of alveoli, producing large cavities

these severely reduce oxygen uptake which can ultimately lead to death

TB is a successful pathogen because:

It is spread by droplet infection, which is the most effective method of infection

It specifically targets epithelial cells in lungs, which means that, when inhaled, it is exactly where it wants to be

It does not kill immediately. This means that it has a large window of opportunity to spread to others

It has a very thick waxy cell wall, which means it is partially protected against lysozyme

It can survive inside macrophages and lie dormant until the immune system is weakened, when it can re-infect

What might a pathologist expect to find in a body of a patient who died of suspected TB? Presence of TB bacteria Enlarged lymph nodes Tubercules (lesions) in lungs Serious lung damage Typical damage to brain, spleen, kidney, bones

Diagnosis of TB

Skin test (Heaf test and Mantoux test); uses protein tuberculin derived from dead bacteria; detects whether body has anti-TB antibodies – inflammation reponse

Culture of TB bacteria from sputum

Prevention of TB

Improvement of living conditions – better ventilation, reduction in overcrowding, better nutrition etc.Immunisation of high risk groups

Treatment of TB

Use of specific antibiotics to kill the bacteria (a course can last more than 6 months and must be completed to ensure all the bacteria are killed)

Antibiotics

Active TB bacteria are killed by using a combination of antibioticsAn antibiotic is a drug that kills or prevents the growth of bacteria.

Antibiotics can be;

Bacteriocidalo Kill bacteria e.g. penicillins

Bacteriostatico Prevent the multiplication of bacteria

Antibiotics are used to kill or slow the reproduction of a pathogen to give the immune system the chance to respond and ‘catch up’ so it can deal with the infection e.g. by phagocytes or antibody production

Antibiotics target processes in bacterial cells but do not affect mammalian cells because: they are eukaryotic do not have cells walls have larger ribosomes and subtle differences in the mechanism of protein

synthesis have different enzymes

Antibiotics do not affect viruses because antibiotics affect the metabolism of bacterial cells but viruses have no metabolism so they cannot be affected.

Antibiotic resistance

In this context, antibiotics are a selection pressure especially when over-used.

Susceptible bacteria are killed but those bacteria with random mutations which produced alleles for resistance (adding to the gene pool but which may confer no selective advantage unless an antibiotic is encountered) are resistant so will survive to pass their alleles on (antibiotic resistance genes are often found on plasmids)

so eventually the bacterial population becomes resistant and the antibiotic is no longer effective

Antibiotic resistance can build up rapidly because:

bacterial numbers can increase very fast mutations occur when DNA divides/bacterial cells divide frequently/ so

mutations occur more frequently so many cells potentially carry mutations

bacteria are haploid so any mutation will be expressed and exposed to selection

many antibiotic-resistant genes are carried on plasmids which can be passed from one bacterium to another (by conjugation) or taken in by bacteria from the environment containing other dead bacteria

so the number of bacteria containing resistance alleles increases further

Antibiotic resistance can develop because:

Antibiotics are often over-prescribed or used when not really needed e.g. for colds, flu, other viral infections

Patients stop taking them before the course in ended when they feel better but not all the bacteria are killed)

Antibiotics used in low doses in diet of farm animals to make them grow faster so get passed to humans in the food chain

The consequence is that the antibiotic is now ineffective so there is a need to:

use combinations of different antibiotics are used to reduce the probability of resistance to both developing

only prescribe antibiotics when absolutely necessary**and complete the full course of treatment

fight infections in other ways; infection control – use of disinfectants, hygiene (e.g. hand washing and antiseptic or alcohol gels ); thorough cleaning of wards, clothing (no ties, wrist watches!) **, use of gloves especially with open wounds

use of isolation wards ** improve diet, housing, living conditions so people more healthy so their

immune systems are better able to combat infections without the need for antibiotics

develop new antibiotics develop other forms of treatment which do not involve antibiotics

*** used to reduce risk of hospital acquired infections such as MRSA

HIV

HIV is found in blood and other body fluids; semen/vaginal secretions/breast milk

HIV infection occurs when blood or the body fluids containing the virus of an infected person gets transferred directly into the body, and subsequently the blood, of an uninfected person by: Unprotected sex Direct blood to blood contact e.g.cuts, grazes, oral sex via gum

damage/intravenous drug abusers sharing needles Mother to child across placenta, during birth or via breast feeding

Viruses reproduce by inserting their nucleic acid into the host cell which is then translated into proteins to build new viruses.

Nature of genetic code.

Each DNA molecule (which makes up a chromosome) contains the genetic code for a large number of proteins.

A gene is a region of a DNA molecule which codes for the synthesis of one particular protein.

The genetic code of a gene is the sequence of bases in the DNA molecule that codes for the order in which the amino acids are assembled into a polypeptide or protein molecule (i.e. the primary structure).

Key concepts about the genetic code

It is a triplet code. A sequence of 3 bases codes for one amino acid (3 bases is the minimum number to produce a code for the 20 amino acids)

A codon is the triplet of 3 bases coding for one amino acid

The code is non-overlapping: the codons are ‘read’ individually and in sequence (just like reading the fat cat sat…) i.e. CTACTC is only read as two codons, CTA and CTC (rather than CTA, TAC, ACT etc if the code was overlapping).

One codon codes for one amino acid only The code is a degenerate code; there are actually 64 possible codons -

most amino acids are coded for by more than one codon, there is also one ‘start’ codon (AUG) and there are 3 codons which do not code for any amino acid and are called ‘stop’ codons.

The code is universal: the same triplet codes for the same amino acid in all organisms.

How the genetic code worksHow the genetic code works.

DNA à transcription à mRNA à translation à protein

too big to leave nucleus

sequence of codonsin DNA gene copied as sequence of codonsin mRNA

small, single stranded molecule which leaves nucleus, attaches to ribosome

sequence of codons in mRNA translated into sequence of amino acids

amino acids joined together to form the protein

Transcription of a gene: learn the wording!

Hydrogen bonds between the DNA bases break so the DNA molecule ‘unzips’

Bases of the gene to be copied are now exposed RNA nucleotides (present inside the nucleus) match up with the

complementary bases on the DNA template strand (NB: A in DNA pairs with U in RNA)

RNA polymerase joins up the RNA nucleotides to make a single strand of messenger RNA.

Why is transcription necessary?

DNA too big to leave nucleus Protein synthesis only takes place in cytoplasm So need mRNA to carry genetic information from DNA in nucleus to

ribosomes in cytoplasm

Post-transcriptional processing of mRNA.

Genes have coding regions (exons) and non-coding regions (introns). Whole gene is transcribed into mRNA. Introns then ‘cut out’ leaving just the exon sections. Exons spliced together to make functional mRNA; the exons can be sliced

together in different ways so that several types of mRNA are produced which will be translated into several different proteins; this is called post-transcriptional processing

So one gene à several related proteins [this is a form of molecular amplification]

Translation: learn the wording

mRNA passes out of nucleus into cytoplasm and attaches to a ribosome on the RER

transfer RNA molecules carrying the amino acids specific to their anticodons pair up with their complementary codons on the mRNA; the first one pairs up with the ‘start’ codon

to get the amino acids in the right place in the primary structure. the amino acids are joined together by peptide bonds to form the protein. process continues until the stop codon (for which there is no tRNA) polypeptide released into the rER the protein then folds to form its specific tertiary structure e.g. a viral capsid

protein.

HIV Infection and AIDS

This can occur from mother to child across the placenta or in breast milk.

This can occur with direct blood-to-blood

transfer through cuts and grazes.

This can occur when sharing needles, whether used illegally or legally.

The weakened immune system makes the patient more prone to opportunistic infections such as pneumonia and TB. There may also be significant weight loss, dementia (memory and intellect loss) and the cancer Kaposi’s sarcoma.

AIDS is usually fatal.

An increased number of viruses in circulation (viral load) and a declining number of T helper cells indicate the onset of AIDS, the disease phase.

There may be no symptoms during this chronic phase, but there can be an increasing tendency to suffer various infections which are slow to go away. Dormant diseases such as TB and shingles can reactivate. The chronic phase can

last for years, especially if combined with drug treatment.

The virus continues to reproduce rapidly, but the numbers are kept in check by the immune system.T killer cells recognise the infected T helper cells and destroy them.

The infected person may experience symptoms such as fever, sweats, headache, sore throat and swollen lymph nodes, or they may have no symptoms.

As the number of viruses increases, the number of host T helper cells decreases. Macrophages, B cells and T killer cells are not activated and the infected person’s immune system becomes deficient.

When a person is first infected by HIV, there is an acute phase of infection. There is rapid replication of the virus and loss of T helper cells.

The new virus particles bud out of the T cell, taking some of the surface membrane with them as their envelope, and killing the cell as they leave.

Once inside, the virus uses reverse transcriptase to produce DNA from its RNA. The DNA is integrated into the host’s DNA by another HIV enzyme, integrase. The viral DNA is transcribed and translated to produce new viral proteins and

assemble new viruses.

HIV invades T helper cells and macrophages. The HIV gp120 molecules attach to their CD4 receptors allowing the virus envelope to fuse with the host cell surface membrane, enabling the viral RNA to enter the cell.

This can occur through unprotected

sex.

HIV infection occurs when the body fluid (blood, vaginal secretions and semen, but not salivaor urine) of an infected person is transferred directly into the body of an uninfected person.

AIDS, acquired immune deficiency syndrome, is caused by infection with the human immunodeficiency virus, HIV.

Course of the disease

Acute phase May suffer fever, sweats, headache, sore throat, swollen lymph nodes –

similar to flu. (Some people have no symptoms) Lasts 3-12 weeks after infection Rapid viral multiplication + loss of T helper cells. Increase in HIV antibodies – now HIV positive T killer cells destroy infected T helper cells, keeping numbers in check, so

reducing rate of viral multiplication, but numbers of helper T cells decreases as they are destroyed

Hopefully start to feel better!

Chronic phase (asymptomless or latent phase) Virus continues to reproduce and infect T cells but numbers kept in check by

immune system – killer T cells destroy infected helper T cells so their numbers continue to decrease

Active virus present so HIV positive individuals are infectious! Reduced immune system efficiency means colds and other minor infections

are slower than normal to shift Also means latent diseases such as TB may reactivate

Disease phase: AIDSAIDS = Acquired immune deficiency syndromeIncrease in the number of viruses + ever declining number of T helper cells weakens the immune system leading to Opportunistic infections – infections normally controlled in healthy people

but potentially life-threatening in HIV infected people: includeso TB, pneumonia and other lung infections, intestinal infections leading

to persistent diarrhoea and vomiting à weight losso also dementia, loss of intellectual functions, certain otherwise rare

cancers e.g. Karposi’s sarcoma AIDS is usually fatal.

Treating HIV

A number of new drugs are being designed to block fusion of HIV with its host cell to prevent infection.

Inhibitors of reverse transcriptase , such as AZT, were the first anti-HIV medications, and are still a critical part of treating infection.

Inhibitors of integrase are under study as a new way to block HIV replication HIV protease inhibitors , one of the most potent types of anti-viral

medications, block the processing of other HIV proteins into their functional forms essential for virus maturation before release

Problems facing treatments for AIDS

HIV infections cannot be cured because: virus attacks and remains in cells of the immune system of the body so the

immune system cannot detect and attack it. HIV actually attacks cells of the immune system itself so weakening it. not easy to develop a drug which attacks the virus without damaging the

cells in which it is found.

once the viral DNA is integrated into the genetic material of the host, it is possible that HIV may persist in a latent state for many years.

HIV surface antigens change as a result of random mutations so lymphocytes and antibodies (memory cells from a previous infection) won’t recognize it.

Random mutations occur rapidly in RNA (because single stranded) due to high multiplication rates of the virus and large numbers of viruses carrying the mutations are produced

The virus can also become resistant to the drugs used (which is why the drugs are often used in combination to reduce the probability of multi-drug resistance)

For this reason, based on our current knowledge, patients must remain on anti-viral therapy for life. The drugs are very expensive and need to be taken for extensive periods of time so they are not available to the vast majority of infected people

An ‘evolutionary arms race’ exists between pathogens and drug developers

• Drug developers produce new drugs effective against pathogens (bacteria or viruses)

• These drugs provide a selection pressure;• Rapid multiplication pathogens produces many with mutations• Any pathogen with mutations that make them resistant to the drug will

be more likely to survive and reproduce; susceptible pathogens killed, resistant ones survive and increase

• Drugs now ineffective against resistant pathogens• Drug developers have to create new drugs.