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. predation
Abiotic factors: environmental factors due to the physical conditions e.g. soil pH
Habitat: the particular place where a community of organisms lives
Population: a group of individuals of the same species living and breeding together in the same
place at the same time
Community: 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

Sampling strategies
• In a uniform environment random
sampling is used
• Quadrats are placed at random to avoid
bias

X
X
X

X
 How?
B Divide the area into a grid (e.g. using
measuring tapes, string with knots in at 1m
intervals)
1 2 3 4 ogenerate random numbers – e.g. use
1 random number generator on a calculator,
dice, random number tables – these give
2 the coordinates of a random quadrat;
oin this example A3, B2 defines the top
A
3 X left hand corner of the shaded quadrat on
the diagram
4 orepeat the procedure for the number of
quadrats to be taken.
5 oplace the each quadrat on its appropriate
coordinates.
oin each quadrat count the number of
organisms of the species under
investigation.

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

X x x x
X or

X x x
X
X x x x
A line transect down a slope,
across a rocky shore Around a pond

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 habitat
e.g. Investigation of the distribution and abundance of heathers on the heathland
Line 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 using
o the H atoms from reduced NADP
o 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

Trophic levels

Secondary consumers (carnivores)

Primary consumers (herbivores)

Primary producers

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’
A trophic level is a feeding level in a food chain

Efficiency of energy transfer

Energy transfer: sunlight  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 NPP

i.e. NPP = GPP – respiration
The energy in the biomass is what is available to the primary consumers.

Energy transfer: producers  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 heat
This 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 decompose
The peat accumulates in successive layers; lowest layers are the oldest: pollen trapped in peat layers
Use 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 occurring
i.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 again
o 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 CO 2
accumulate in the biomass (so effectively lock out of the cycle)
 Fossil fuels
o fossil fuels e.g. coal reserves are carbon sinks
o 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 equilibrium
But 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 rise
o 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 from

o anaerobic decay in paddy fields and of domestic refuse in landfill sites
o flatus from herds of beef and dairy cattle
o 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 knowledge
Models 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 produced
o 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 trees
o 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 CO 2
contributing to global warming)
o May slow down further increase in atmospheric CO 2 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 [CO 2
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 glaciers
o 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 6
Topic 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 Contents
Polymerase chain reaction...................................................................................18
Producing a DNA profile.......................................................................................18
Determination of the time of death.....................................................................19
Causes of decomposition.....................................................................................20
Forensic entomology............................................................................................20
Non-specific responses to infection....................................................................22
TB..........................................................................................................................24
Antibiotics.............................................................................................................25
HIV.....................................................................................................................27
Nature of genetic code.........................................................................................27
HIV 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 profiling

Works on the premise that everyone’s DNA is unique

Polymerase chain reaction

Use 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 temperature

Body 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 contraction

On 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 decomposition
Autodigestion or autolysis due to action of hydrolytic enzymes (= self-digestion!) begins about 4
mins after death!
 In gut
 from lysosomes in cells
Causes 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 entomolog
This 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

Structure of a virus

Much smaller than bacteria

20 – 400 nm
[1 nm = nanometre = 10-6 mm]
A virus is a very simple structure which consists of:
•Protein coat or capsid made up from subunits of individual protein molecules
(called capsomeres) and glycoproteins
•Nucleic acid (contains the genes for the structure of the virus). This can be
•DNA e.g. in adenovirus, the flu virus
•RNA e.g. in HIV, hepatitis virus
•Some viruses also have an outer envelope derived from the host cell
membrane (so consists of lipids and proteins) e.g. HIV, measles
•No cytoplasm, membrane systems or organelles; no metabolism

Comparison of bacteria and viruses

Bacteria Viruses
• Prokaryotic cells • No cellular structure
• Cell wall, cell membrane, cytoplasm, no • Protein coat surrounding nucleic acid
organelles, DNA not in a membrane- molecule. May have outer envelope
bound nucleus. May have mucilage derived form host cell
capsule
• Typically 10 mm in size • Typically up to 400 nm in size, so very
(x 25 times bigger) much smaller
• Genetic material is DNA • Genetic material is DNA or RNA
• Reproduce by binary fission (asexual) • 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-destruct
Significance
• 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 defence
Both 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.

erculosis (TB) is a contagious disease caused by the bacterium Mycobacterium tuberculosis. Respiratory or pulmonary TB is the most common form.

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

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

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

aerobic tissue masses known as a granuloma or tubercules form in response to infection. They contain dead bacteria and macrophages at their centre.

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

may survive inside macrophages. The bacteria have very thick waxy cell walls, making destruction inside the macrophages very difficult. The bacteri

uberculosis) occurs if there are too many bacteria for the immune response to deal with, or if an old infection breaks out because the immune system is

The bacteria multiply rapidly and destroy the lung tissue, creating holes or cavities.

The lung damage will eventually kill the sufferer if they are not treated with an appropriate antibiotic.
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 antibiotics
An antibiotic is a drug that kills or prevents the growth of bacteria.

Antibiotics can be;

 Bacteriocidal
o Kill bacteria e.g. penicillins
 Bacteriostatic
 o 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 works

How the genetic code works.
DNA  transcription  mRNA  translation  protein
sequence small, sequence of amino
too big single
of codons codons in acids
to leave stranded
in DNA mRNA joined
nucleus molecule
gene translated into together
copied as which sequence of to form
sequence leaves amino acids the
of codons nucleus, protein
in mRNA attaches to
ribosome

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

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

This can occur

This
through
can occur
unprotected
when sharing
sex. needles,
This can
whether
occurused
withillegally
direct blood-to-blood
or legally.
This can occur
transfer
fromthrough
mothercuts
to child
and grazes.
across the placenta or in breas

crophages. The HIV gp120 molecules attach to their CD4 receptors allowing the virus envelope to fuse with the host cell surface membrane, enabling

e 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

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.

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.

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 sys

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

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.

an increasing tendency to suffer various infections which are slow to go away. Dormant diseases such as TB and shingles can reactivate. The chronic

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.

re prone to opportunistic infections such as pneumonia and TB. There may also be significant weight loss, dementia (memory and intellect loss) and t
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: AIDS

AIDS = Acquired immune deficiency syndrome
Increase 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: includes
o TB, pneumonia and other lung infections, intestinal infections leading to persistent
diarrhoea and vomiting à weight loss
o 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.