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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 dont
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 dont 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 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 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

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 isnt 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 1C

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 Earths 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 Earths
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 CO2 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: (dont 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 CO2 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 [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 dont grow
above the tree line)

Effects of global warming

Changing rainfall patterns


some areas will get increased rainfall, including torrential rainstorms
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 dont get pollinated which will reduced their numbers, and the
insects dont 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
youngor insect life cycles speed up so that larvae or adults are produced
before the food plants
Seeds may not germinate if dont get the cold stimulus from a cold winter;
over-wintering stages of insect pests wont 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 bodys 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 bodys 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 persons dental records are fairly unique so they can be as reliable
as fingerprints

Identification by DNA profiling


Works on the premise that everyones 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 peoples 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

Comparison of bacteria and viruses

Bacteria Viruses
Prokaryotic cells No cellular structure
Cell wall, cell membrane, Protein coat surrounding nucleic
cytoplasm, no organelles, DNA acid molecule. May have outer
not in a membrane-bound envelope derived form host cell
nucleus. May have mucilage
capsule Typically up to 400 nm in size, so
Typically 10 mm in size very much smaller
(x 25 times bigger) Genetic material is DNA or RNA
Genetic material is DNA Reproduce by inserting nucleic
Reproduce by binary fission acid into host cell which reads
(asexual) 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 pathogens 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 dont
need to happen)
more cells are produced much faster than in 1 o 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.Tuberculosis (TB) is a contagious disease caused by the bacterium Mycobacterium tuberculosis. Respiratory or pulmona

Herd immunity
Achieved when enough people in a community are immunized against
certain diseases so it is more
Infection difficult
may occur fortuberculosis
when M. that disease
bacteria to get passed
are inhaled and lodgebetween
in the lungs. Here they star
those who aren't immunized.

TB
The first phase (primary infection) can last for several months; it may have no symptoms
Tuberculosis is caused by the bacterium Mycobacterium tuberculosis. Course
of the disease.

An inflammatory response by the hosts immune system occurs. Macrophages engulf the bac

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

After 38 weeks, the infection is controlled and the infected region of the lung heals.

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

The second phase (active tuberculosis) occurs if there are too many bacteria for the immune response to deal with, or if an old infection breaks

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 an
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

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 in

HIV infection occurs when the body fluid (blood,


or urine) of an infected person is transferred dire

This can occur


This
through
can occur
unprotected
when sharing
sex. needles,
This can
whether
occurused
withillega
direc

HIV invades T helper cells and macrophages. The HIV gp120 molecules attach to their CD4 receptors allowing

Once inside, the virus uses reverse transcriptase to produce DNA from its RNA. The DNA is integrated into the hosts DNA by anothe

The new virus particles bud out of the T cell, taking some of the surface mem

When a person is first infected by HIV, there is an acute phase of infectio

As the number of viruses increases, the number of host T helper cells decreases. Macrophages, B cells

The infected person may experience symptoms such as fever, sweats, headach

The virus continues to reproduce rapidly, but the num


T killer cells recognise the infected T

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 awa

An increased number of viruses in circulation (viral load) and a declining n

The weakened immune system makes the patient more prone to opportunistic infections such as pneumonia and TB. There may a
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 weight loss
o also dementia, loss of intellectual functions, certain otherwise rare
cancers e.g. Karposis 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) wont
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.

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