Bio topic 6 - Immunity, infection and forensics

Q1. b) (iii) Explain why there is a decrease in mass of the leaves (4)

Decomposers release enzymes in decomposition
Soluble AAs formed and taken up by organisms
Respiration of glucose takes place
co2 released
Water is evaporated
Animals eat the leaves

(iv) Suggest what effect an increase in temperature would have on the rate of decomposition of these leaves (4)

Increase in temp would increase the rate of decomposition (up to an optimum temp)
Increased KE results in increase in no. of collisions which increases no. of enzyme-substrate complexes formed
Increased temp increases rate at which bacteria increase
Above a certain temperature rate of decomposition would decrease
At higher temps, enzymes become denatured

Q2. Describe the role of decomposers, such as microorganisms, in the carbon cycle (2)

Break down organic material from dead body and release enzymes in decomposition
Respire and release co2 into atmosphere

Q3. *(i) Describe how a DNA profile was produced from this small sample of DNA (6)

Multiple copies of DNA made using PCR
Primers are used
Restriction enzymes produce DNA fragments
Carry out gel electrophoresis by loading DNA onto gel
Apply potential difference / current across gel
Use UV dye to visualise bands

(ii) Suggest how these DNA profiles were compared (3)

Compare total no. / position / size of bands

Q4. Explain how gel electrophoresis could be used to find out if this DNA came from a black panther (5)

Obtain DNA from panther using restriction enzymes
Load DNA onto agarose gel
Apply potential difference / current across gel
Use UV dye to visualise band
Compare position / no. of bands
A match would indicate DNA from black panther present

Q5. (e) In addition to body temperature, forensic scientists would look for other evidence of time of death.
Give 2 other pieces of evidence that allow for an estimation of TOD (2)

Rigor mortis
Degree of decomposition
Forensic entomology

Q3. Suggest why cephalosporins are bactericidal antibiotics (2)

Destroying / death of bacteria cells
Bacteria / cells burst

(ii) Suggest why quinolones are bacteriostatic antibiotics (2)

inhibit multiplication
No cell division

Q4. (ii) Explain why the mean levels of antibody in group B are different from group A in the first fifteen days (3)

Antibodies and memory cells present from first vaccination (secondary immune response)
Memory cells mean antibodies are produced immediately on exposure to same antigen

(c) Using the information in the graph, explain the advantage of vaccinating people tw against yellow fever (2)

Virus destroyed quicker
More memory cells present so higher lvls of antibodies

Q5. Human diseases can be caused by many different types of organism, such as bacteria and viruses.
(a) Give two differences between the genetic material of bacteria and viruses (2)

Bacteria have DNA, viruses have DNA or RNA
Bacteria are circular, viruses are linear
Bacteria are double stranded, viruses are single or double
Bacteria may have plasmids, viruses don’t

(i) Describe how macrophages ingest the bacteria (2)

Phagocytosis (engulfing)
Detects presence of pathogen (receptors bind to antigens) -> Phagocyte wraps its cytoplasm around pathogen and engulfs it
Pathogen within vesicle (phagosome) fuses w lysosome to form phagolysosome

(ii) Suggest why treatment with antibiotics may not be effective against the dormant bacteria in the tubercles (2)

Bacteria need to be accessible to antibiotics
Bacteriostatic antibodies affect dividing bacteria (they develop antibiotic resistance)

(iii) TB can be prevented by vaccination. Explain how a person can develop artificial active immunity following vaccination (3)

Dead organisms put into person
Stimulation of specific / primary immune response
T helper cell activation (release cytokine to activate B cells)
T killer cell activation (destroy any cells which have been infected w pathogen)
Production of memory cells (remain in low lvls in case reinfection occurs)

(c) In a person with TB, the dormant bacteria in tubercles may be activated after several years. The bacteria multiply rapidly, resulting in severe lung damage. The bacteria are released from the tubercles. These bacteria can inhibit the activity of T cells and infect other organs.
Explain why the activity of these bacteria and the inhibition of T cells means that a person may quickly develop severe symptoms leading to death (4)

Further lung dmg / severe breathing problems (can’t get enough o2)
Mycobacterium get into blood
Organ failure leads to death
Weakened immune response due to loss of T cells
T helper cells (release cytokine to activate B cells)
No T killer cells = infected cells won’t be destroyed
No B cells = no antibody produced
Secondary / other infections causing death

(i) State two characteristic features of antibodies (2)

Chains of aas
Specific 3D shape, 4 peptide chains, disulphide bridges b/w peptides
Variable region
Constant region
Produced by plasma cells (present on B cells)
Role = immobilisation / agglutination / lysis

*(ii) The antibody 2G12 is produced in response to part of a glycoprotein found on the surface of HIV. Synthetic molecules have been made that resemble this part of the glycoprotein. The antibody 2G12 binds to these synthetic molecules.
Suggest how this may enable scientists to develop a means of producing active immunity to HIV infection (5)

 Artificial (active) immunity
Vaccination containing synthetic antigen / glycoprotein
Stimulates specific immune response to synthetic antigen
B cells produced by T helper cells activating them (release cytokine)
2G12 antibodies produced faster on reinfection (secondary immune response)

Suggest why data about HIV infections are often estimates (2)

Doesn’t always produce symptoms
Virus is dormant
Only ppl who suspect they may have contracted HIV test
Some ppl wouldn’t wanna be tested
Symptoms common to other diseases
New cases arising all the time

Q7. (i) Suggest why common cold viruses cannot infect cells if they land on unbroken skin (2)

Keratin in skin prevents entry by acting as a barrier
Skin has diff receptors

(ii) Suggest why common cold viruses cannot infect cells if they enter the blood through a cut in the skin.(2)

Viruses only attach to specific receptors (host cells)
Receptors not present on endothelial / blood cells
Phagocytes destroy viruses

(b) Compare the action of the RNA in the common cold virus with that found in HIV (2)

Reverse transcriptase required in HIV but none in cold virus
DNA formed using RNA in HIV (no DNA formed in cold)
Delay in virus formation in HIV infection / immediate formation of virus particles in cold 

Q8. (ii) Explain the changes in mean level of antibody A after infection with Bordetella pertussis (3) 

Secondary immune response
Memory cells differentiate into plasma cells
In secondary response, antibodies released from plasma cells

(b) (i) Suggest why antibody B was not present in the blood of these rats until after infection with Bordetella pertussis (2)

Antibodies only present if antigen present
Antigen B not present in vaccine
Vaccination failed to stimulate immune response 

Q9. A person who has been vaccinated becomes infected with HPV-16.
Explain the role of the T cells in the body of this person (3)

T memory cells alr present and recognise antigens specific to HPV-16 virus
T helper cells activate B cells
Formation of T killer cells destroy cells infected w virus

Q10. (a) (i) Describe how the production and action of interferon differs from the production and action of lysozyme (3)

Interferon involved in viral infections, Lysozyme affects bacteria
Interferon produced by infected cells, Lysozyme present in phagocytes
Interferon inhibits replication of viruses, Lysozyme kills bacteria

(ii) Suggest why the protein structure of lysozyme is important to the way in which it acts against pathogens (4)

Lysozyme is an enzyme with a specific shape that acts on cell wall of bacteria

(b) (i) Explain why an insect bite, which breaks the surface of the skin, may lead to inflammation around the injury (3)

Histamine released due to dmged cells
-> released from platelets / WBCs
Histamine leads to increased blood flow
Inflammation causes oedema / swelling (increases temp)

(ii) In order to reduce inflammation, a cream containing antihistamines might be applied to the skin, around an insect bite. Suggest why applying this cream might be better than taking tablets containing antihistamines (3)

Histamines produced around bite area (only local reaction produced)
Cream applied to actual site of production of histamine
More immediate relief / effect
Higher conc. Of antihistamine at site n won’t be destroyed by acid
Tablets may lead to side effects

Q11. One role of the skin is to protect the body from infection. (i) Explain how skin flora protect the body from infection (2)

Prevent growth of bacteria and release chemicals / enzymes
Competition for nutrients / water / space

Q12. (a) Explain why antibiotics are not used to treat Ebola haemorrhagic fever (2)

Targets organelles in bacteria so viruses are unaffected

(b) Explain why the blood plasma from survivors can be used to treat new cases of Ebola infection (3)

Survivors will have antibodies specific to the virus in their plasma
Antibodies given to individuals infected w Ebola will provide passive immunity
Antibodies given will therefore agglutinate virus particles

(c) A study of the 2014 Ebola outbreak in Sierra Leone found that the Ebola virus was evolving rapidly. Explain why the evolution of the virus might reduce the effectiveness of any vaccine being developed (4)

Vaccine stimulates immune response to make antibodies specific to viral proteins
Mutations in virus nucleic acid result in change in shape of viral proteins antibodies can no longer bind to virus