week4

Question 1

Revise criteria used for virus classification

Answer 1

type and organisation of genome (DNA/RNA) - single or double stranded

viral replication strategy- reverse transcription?

stricture + size of the viron (envelope?)

host range

Question 2

Revise replication cycle of herpes simplex

Answer 2

herpes: cell membrane is derived from a host lipid bilayer, fusion initiated between host and virus and caspid is injected into cytoplasm.

parental capsid docks onto a host nuclear pore complex (NPC)

viral genome then translocates through the nuclear pore into the nucleoplasm, where it is transcribed and replicated to propagate infection

Question 3

Describe the replication cycle of rotavirus.

Answer 3

Question 4

Revise replication cycle of HIV

Answer 4

Question 5

describe the clinical features and structure of HIV

Answer 5

Human Immunodeficiency virus, inner cone shaped core with 2 strands of single RNA. surrounded by matrix protein and lipid membrane.- usual infection symptoms, weight loss can be noticeable.

Question 6

describe the clinical features and structure of herpes simplex

Answer 6

herpes viruses, four layered structure: a core containing double-stranded DNA genome, icosapentahedral capsid, amorphous protein coat called the tegument, glycoprotein-bearing lipid bilayer envelope. Traditional sores apperance.

Question 7

describe the clinical features and structure of hep A

Answer 7

HEP A- enteric picornavirus. genome single stranded RNA. naked, icosahaedral. Upper right quadrant pain, loss of appetite, dark urine,

Question 8

describe the clinical features and structure of hep B

Answer 8

B Icosahedral nucleocapsid- circular dna partially double stranded. Symptoms same as hep A but also jaundice + hives

Question 9

describe the clinical features and structure of hep C

Answer 9

C viruses, Enveloped Icosahedral nucleocapsid, Single stranded RNA, enveloped mainly by E proteins. Jaundice, ascites, easily bleeding/ bruising.

Question 10

describe the clinical features and structure of influenza

Answer 10

influenza virus,- flu like symptoms outer host membrane sphere- protein M1 shell, 8 RNA single strands

Question 11

describe the clinical features and structure of rotavirus

Answer 11

rota virus, 11 double stranded DNA segments non enveloped triple layered caspid. Icosahedral structure. Causes fever vomiting diarhoea, abdominal pain.

Question 12

describe the clinical features and structure of measles

Answer 12

measles- fever, cough, runny nose + sore throat small white spots –> rash. Enveloped RNA single strand. Pleomorphic.

Question 13

describe the clinical features and structure of mumps

Answer 13

Mumps- fever, muscle ache, fatigue, swollen saliva glands. structure: enveloped pleomorphic, single strand RNA. Helical nucleocaspid.

Question 14

describe the clinical features and structure of rubella

Answer 14

rubella viruses,- fever, rash, coughing. Birth defects if acquired by pregnant women. Structure: icosahedral enveloped single strand RNA.

Question 15

describe the clinical features and structure of enteroviruses

Answer 15

Enteroviruses- single strand RNA, icosahedral caspid. fever, runny nose, sneezing, cough, skin rash, mouth blisters, and body and muscle aches

Question 16

describe the clinical features and structure of rhinovirus

Answer 16

rhinovirus - sore throat, runny nose, coughing, sneezing, watery eyes, headaches, and body aches. enveloped virus with a positive-sense single-stranded RNA

Question 17

describe the clinical features and structure of adenovirus

Answer 17

Adenovirus- most commonly respiratory illness. Icosahedral, double stranded DNA, no envelope.

Question 18

List factors that determine host susceptibility to viral infection

Answer 18

immuno supression
at risk activities for transmission
lifestyle (exposure, sexual activity)
age
nutritional status
pre-existing chronic diseases
genetics

Question 19

Describe primary and secondary infection, re-infection and reactivation of infection and provide examples for each

Answer 19

primary- first encounter with virus
s’- an infection that occurs during of immediately after another infection.

re-infection: infected–> recovered–> infected. e.g rhinovirus

re-activation- doesn’t replicate for periods of time. then when immunosupressed will begin and cause disease. - varicella zoster

Question 20

Using Varicella Zoster virus as an example describe mechanisms that viruses use to spread within the body

Answer 20

Question 21

Describe mechanisms used by viruses to persist within the host

Answer 21

make very few viral proteins and do not replicate (become dormant)

down regulate MHC1 and hinder antigen presentation.

replicate in privileged sites

change viral proteins

Question 22

Describe pathogenesis of viral infections with reference to viruses that cause cancer

Answer 22

papilloma virus
virus replication depends on host cell machinery.
several layers in epithelia aren’t replicating- which is where the virus migrates to.

inserts DNA into host cell genes at E2. this causes E6- to suppress p53 protein and E7 to suppress Retinoblastoma gene. causing decreased regulation of cell proliferation.

E6 also activates telomerase gene- which makes cells live a lot longer and go through more cycles of replication

Question 23

Define the terms: antigenic variation; phase variation; antigenic drift; antigenic shift

Answer 23

antigenitic variation- an invading pathogen changed the proteins (antigens) on its surface during infection to avoid immune response.
phase variation - ON/OFF of an antigen at low frequency

Drift consists of small changes (or mutations) in the genes of influenza viruses

shift- an abrupt major change in antigen conformation.

Question 24

Explain the concept of viral antigenic diversity and show how this influences infectivity and disease spread, using influenza as an example

Answer 24

altering the proteins on its surface to evade host defence.

if drifts- usually mutation + selection- leads to epidemics

if gene re-arrangement occurs- leads to pandemics.

Question 25

Outline, with bacterial and viral examples, survival strategies used by pathogens to avoid the adaptive and innate immune systems

Answer 25

Both- hide in cells

bacteria- inhibit opsonins + complement. c3a + C5a proteases- inhibit inflam response.

viruses- down reg MHC, dysreg apoptosis, immune suporession (dec cd4), rapid growth and transmission prior to immune response.

Question 26

Describe the role of bacterial capsular polysaccharides in pathogenesis

Answer 26

facilitate adhesion to surfaces + other bacterial cells.

Question 27

Outline the general principle of antigenic variation in Neisseria gonorrhoeae

Answer 27

Question 28

Provide an overview of how viral infections are diagnosed with emphasis on laboratory diagnosis

Answer 28

fluorescent tags used in pcr replication

genome sequencing

electron microscopy

culture growing is not very effective.

haemagglutination assey

Question 29

Understand the science behind the different methods of diagnosing viral infections

Answer 29

pcr- exponential growth of viral dna in the assey makes it easier to detect.

matched tags to specific viruses emit fluorescence when a match is made.

Question 30

Demonstrate an appreciation of the advantages and limitations of the different viral diagnostic tests allowing the most appropriate sample and test to be chosen and the correct diagnosis to be made

Answer 30

weigh up the benefits of each of the testing methods, cost vs effective vs time consuming.

Question 31

List four different types of antiviral agent which interfere with viral RNA and DNA strand synthesis

Answer 31

influenza- oseltamivir (inhaled version is zanamivir) - inhibit virus release from infected cells (inhibition of neuraminidase)

herpes Rx- aciclovir - competitivly inhibits guanosine binding and stops DNA chain continuation, low cellular toxicity.

gancyclovir- analogue of guanosine- inhibits polymerase.

valaciclovir- prodrug of acyclovir (anti CMG prophylaxis)

valganciclovir- prodrug/ ester of gancyclovir (CMv infection)

Question 32

List other agents used for the treatment of viral infections

Answer 32

hep B drugs Lamivudine, tenofovir,
entecavir, adefovir

HIV drugs in picture.

Question 33

Outline the pathophysiology underlying types I-IV hypersensitivity reaction

Answer 33

1. (POLLEN, ANIMAL HAIR, athsma) B lymphocite sensitisation + subsequent recog. presentation to TH2. release Il-4- induce class switch to IgE producing cells. IgE cells link with mast cells- when pollen activates 2 IgE at same time- induce degranulation- release histamine + cytokines.

2- (myasthenia gravis, graves) Igm + IgG mediatied. antibody antigen interaction. block a receptor (functioning as antigen) in open/ closed position- resulting in overstim/ lack of stim.

3- (SLE) similar to type 2 but with soluble circulating antigen- can be own or foreign tissue. forms immune complexes- fix complement- complexes become so big they can be trapped in kidney. immune complexes not cleared by phagocytes.

4- delayed hypersensitivity (mantoux test) T cell mediated. macrophages present antigen, TH activated- release cytokines- activate macrophages. firm red swelling of skin.

Question 34

Describe immunological factors involved in the development of autoimmunity

Answer 34

genetics- HLA genes
infections- can sensitise/ trigger
specific autoantigens- some proteins are highly conserved across pathogens and humans.
drugs
immunodeficiency
age + gender

Question 35

List examples of autoimmune diseases

Answer 35

graves, sle, rheumatoid arthritis, psoriasis, chrons, colitis.

Question 36

List examples of primary immunodeficiency

Answer 36

People with primary immunodeficiency (PI) have an immune system that does not work correctly.

T Cell deficiency (no thymus) - di george syndrome
b cell deficiency- lack of stem cell –> b cell.
chediak-higashi syndrome

c1q inhibitor deficiency
c3 deficiency

Question 37

Distinguish between primary and secondary immunodeficiency

Answer 37

2’ is acquired- HIV, tumours, malnutrition, cytotoxic drugs, blood cancers.

Question 38

1) Explain why maternal morbidity and mortality is important

Answer 38

a young patient demographic with one/ more children present. generally come in healthy

Question 39

2) List key microbes that can cause maternal, congenital, and neonatal infection

Answer 39

Question 40

3) Outline antenatal tests for women in the UK and why they are done

Answer 40

HIV
Hepatitis B
Syphylis

can be treated whilst the baby is still in the womb without any significant damage/ harm to mum or baby

Question 41

4) Identify the vaccinations relevant to pregnant women in the UK schedule and explain why they are given

Answer 41

Flu, pertussis, covid 19

pertussis most infections occur before newborns vaccine is effective
COVID -19 reduced the chance of early birth.

Question 42

5) Recognise key maternal infections such as chicken pox, parvovirus and genital herpes, the clinical presentation, investigations, and the effect of these infections on the baby

Answer 42

if mother is exposed, call micro on call. they will test bloods taken at 8 weeks and see if there are antibody titers. if there are no biggy, if not need treatment with immunoglobulins.

Question 43

6) Understand the difference in immune susceptibility in pregnancy compared to when people are not pregnant

Answer 43

possibly more prone to infections but research is limited and reports different findings.
more likely to become significantly ill with the same diseases.

Question 44

7) Demonstrate an understanding of the key importance of sepsis during pregnancy and childbirth and outline typical microbial causes such as Group A Strep and Group B strep

Answer 44

presentation day 3 post birth. smelly discharge

significant disease with good treatment if given abx within the hour.

Question 45

Explain the term ‘vaccine’ and the concept of ‘protective immunity’

Answer 45

protective immunity- the ability to defend and resist against a virus

vaccine- a substance used to stimulate the immune system to produce antibodies and provide immunity.

Question 46

Describe types of vaccine, and relate to common clinical examples

Answer 46

live attenuated- MMR, BCG
killed whole organism- require boosting- Polio
toxoid- tetanus
viral vectors
RNA
proteins

Question 47

Discuss the considerations for when, how and who a vaccine is given to in relation to common bacterial and viral vaccines used in the immunisation schedule in the UK

Answer 47

vaccine has to be given before individuals are susceptible to the disease- i.e may need to vaccinate in pregnancy to protect newborns.

putting may vaccines in one help with administration and adherence

at risk groups and also whole populations to reduce incidence of the disease and induce herd immunity

Question 48

Outline the reasons for vaccine booster doses

Answer 48

igm +igg can reduce over time
giving boosters quickly increased the amount of circulating IgG and can make memory cells last for long times post booster.