week4 Flashcards
Revise criteria used for virus classification
type and organisation of genome (DNA/RNA) - single or double stranded
viral replication strategy- reverse transcription?
stricture + size of the viron (envelope?)
host range
Revise replication cycle of herpes simplex
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
Describe the replication cycle of rotavirus.
Revise replication cycle of HIV
describe the clinical features and structure of HIV
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.
describe the clinical features and structure of herpes simplex
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.
describe the clinical features and structure of hep A
HEP A- enteric picornavirus. genome single stranded RNA. naked, icosahaedral. Upper right quadrant pain, loss of appetite, dark urine,
describe the clinical features and structure of hep B
B Icosahedral nucleocapsid- circular dna partially double stranded. Symptoms same as hep A but also jaundice + hives
describe the clinical features and structure of hep C
C viruses, Enveloped Icosahedral nucleocapsid, Single stranded RNA, enveloped mainly by E proteins. Jaundice, ascites, easily bleeding/ bruising.
describe the clinical features and structure of influenza
influenza virus,- flu like symptoms outer host membrane sphere- protein M1 shell, 8 RNA single strands
describe the clinical features and structure of rotavirus
rota virus, 11 double stranded DNA segments non enveloped triple layered caspid. Icosahedral structure. Causes fever vomiting diarhoea, abdominal pain.
describe the clinical features and structure of measles
measles- fever, cough, runny nose + sore throat small white spots –> rash. Enveloped RNA single strand. Pleomorphic.
describe the clinical features and structure of mumps
Mumps- fever, muscle ache, fatigue, swollen saliva glands. structure: enveloped pleomorphic, single strand RNA. Helical nucleocaspid.
describe the clinical features and structure of rubella
rubella viruses,- fever, rash, coughing. Birth defects if acquired by pregnant women. Structure: icosahedral enveloped single strand RNA.
describe the clinical features and structure of enteroviruses
Enteroviruses- single strand RNA, icosahedral caspid. fever, runny nose, sneezing, cough, skin rash, mouth blisters, and body and muscle aches
describe the clinical features and structure of rhinovirus
rhinovirus - sore throat, runny nose, coughing, sneezing, watery eyes, headaches, and body aches. enveloped virus with a positive-sense single-stranded RNA
describe the clinical features and structure of adenovirus
Adenovirus- most commonly respiratory illness. Icosahedral, double stranded DNA, no envelope.
List factors that determine host susceptibility to viral infection
immuno supression
at risk activities for transmission
lifestyle (exposure, sexual activity)
age
nutritional status
pre-existing chronic diseases
genetics
Describe primary and secondary infection, re-infection and reactivation of infection and provide examples for each
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
Using Varicella Zoster virus as an example describe mechanisms that viruses use to spread within the body
Describe mechanisms used by viruses to persist within the host
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
Describe pathogenesis of viral infections with reference to viruses that cause cancer
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
Define the terms: antigenic variation; phase variation; antigenic drift; antigenic shift
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.
Explain the concept of viral antigenic diversity and show how this influences infectivity and disease spread, using influenza as an example
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.
Outline, with bacterial and viral examples, survival strategies used by pathogens to avoid the adaptive and innate immune systems
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.
Describe the role of bacterial capsular polysaccharides in pathogenesis
facilitate adhesion to surfaces + other bacterial cells.
Outline the general principle of antigenic variation in Neisseria gonorrhoeae
Provide an overview of how viral infections are diagnosed with emphasis on laboratory diagnosis
fluorescent tags used in pcr replication
genome sequencing
electron microscopy
culture growing is not very effective.
haemagglutination assey
Understand the science behind the different methods of diagnosing viral infections
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.
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
weigh up the benefits of each of the testing methods, cost vs effective vs time consuming.
List four different types of antiviral agent which interfere with viral RNA and DNA strand synthesis
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)
List other agents used for the treatment of viral infections
hep B drugs Lamivudine, tenofovir,
entecavir, adefovir
HIV drugs in picture.
Outline the pathophysiology underlying types I-IV hypersensitivity reaction
- (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.
Describe immunological factors involved in the development of autoimmunity
genetics- HLA genes
infections- can sensitise/ trigger
specific autoantigens- some proteins are highly conserved across pathogens and humans.
drugs
immunodeficiency
age + gender
List examples of autoimmune diseases
graves, sle, rheumatoid arthritis, psoriasis, chrons, colitis.
List examples of primary immunodeficiency
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
Distinguish between primary and secondary immunodeficiency
2’ is acquired- HIV, tumours, malnutrition, cytotoxic drugs, blood cancers.
1) Explain why maternal morbidity and mortality is important
a young patient demographic with one/ more children present. generally come in healthy
2) List key microbes that can cause maternal, congenital, and neonatal infection
3) Outline antenatal tests for women in the UK and why they are done
HIV
Hepatitis B
Syphylis
can be treated whilst the baby is still in the womb without any significant damage/ harm to mum or baby
4) Identify the vaccinations relevant to pregnant women in the UK schedule and explain why they are given
Flu, pertussis, covid 19
pertussis most infections occur before newborns vaccine is effective
COVID -19 reduced the chance of early birth.
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
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.
6) Understand the difference in immune susceptibility in pregnancy compared to when people are not pregnant
possibly more prone to infections but research is limited and reports different findings.
more likely to become significantly ill with the same diseases.
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
presentation day 3 post birth. smelly discharge
significant disease with good treatment if given abx within the hour.
Explain the term ‘vaccine’ and the concept of ‘protective immunity’
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.
Describe types of vaccine, and relate to common clinical examples
live attenuated- MMR, BCG
killed whole organism- require boosting- Polio
toxoid- tetanus
viral vectors
RNA
proteins
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
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
Outline the reasons for vaccine booster doses
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.
