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Phase 1 > Viruses and Immune Response > Flashcards

Viruses and Immune Response Flashcards

1
Q

what are capsids? what is the structure of a capsid and a unit of nucleic acid called?

A
  • protein shell where genetic material of a virus is stored

* a nucleocapsid

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2
Q

what are the 3 general shapes of capsids?

A
  • helical
  • icosahedral
  • complex
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3
Q

what is the a virion?

A

form a virus takes outside of a cell

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4
Q

when virions have an outer lipid membrane, how is this formed?

A

made up of host cell’s plasma membrane, into which virus proteins / glycoproteins are inserted

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5
Q

what are the 4 mains routes of viral entry? give examples of each

A
  • inhaled droplets - rhinovirus, influenza virus, SARS-CoV-2
  • in food / water - hep A virus, norovirus
  • direct transfer from other infected hosts ie. body fluids - HIV, hep. B virus, Ebola virus
  • bites of vector arthropods - yellow fever virus, Zika virus
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6
Q

what are the 3 categories of single-stranded RNA viruses?

A
  • +ve sense - like mRNA, directly translated
  • -ve sense - complementary to mRNA, converted to +ve using RNA polymerase, then translated
  • retrovirus - RNA reverse transcribed to DNA
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7
Q

how do viruses replicate?

A

assembly of individual components (not binary fission)

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8
Q

what is viral tropism? (3)

A

the ability of a give versus to productively infect a:
• particular cell (cellular tropism)
• particular tissue (tissue tropism)
• a particular host species (host tropism)

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9
Q

how is host range of a virus determined?

A

host attachment sites (cellular) and cellular factors (internal environment)

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10
Q

give examples of the 4 mains virus types: DNA (6), RNA ss+ (10), RNA ss- (4), RNA ds (1)

A
  • DNA : adenovirus, Epstein-Barr virus, herpes simplex 1 + 2, hep. B virus
  • RNA ss+: poliovirus, rhinovirus, norovirus, hep. A virus, hep. E virus, dengue virus, yellow fever virus, zika virus, SARS-CoV-2, rubella virus
  • RNA ss-: mumps virus, measles virus, influenza virus, Ebola virus
  • RNA ds: rotavirus
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11
Q

describe the pathology of respiratory viruses eg. coronaviruses, rhinovirus (4)

A
  • common cold
  • bronchiolitis - progression to coughing, wheezing, breathing difficulties
  • croup - harsh brassy, barking cough
  • viral pneumonia
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12
Q

what are the 3 types of influenza viruses? which cause significant human illness?

A
  • A, B and C

* A and B

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13
Q

what are symptoms associated with flu (7)

A

fever, chills, headache, muscle pain, fatigue, dry cough, sore throat

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14
Q

what are the 2 important surface proteins on influenza A?

A

haemagglutinin and neuraminidase

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15
Q

what are the two types of human herpes virus? what are their features?

A
  • herpes simplex - cold sores triggered by UV light, stress etc. (persistent due to latent phase)
  • Varicella zoster - chicken pox, re-emerges as shingles
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16
Q

what is a distinguishing feature of mumps? what complications can it have?

A
  • swelling of parotid glands (jaw)

* viral meningitis, infertility

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17
Q

what are the common symptoms of measles (4)? what can be a serious complication?

A
  • acute rash, cough, fever, conjunctivitis (widespread rash remains while other symptoms decline)
  • encephalitis
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18
Q

what serious consequences can the rubella virus have?

A

preventable congenital defects (also miscarriage and stillbirth)

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19
Q

what can be a serious complication of Zika virus infection during pregnancy?

A

microcephaly

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20
Q

what are the 2 ways that viruses enter host cells?

A
  • attach to specific receptors to produce a conformational change in capsid proteins / lipid envelope allowing fusion of viral and cellular membranes
  • conventional endocytosis (some DNA viruses)
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21
Q

how is viral nucleic acid exposed once inside the cell?

A

capsid is shed by viral or host enzymes

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22
Q

what is an ‘eclipse phase’

A

period of time where the virus has entered the cell but is not infective because new viral particles have not been assembled

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23
Q

describe how mRNA is produced from different virus types: 1. DNA (not reterovirus), 2. RNA ss+, 3. RNA ss-, 4. RNA ds

A

1 - cell’s own RNA polymerase used to transcribe viral DNA
2 - viral RNA acts as mRNA
3 - viral RNA polymerase transcribes -ve strand into +ve strand mRNA
4 - -ve sense strand is transcribed by viral polymerase into mRNA

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24
Q

why is a host cell mRNA displaced from ribosomes during viral infection?

A

so viral proteins are synthesised preferentially

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25
Q

how does a virus replicate? (3)

A

1 - viral polymerase is either translated from viral genome or is already present from entry
2 - template strand is synthesised from which new strands of viral DNA / RNA are synthesised
3 - capsomeres (individual unit of capsid) associate with new genetic material to form the nucleocapsid

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26
Q

how does a nucleocapsid modify the host cell membrane before budding off?

A

inserts own envelope proteins and glycoproteins into plasma membrane (localised in part where virus will bud off)

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27
Q

describe the lytic pathway (2)

A

1 - virus goes through replication to produce many more particles
2 - causes host cell lysis and destruction to release particles and infect more cells

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28
Q

describe the latent pathway

A

1 - virus undergoes replication but remains in quiescent state
2 - genetic material either incorporated into host DNA or remains in cytoplasm
3 - a trigger will release the virus from latency
4 - virus will replicate again and release new formed particles

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29
Q

what types of mutations are highly common in viruses?

A

deletion and insertion

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30
Q

why are some mutations more common in RNA viruses?

A

lack ‘proof reading’ mechanisms

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31
Q

what is antigenic drift? why is this useful? (3)

A
  • small antigenic changes
  • creates new strain of virus (same sub-type)
  • reduces the effectiveness of T/B cell immunity
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32
Q

what is antigenic shift? (2)

A
  • exchange of genetic material from different origins - gene reassortment (large genetic change)
  • results in formation of a new subtype which can result in pandemics (eg. Spanish Flu)
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33
Q

why can influenza rapidly generate new strains?

A

segmented genome (allows genetic reassortment like a human genome where genes are swapped between different chromosomes)

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34
Q

what is the structure of HIV? (3)

A
  • single stand RNA retrovirus
  • enveloped with gp120 glycoprotein antigen
  • high rate of mutation due to many virions that are released at the height of infection and with the low fidelity of reverse transcriptase (does not correct coding mistakes)
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35
Q

which cells does HIV usually infect?

A

cells with CD4 on cell surface: T helper cells, monocytes, dendritic cells

36
Q

where does HIV multiply in the body?

A

mucosa and draining lymphatic tissues

37
Q

how does HIV enter the cell?

A
  • CD4 has a high affinity binding site for the gp120 glycoprotein
  • association causes conformational change that produces a fusion pore for viral entry
38
Q

describe the process of replication for HIV (6)

A

1 - virus is uncoated by viral protease
2 - DNA copy of RNA synthesised by reverse transcriptase enzyme
3 - viral DNA incorporated into cellular DNA using integrate enzyme (viral DNA now called provirus)
4 - T is activated in response to HIV antigens or another infection, provirus may also be activated -> production of new RNA and proteins
5 - new virions bud off and infect other cells
6 - DNA remains dormant for years in viral reservoirs

39
Q

describe the initial immune response to HIV infection in terms of CD4+ cells (6)

A

1 - CD4 cells in musical surfaces at sites of entry and in lymphoid tissues are infected
2 - may be considerable destruction of T cells
3 - activation of T cells causes infection to spread
4 - infected and unaffected CD4 T cells destroyed
5 - macrophages attempt phagocytosis, but lose ability to kill / become APCs - also infected
6 - dendritic cells also infected, and may be responsible for spread to lymphoid tissue

40
Q

how do virus specific CD8 T cells try to limit acute HIV syndrome? (2)

A
  • try to reduce viral load (viraemia) by producing interferon-gamma and tumour necrosis factor-alpha (cytokines)
  • inhibit HIV replication and block entry to CD4 cells
41
Q

what are the features of HIV antibodies in early infection? (2)

A
  • produced in low level

* non-neutralising

42
Q

why does HIV become resistant to CD8 T cell actions? (2)

A
  • latency means virus is undetected by immune system

* high mutation rate, therefore genes that allow HIV to become resistance to CD8 T cells are selected for

43
Q

describe how the humoral response develops as HIV infection becomes chronic (3)

A
  • more neutralising antibodies produced which target entry to cell
  • target variable region of gp120, CD4 binding sites, chemokine receptors and transmembrane protein gp41
  • antibodies allow some people to control virus - remain symptom free, and maintain high CD4 count
44
Q

what are the features of acute HIV syndrome? (3)

A
  • may experience mild acute illness
  • fever, malaise (general unwell feeling)
  • initial viraemia (subsides in a few days)
45
Q

describe the clinical features associated with HIV’s progression to a latency phase (3)

A
  • progressive loss of CD4+ T cells in lymphoid tissue + destruction of tissue structure
  • circulating CD4+ T cell count declines to under 200 cells / mm3 - classed as having AIDS (normal = 1500)
  • patients become more susceptible to opportunistic infections
46
Q

describe the basic clinical features of patients who have progressed to AIDS (2)

A
  • increased infections by microbes usually combated with T-cell immunity (opportunistic infection)
  • can also trigger activation of other latent viruses
47
Q

give examples of opportunistic infections that often present in AIDS patients (3)

A
  • Pneumocystis jiroveci - fungal infection, causes pneumocystis pneumonia
  • Candidiasis - caused by group of fungi (Candida) in various parts of the body
  • toxoplasmosis - parasitic disease caught from infected meat or cat faeces
48
Q

give examples of latent viruses that can be reactivated in AIDS patients (2)

A
  • Epstein-Barr virus - causes mononucleosis (glandular fever), then latency, can cause hairy leukoplakia (oral lesions) and lymphoma in AIDS patients
  • TB - caused by mycobacterium tuberculosis (leading cause of death in AID patients)
49
Q

give an example of a malignancy that AIDS patients are more susceptible to

A

Kaposi’s sarcoma - caused by human herpes virus 8 (HHV-8), presents with pigmented brown lesions

50
Q

give examples of antiretrovirals and how they work (6)

A
  • nucleoside reverse transcriptase inhibitors (NRTIs) - block enzyme required for reverse transcription
  • non-nucleoside reverse transcriptase inhibitors (NNRTIs) - block same enzyme in different location (same effect)
  • protease inhibitors - block the proteolytic cleavage of viral protein precursors, no new virions can be synthesised
  • post-attachment inhibitors - bind to CD4 to prevent HIV from binding to co-receptors after attaching to CD4, so protein cannot enter cell (POST-attachment)
  • CCR5 - block CCR5 co-receptor
  • integrase strand transfer inhibitors (INSTIs) - blocks integrase which incorporates viral DNA into host DNA
51
Q

what does the U=U aim to spread awareness about? (3)

A
  • undetectable = untransmittable
  • it has been proven that people with undetectable viral load cannot pass the disease on even during unprotected sex, and are prevented from developing AIDS
  • aims to tackle the stigma associated with having the disease
52
Q

what is PrEP? (2)

A
  • pre-exposure prophylaxis
  • medication (antiretrovirals) are taken before being exposed to the virus to prevent the spread - do not need to be taken consistently
53
Q

what is the difference between sterilising and non-sterilising immunity?

A
  • sterilising immunity clears the pathogen completely from the body, allowing recovery
  • non-sterilising immunity produces a good immune response, but it is not enough to clear the infection -> leads to chronic infection
54
Q

what are 2 examples of non-sterilising immunity? what is an example of an infection which produces an atypical immune response, but can produce sterilising immunity?

A
  • non-sterilising: HIV and Tuberculosis

* atypical: Dengue

55
Q

what bacteria causes TB? what are its cellular characteristics?

A
  • Mycobacterium tuberculosis

* appears G+ or G-, bacillus, forms clusters

56
Q

what property of the bacteria may contribute to TB being hard to diagnose?

A

• very slow replication rate (18-24 hours)

57
Q

why does TB particularly affect the lungs?

A

• thrives in high partial pressures of oxygen - usually more prevalent in the superior parts of the lung

58
Q

what type of necrosis does TB cause in the lungs?

A

• caseous - cheese-like, yellow and crumbly

59
Q

what is a granuloma? (2)

A
  • an aggregation of macrophages, epithelioid cells, T+B cells and fibroblasts
  • occurs when immune system attempts to isolate a foreign substance but fails to eliminate it
60
Q

what are epithelioid cells? (2)

A
  • activated form of macrophages

* aggregate forming multinucleated giant cells

61
Q

what is the basic pathogenesis of TB? (4)

A
  • after entrance of M.tb, 90-95% remain asymptomatic - enters latent phase
  • 10% develop active TB
  • reactivated eg. HIV infection, smoking, old age
  • progression to cavitary TB -> becomes infectious and is spread through coughing
62
Q

what is the initial immune response to TB infection? (3)

A
  • T-cell mediation, macrophages act as controlling cell
  • production of interferon gamma
  • attempted phagocytosis, but M.tb will survive in cells
63
Q

why can M.tb survive in phagocytes? (3)

A
  • bacterium will coat the phagosome with coronin (actin associated)
  • resists post-endocytosis trafficking to lysosome and so is not destroyed
  • also resists lysosomal action by pumping protons out of the vesicles to inhibit digestive enzymes
64
Q

what is an example of a genetic risk factor for severe TB infection?

A

lack interferon gamma receptor, so disease can spread to affect multiple organs

65
Q

what test and vaccine is used to detect / screen for high risk individuals (TB)?

A
  • BCG vaccine (Bacillus Calmette-Guérin) - weakened TB strain
  • Mantoux test - Tuberculin (TB proteins) are injected, if high risk (or actively infected), then a hypersensitive reaction will occur causing local inflammation -> diameter of inflammation is measured
66
Q

describe the T-spot test (3)

A
  • interferon gamma release assay
  • counts the number of leukocytes that release interferon gamma in a blood sample
  • can be used to detect latent TB infection
67
Q

how does dengue spread?

A

Aedes aegypti - mosquito bites (viral vector)

68
Q

what proportion of people infected with dengue go on to have symptoms?

A

15% experience mild symptoms, 5% develop severe disease (80% asymptomatic)

70
Q

what cells does dengue infect in the human body? what is a clinical consequence of this?

A
  • white blood cells

* increased cytokine and interferon release which may be the cause of some symptoms (fever and pain)

71
Q

why is a second dengue infection associated with increased risk of dengue haemorrhagic fever? (3)

A
  • 4 types of dengue strains
  • recovery from one strain gives lifelong immunity to that strain
  • a second infection from a different strain increases risk of severe disease because antibodies from the first strain actually increase uptake of the virus of the second strain
72
Q

what is the difference between primary and secondary imunodeficiency?

A
  • primary is congenital - results from genetic defects which are inherited from parents
  • secondary is acquired as a result of other diseases (eg. HIV, malnutrition, immunosuppression)
73
Q

what is a genetic characteristic of most primary immunodeficiencies?

A

recessive inheritance

74
Q

what clinical features develop from primary immunodeficiencies? (5)

A
  • recurrent infection in young
  • allergy
  • autoimmunity
  • abnormal lymphocyte proliferation (eg. lymphomas, leukaemias)
  • other cancers
75
Q

what is a common consequence of B cell / innate immune deficiency?

A

pyrogenic (fever-causing) bacterial infections

76
Q

what are 2 common consequences of T cell deficiencies?

A
  • viral and other intracellular microbial infections (unusually severe)
  • virus-associated malignancies (eg. EBV-associated lymphomas)
77
Q

what is an example of a severe combined immunodeficiency? what are its features (3)

A

X-linked SCID (severe combined immunodeficiency disease)
• “bubble boy” - David Vetter
• mutations in cytokine receptors - cytokines cannot bind
• T and NK cells fail, B cells normal but cannot produce efficient antibody responses

78
Q

what is an example of a less severe combined immunodeficiency? what are its features? (3)

A

Hyper IgM Syndrome
• high IgM (antibody that is produced first), but low of other antibodies (IgM not converted to other forms)
• more susceptible to infection
•fault on T cells -> impaired T/B cell interactions

79
Q

what is an example of a combined immunodeficiency with syndrome features? what are its features? (3)

A

FoxN1 deficiency
• athymic (no T cells)
• alopecia - syndrome feature
-> caused by lack of hair/thymic epithelium development

80
Q

what are the consequences of faulty antibody function (caused by antibody / humoral deficiencies)? (4)

A
  • recurrent sepsis
  • bacterial infections (often airways)
  • chronic gastroenteritis
  • failure to thrive
81
Q

what type of immunodeficiency is Bruton’s agammaglobinaemia? what are its features? (3)

A

• humoral defect (antibody deficiency)

  • mutation in tyrosine kinase gene
  • prevents B cell development
  • results in low antibody levels
82
Q

what type of immunodeficiency is IgA deficiency? what are its features (2)

A

• humoral (antibody deficiency)

  • IgA plasma cells do not develop
  • often asymptomatic (children sometimes outgrow the deficiency)
83
Q

what type of immunodeficiency is Chronic Granulamtous Disease (CGD)? what are its features? (2)

A

• congenital defect of phagocytes

  • no superoxide burst (used by macrophages to kill bacteria)
  • multiple granulomas form, ineffective elimination of bacteria
84
Q

what type of immunodeficiency is chronic mucocutaneous candidiasis an example of?

A

• defects in innate immunity (multiple causes)

85
Q

what type of immunodeficiency is Familial Mediterranean Fever an example of? what are its features? (2)

A

• autoinflammatory disorders

  • defect in inflammasome regulators
  • release too much IL-1 (inflammation attacks)
86
Q

what are the 3 phases of dengue infection? include typical symptoms for each

A
  • febrile: fever, pain, headache and rash
  • critical - some progress to critical phase as fever resolves: plasma leakage leading to fluid accumulation and decreased blood supply (can cause shock and haemorrhage)
  • recovery phase - fluid reabsorption: may have decreased heart rate and severe itching

Phase 1 (14 decks)

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