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CB of Immunity > Immune response to viral infections > Flashcards

Immune response to viral infections Flashcards

1
Q

Obligate intracellular viruses

A

dependent on host proteins for replication (contain as few as 3 genes). genomes enclosed within caspids

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2
Q

Cytopathic viruses (lytic)

A

e.g. poliovirus and influenza virus - lyse cell by inducing autophagy or apoptosis

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3
Q

Latent virus

A

e.g. herpes - initial infection then just lay dormant for 30 years until the immune system becomes weakened

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4
Q

Non-cytopathic viruses

A

e.g. hepatitis B - don’t induce cell destruction

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5
Q

intestinal viruses

A

e.g. poliovirus enter via antigen-sampling M cells

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6
Q

respiratory viruses e.g.

A

influenza virus establish infection in the epithelial cells of the airways

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7
Q

insect vectors for transmission

A

e.g. dengue virus and West Nile virus

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8
Q

bloodborne viruses

A

e.g. HIV and hepatitis B can invade through mucosa or epithelia following physical trauma,

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9
Q

Tissue tropism

A

Viruses bind to receptors on the outside of the cell which causes a conformational change, allowing them to enter into the cell

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10
Q

Tissue tropism of HIV

A

use CD4 receptor on outside of t cells, chemokine receptors (CXCR4 and CCR5) and c-type lectin receptors (CD209)

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11
Q

innate immunity against viruses

A

mediatd via type 1 interferons, complement and NK

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12
Q

adaptive immunity against viruses

A

mediated via antibody and cytotoxic T lymphocytes

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13
Q

Fc-gamma-RIII

A

found on NK cells which bind to Fc region of IgG (bound to viral particle)

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14
Q

Epidemic

A

classification of a disease that appears as new cases in a given human population, during a given period, at a rate that substantially exceeds what is “expected” based on recent evidence

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15
Q

pandemic

A

an epidemic that spreads through human populations across a large region, e.g. a continent, worldwide

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16
Q

HIV

A

human immunodeficiency virus

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17
Q

AIDS

A

acquired immune deficiency syndrome

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18
Q

HIV causes AIDS. How?

A

destroys CD4+ T cells

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19
Q

PCP

A

pneumocystis carinii pneumonia. highly prevelant but affects immunosuppressed

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20
Q

GRID

A

gay-related immune deficiency in 1980s

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21
Q

ART

A

anti-retroviral therapy

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22
Q

HIV-1

A

most cases of human AIDS caused by this particular virus

23
Q

HIV-1 (simian immunodeficiency virus)

A

originates from chimpanzees. retrovirus.

24
Q

HIV enters epithelial barriers

A

M cells can take up whole virion and transcytose it.
Vaginal epithelium doesn’t have M cells - Langerhan’s cells.
Small intestine epithelial cells express CCR5 (chemokine receptor. CCR5 binds HIV via viral envelope glycoprotein gp120.

25
Q

HIV transport to lymph nodes

A

Once passed epithelial cells, HIV encounters sub-endothelial DC, which have C-type lectin receptors (CLRs) that bind the high-mannose oligosaccharide on gp120. DC migrates to lymph nodes then presents HIV to interact with T cells.

26
Q

Small intestine and HIV

A

Predominant site of HIV replication in early stage replication is in the small intestine - large number of T cells expressing CCR5 in this organ

27
Q

gp120

A

viral envelope glycoprotein. mediates HIV entry into cells, which then binds to CD4 of chemokine (CCR5 or CXCR4) receptors on host surfaces.

28
Q

gp41

A

binding with receptor leads to a conformational change in gp120, exposing the transmembrane component of the envelop protein gp41. gp41 mediates fusion of the virus envelope with host cell membrane.

29
Q

Immunological consequences of HIV infection

A

DC translocates HIV from mucosa within 30 minutes and takes to CD4.
Wave of viral proliferatio in lymph nodes peaks 4-7 days after infection.
Viremia peaks at 14 days and all lymphoid tissues infected by 3 weeks.
>99% of virus is produced by newly infected CD4 T cells.
Loss of helper activities (mainly through loss of cytokine stimulation) leads to a loss in CD8 maintenance and antibody response of B cells.

30
Q

Quiescent

A

HIV is in a state of dormancy within resting CD4 T cells (years). on T cell activation, virus production is also activated and the host cell dies.

31
Q

progression of untreated HIV

A

Flu like symptoms initially due to drop in CD4.
Flush of CD8 is responsible for prolonged period of stable viremia = VIRAL SET POINT.
normally asymptomatic until CD4 levels decline further below threshold of <200 cells/ul. Opportunistic infections arise and even developing lymphocytes in bone marrow and thymus get infected and are unable to replace lost T cells.
Death by 2 years.

32
Q

AIDS and microbial infection

A

cryptococcal meningitis. Candidasis. Pneumocystis carinii pneumonia. Tuberculosis. Herpes simplex. Shingles. Genital herpes. Human papillomavirus.

33
Q

Influenza

A

A, B and C subtypes.
A and B cause disease.
A causes pandemic.
Avian (birds) disease that adapted to humans.
Aerosol spores that cause cytolytic infection in respiratory tract.

34
Q

Hemagglutinin

A

HA. Trimeric. Mediates binding to cell surface and internalisation.

35
Q

Neuraminidase

A

NA. Tetrameric. Cleaves sialic acid and promotes viral release from cells.

36
Q

Binding and Budding of Influenza A virus

A

Influenza A binds to the cell membrane HA interacting with a membrrane protein Sialic Acid. It is endocytosed and uncoates, enters the nucleus for RNA replication. Viral proteins come together in the cytosol and with NA, it starts to bud and is then released from the cell as a new viral molecule/.

37
Q

influenza genotypes

A

H1-H15. N1-N9.

38
Q

avian viruses, human viruses and pig viruses (influenza)

A

Avian influenza viruses prefer receptors (primarily in the intestinal cells) that have alpha-2,3 sialic acid linkage to galactose.
Human viruses prefer the alpha-2,6 linkage on respiratory epithelial cells.
Pig viruses express both types of linkage on respiratory epithelial cells

39
Q

When does influenza enter the human population.

A

When humans, pigs, waterfowl and domestic chickens are in close proximity.
Pigs can be infected by both avian and human influenza –> exchange of segments between viral genomes in the pig can give rise to variants expressing novel surface proteins together with human-adapted virulence determinants.

40
Q

immune response to influenza

A

Neutralising antibodies to prevent the binding to sialic acid receptors.
NA-specific antibodies tether to the virus as it leaves the cell - not able to infect other cells.
adaptive response mainly through CD8+ and NK cells - perforin and granzyme (MHCI)

41
Q

Epidemic of influenza and ANTIGENIC DRIFT

A

when point mutations accumulate in surface HA or NA and antigenic drift occurs - neutralising antibodies from previous infections no longer recognise the NA or HA

42
Q

Pandemic of influenza and ANTIGENIC SHIFT

A

Human and avian influenza virus infect a pig - re-assortment of the two genomes lead to the expression of avian HA or NA in a virus otherwise adapted to infect humans = ANTIGENIC SHIFT

43
Q

Neutralising antibodies

A

Neutralise the ability of the virus to bind and infect the cell

44
Q

influenza pandemic

A

human infections are generally, but not exclusively, limited to viruses that express the following subtypes: H1, H2 or H3, AND N1, N2 and possibly N8

45
Q

Spanish flu pandemic

A

1918-1920, H1N1

46
Q

Asian flu pandemic

A

1957-1958, H2N2

47
Q

Hong Kong flu pandemic

A

1968-1970, H3N2

48
Q

21st century global pandemic expected deaths

A

2 million - 360 million and even up to 1 billion. Analogue to the Spanish flu is thought inevitable!

49
Q

Spanish flu

A

Influenza A H1N1. 50-100 million deaths (25million in first 25 weeks) - deadlier than AIDS.
Caused by hypercytokinemia (cytokine storm)

50
Q

Cytokine storm (hypercytokinemia)

A

Systemic expression of a healthy and vigorous immune system. Release of >150 inflammatory mediators (pro/anti-inflammatory cytokines, free radicals, coagulation factors, etc.)
Leads to massive damage of epithelial cells.
Seen in many infectious and non-infectious diseases, e.g. Ebola, sepsis, ARDS, avian influenza.

51
Q

Why is a 21st Centrury flu pandemic inevitable?

A

Highly Pathogenic Avian Influenza (HPAI) express H5, H7 or H9 - established in poultry through China and Southeast Asia.
HPAI H5N1 viruses transmitted to individuals exposed to poultry during outbreaks in Hong Kong 1997.
Pigs in China infected with avian H5N1 and human H3N2 virus strains, responsible for HK 1968-70 outbreak.

52
Q

Ebola Hemorrhagic Fever

A

Enzooti cycle (bats) and epizootic cycle (bats-chimpanzees). Human infection through eating bushmeat.

53
Q

Ebola genes

A

ssRNA (19kB genome).
7 genes.
Important gene is glycoprotein (GP) that codes for two forms:
1. trimeric transmembrane GP (allows virus to enter monocytes and macrophages, causing cytokine dysregulation and vascular instability shock.
2. soluble dimeric form (sGP) which is secreted after infection and prevents neutrophil activation

CB of Immunity (12 decks)

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