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3 IIH > 3.2 Intro to Virology > Flashcards

3.2 Intro to Virology Flashcards

1
Q

What is the difference between enveloped and non-enveloped viral structures?

A

enveloped have envelope from plasma membrane of previous host cell

(with some viral glycoproteins)

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2
Q

What are the 7 baltimore classifications of viruses?

A 
I - dsDNA (+/-)
II - ssDNA (+)
III - dsRNA (+/-)
IV -  ssRNA (+)
V - ssRNA (-)
VI - ssRNA (+) (RT)
VII - dsDNA (+/-) (RT)
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3
Q

What are the 2 ways a virus can enter a host cell?

A

direct fusion

receptor mediated endocytosis

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4
Q

What 2 steps in the viral life cycle are more specific to Herpes?

A

glycosylation

glycoprotein export

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5
Q

what drugs target virion uncoating and what are they used for?

A

amantadine, rimantadine

influenza

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6
Q

What drugs target DNA polymerase and what are they used against?

A

Nucleoside analogues

Herpes
HIV

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7
Q

What drugs target reverse transcriptase and what are they used against?

A

nucleosides

HIV

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8
Q

What drugs target Viral protease and what are they used against?

A

Ritonavir
liponavir

HIV

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9
Q

What drugs are used against viral neuraminidase, and what are they used against?

A

Sanamivir, oseltamivir

influenza A and B

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10
Q

What 2 main glycoproteins do we consider with influenza and what RNA segments are they associated with?

A

haemagglutinin (4)

neurominidase (6)

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11
Q

How many RNA segments does influenza have?

A

8

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12
Q

Which type of influenza causes pandemics?

A

A

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13
Q

How many subtypes of haemagglutinin are there?

A

18

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14
Q

How many subtypes of neurominidase are there?

A

11

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15
Q

What is the function of haemgglutnin for influenza?

A

mediates entry into target cells on airway epithelium

via alpha-2,3 sialic acid in humans

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16
Q

What is the immune response to influenza in the respiratory tract?

A

neutralising antibodies bind to HA on its’ binding site with alpha-2,3 sialic acid

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17
Q

What 2 types of antigenic variation do we associate with influenza?

A

genetic drift

genetic shift

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18
Q

Why do RNA viruses expereince genetic drift?

A

RNA polymerase does not posses the checking ability which DNA polymerase does

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19
Q

What is antigenic drift?

A

minor changes accumulating over a small amount of time, eventually ends up in a loss of immunity

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20
Q

What happens in antigenic shift?

A

if you get 2 different infections in one cell, the RNA segments can swap, resulting in new combinations of surface proteins

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21
Q

What is the distribution of sialic acid receptors in the human resporatory tract, and in birds?

A

alpha-2/6 receptors are kinda everywhere (notably in URT)
alpha-2/3 are confined to LRT

in birds, the alpha-2/3 receptors are everywhere, including URT

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22
Q

How does genetic shift navigate birds, and pigs to allow new influenza strains to reach humans?

A

avian influenza gets into pigs, human influenza coinfect the pig, they form a new virus that infects humans

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23
Q

What is the structure of Hep B?

A 
small
enveloped
ddDNA
Hep B surface antigen
Hep e antigen (HBeAg)
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24
Q

Name one characteristic of HBeAg

A

it is only expressed during replication

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25
Q

Name one characteristic of HBsAg

A

it has 3 sizes
smol
mediom
lorg

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26
Q

How many different viral genotypes are there of Hep B?

A

8

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27
Q

How infectious is Hep B, and how long can it survive outside the body?

A

very infectious, 50-100x more than HIV

7 days

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28
Q

How is Hep B usually transmitted?

A 
perinatal
parenatal (blood, blood products)
needles (inc body modifications)
sexual
body fluids
medical surfaces
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29
Q

name 7 high risk groups of Hep B

A 
homosexual sex doers
many sex doers
HCW's
IV drug users
blood transfusion recipients
solid organ transplant recipients
infants of HBV carrier mothers
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30
Q

What is the incubation period of HepB?

A

30-180 days

75 average

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31
Q

How serious is Hep B for adults and children?

A

children not so much, 80-90% are infected in their first year of life

adults bit worse, 20-30% who are chronically infected will develop cirrhosis and/or liver cancer

32
Q

What is the testing process for Hep B?

A

antibodies

one of the first thing we would see is HBeAg

33
Q

Which specific part of Hep B is the target for vaccination?

A

HBsAg

34
Q

Name 3 markers of a good immune response to HepB

A

loss of HBeAg
appearance of HBe antibodies
clearance of HBV DNA and HBsAg

35
Q

What will be evident in the serum of chronic Hep B sufferers, and why

A

Viral DNA
HBsAg
HBeAg
elevated serum ALT and AST levels

virus replication will come on and stay on

36
Q

When was Hep C and its’ vaccine discovered?

A

1989

we still don’t have a vaccine

37
Q

What is the structure of Hep C?

A

enveloped
ssRNA
small

38
Q

What is odd about Hep C down the microscope?

A

either attached to or around many lipid droplets

LDL’s interact with the cell surface to bring virus in close proximity with the cell and facilitate viral entry

39
Q

How is Hep C transmitted?

A

bloodborne only

so on equipment or during some sexual practices

40
Q

What is the incubation period for Hep C?

A

2 weeks - 6 months

41
Q

What proportion of Hep C holders show sympotms?

A

20%

42
Q

What proportion of adults and children develop chronic infection with Hep C?

A

infants (50-60%)

adults (50-90%)

43
Q

What is the lab test process for Hep C?

A

initial antibody screening
then viral nucleic acid (chronic infection?)
then cirrhosis test

44
Q

Why does Hep C have 6 different genotypes?

A

because it is an RNA virus and hence develops mutations - genetic drift

45
Q

What is the structure of HIV?

A

enveloped
ssRNA(+)
gp41 and gp120 surface glycoproteins

46
Q

What is the significance of HIV’s glycoproteins?

A

gp41, gp120

target the CD4 receptor and CXCR4 and CCR5 coreceptors

47
Q

Who are at risk of contracting HIV?

A 
heterosex (49% of new infections
homo sex
IV drug users
sex workers + clients
mother to child
48
Q

What is the incubation period of HIV?

A

2-4 weeks

49
Q

How does HIV integrate its’ genetic material into the host?

A

ssRNA reverse transcribed into dsDNA

50
Q

What happens to HIV RNA copies over time?

A

initially rapid increase, then slow increase until exponential growwth during opportunistic disease and ultimately death

51
Q

What happens to CD4 TL count after infection with HIV?

A

rapid decrease, increase only after HIV RNA copies subsides

then long term steady decrease to death

52
Q

What facilitates the rapid division when HIV reappears?

A

the CD4 T cell count drops below a certain point, the BANG

53
Q

Name 3 AIDS defining opportunistic infections

A

cryptococcal meningitis
toxoplasmosis
pneumocystis pneumonia

54
Q

How long do people survive with AIDS?

A

maximum of 3 years

55
Q

What sort of cancer can AIDS result in?

A

Kaposi’s sarcoma

56
Q

Can HIV be transmitted through saliva?

A

NO

57
Q

What are the lab tests available for HIV?

A

HIV antibody test in screening
Nucleic acid test
antigen / antibody test

58
Q

When might we use a nucleic acid test for HIV?

A

only used for high risk exposures

59
Q

What antigen is targeted for testing in HIV patients?

A

p24, which is made by infected cells and detected before antibodies

60
Q

What proportion of all HIV sufferers are HIV-1, what are the subtypes, and where does HIV-1 come from?

A

95%
MNOP
Gorillas and chimpanzees

61
Q

Where do we tend to see HIV-2, and what are the differences between HIV-2 and HIV-1?

A

concentrated in West Africa

less infectious progresses more slowly

62
Q

What are NNRTI drugs and how do they work with HIV-2?

A

nucleoside and nucleotide reverse transcriptase inhibitors

they don’t this is bad

63
Q

How many subgroups of HIV-2 are there, and where are they from?

A

8

developed from SIV in Sooty Mangabeys

64
Q

Do HIV subgroups really matter?

A

nope, we don’t really understand them

most antibodies are tested against HIV-1 MB as it’s the most prevalent in the west

65
Q

Name the 8 types of Herpes virus

A 
Herpes Simplex 1 (HSV 1)
Herpes Simplex 2 (HSV 2)
Human Cytomegalovirus (HCMV)
Varicella Zoster Virus (VZV)
Epstein Barr Virus (EBV)
Human Herpes VIrus 6A/6B (HHV-6A/6B)
Human Herpes Virus 7 (HHV 7)
Haposi's Sarcoma associated Herpes Virus (KSHV / HHV 8)
66
Q

What kind of proteins are in Herpes viruses?

What do they do?

A

tegument proteins

innate immunity recognises them, although the tegument proteins ulitmately lead to their destruction

67
Q

How is Herpes transmitted?

A

moscontagious when symptoms are present

oral - oral - genital- genital

68
Q

Why might women be worse off with herpes?

A

genital herpes (HSV 2) will have excruiciating outbreaks during menstruation

69
Q

What does the Lytic cycle cause?

A

stomatitis

70
Q

What are the stages of the Lytic cycle?

A

infection of muscoepithelial cells
replication of musculopepithalial cells
infectious virus release

71
Q

What are the stages to latency with Herpes?

A

immunologicall silent infection by turning off viral gene expression
reactivation occurs periodically
replication in mucoepithelial cells
infectious virus release

72
Q

How does Herpes interact with the nervous system?

A

silent in Trigeminal ganglia (HSV 1)
silent in sacral ganglia (HSV 2)

HSV and VZV can go to CNS and cause meningitis and encephalitis

73
Q

What is the difference between primary and secondary infection of VZV?

A

priamry - chicken pox

secondary - shingles

74
Q

How does shingles cause skin issues?

A

when it reactivates it moves down the nerve and to the dermatome

75
Q

What is Epstein Barr virus?

A

tumour virus, causes lymphoma is uncontrolled

76
Q

What can CMV cause?

A

retinitis (blindness)

GVHD

3 IIH (23 decks)

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