viruses Flashcards

1
Q

non- enveloped vs enveloped?

A

NAKED (non-enveloped):

  • survive well
  • may be bile resistant
  • tougher capsid - harder to disinfect
  • faecal oral route transmission

ENVELOPED:

  • survive transiently outside
  • spread by close contact/intimacy/blood/sneezes and coughs etc…
  • capsid can dry out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the envelopes made of?

A

lipid bilayer of host origin
PLUS viral-encoded glycoprotein spikes that:
- have receptors to target next cell to attack
- help attach to new cell and facilitate entry
- are the targets for antibodies of host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pox virus - capsid symmetry? and is it enveloped?

A

COMPLEX enveloped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the 3 capside symmetries

A

Complex, helical and icosahedral. They can all be DNA strands and can all be enveloped.

COMPLEX can only be DNA strand and can ONLY be enveloped

HELICAL can be DNA or RNA but ONLY enveloped also

ISOHEDRAL can be anything.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

HIV virus? enveloped? capsid? RNA/DNA?

A

retrovirus so - enveloped + ICOSAHEDRAL + RNA strand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do retroviruses work?

A

use reverse transcriptase to turn their RNA strand into cDNA and then integrate that into host DNA using integrase before transcribing itself again and reproducing and releasing itself out to infect more cells - a process requiring protease to cleave GAG into matrix, capsid and nucleocapsid (enabling it to be infectious)

(3 enzymes to rmb: reverse transcriptase, integrase, protease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does HIV require to get into the cell?

A

CD4 and chemokine receptors either CCR5 or CXCR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the important viral load figures to remember?

A

less than 50 means it’s very controlled and AIDS free. Over 200 = AIDS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TAT?

A

activator of viral transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

REV?

A

mediates RNA nuclear export

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

VIF?

A

works against APOBEC to ensure virus not too mutated and still functional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is APOBEC?

A

protein that mutates virus by changing C to U on DNA strand - can be both good and bad (APOBEC3 is host protein that also inhibits RT), but mutations can also cause virus to evade immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NEF?

A

removes CD4 from surface of cell - stops T-cells from working

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

VPU

A

destroys tetherin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What’s tetherin?

A

protein that inhibits release of virus from cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SERIN C?

A

interferes with viral entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SAMHD1

A

suppresses RT in myeloid cells by hydrolyzing dNTPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what cells are affected by HIV?

A

Mainly CD4 depletion, loss of memory t-cells,
DC, macrophages also affected and can enhance t-cell infectivity
GALT also affected and can never recover even with therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which cell controls the acute infection phase of HIV?

A

CD8 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is HIV diagnosed?

A

ELISA to look for anti-p24 (capsid) antibodies IF already seroconverted (usually after 3 months)
pre conversion must use RT-PCR - blood test to confirm (pinprick needed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

List some opportunistic infections that are associated w HIV

A
Kaposi's sarcoma
CMV
pneumococi jirovecii
candida
pneumocystis carinii
toxoplasmosis
reactivation of herpes simplex
MCB TB
MCB avium complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe HAART

A

combination of 3 HIV drugs used to fight mutation

Usually 2 NRTI (nucleoside reverse transcriptase inhibitors) + 1 NNRT (non-NRTI) OR 1 protease inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

positive RNA strands means? negative strand means?

A

positive RNA strands are equivalent to mRNA strand so can immediately be translated, unlike negative strands that must first be converted to positive strands. cells with negative RNA strands need replicative polymerase enzyme to make new negative strands from positive strands because cells don’t contain that enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In any lymphoma/ see lymph nodes what virus should you suspect?

A

EBV

also in nasopharyngeal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what cancers can HPV cause?

A

cervical carcinoma

anogenital & vulvo-perineal tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the body’s first line of defence against viruses?

A

interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

DNA viruses are HHAPPPPy

A

Herpes, Hepad, Adeno, Papilo, Parvo, Polyoma, Pox

Hs and Pox have envelope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the name of the stage for the time between exposure and onset of a specific clinical sign?

A

Incubation period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the name of the stage where non-specific symptoms like fever and loss of appetite occur?

A

Prodrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What do superantigens increase the process of?

A

SEPSIS

31
Q

How to diagnose hepatitis

A

LFTs ALT:AST ratio should be both raised and abount 1:1
ALT is the more important marker for inflammation

Should look for Hx viral load, HbeAg, Hx core IgM (if seen had infection within last 6 months)

Alpha-fetoprotein - if raised is indication of possible cirrhosis, hepatitis and is risk factor for hepatocellular carcinoma

Antibodies: look for ANA + ASMA = HEPC
ANA + SMA = autoimmune hepatitis

Fibroscan and ultrasound to truly diagnose - assess liver fibrosis level, fatty deposits and general composition

Might biopsy depending on other results.

32
Q

How are Hep A and Hep E alike?

A

Both ss-RNA naked

Both don’t cause chronic illnesses usually.
(Hep E can be chronic in immunosuppressed individuals.)

Have similar incubation periods (A: 3-5/E:6), lab diagnosis and transmission (faeco-oral/person to person transmission: hep A - raw fruit, shellfish; hep E - uncooked raw meat, sewage contaminated water and blood transmission)

Both diagnosed by looking for HA/EV IgM in blood samples

33
Q

Which Hep viruses can cause chronic infection? What symptoms are associated with this?

A

B, C, D, (E only in immunocompromised)
You can only get D if also B positive surface antigens present.

Associated with chronic liver disease, chronic active/persistent hepatitis, cirrhosis which can lead to hepatocellular carcinoma

34
Q

What are some non-specific symptoms of hepatits?

A
Jaundice
Right hypochondriac quadrant pain
Dark urine (bilirubin)
Clay coloured faeces (bilirubin)
Nausea and vomiting
Malaise
Fever
Headache
35
Q

HEP E mortality in pregnancy?

A

20-40%

36
Q

How to treat Hep A?

A

No real treatment, mainly symptomatic control
There is a Hep A vaccine to prevent spread - offered to high risk individuals e.g. travelling to a poor country that might be less hygienic

37
Q

How to treat Hep E?

A

Persistent infection in immunocompromised patients can be treated with ribavirin (antiviral agent) or interferon (immunomodulator)

38
Q

How do you interpret serology for Hep B

A

HbsAg - only seen when infection actively happening (can be acute or chronic)
Hb c Ab - seen in anyone who’s ever been infected or is currently infected
Hb core IgM - seen in anyone who’s been acutely infected within last 6 months
Hb e antigen/antibody - if present, and Hb core IgM is high, could be chronic infection as it raises IgM.
Hb surface antibody - if above 10 mIU/ml = no infection - either had it way in past or is vaccinated for it.

39
Q

Describe how Hep B works

A

it is a dsDNA with reverse transcriptase
incubation period of a few months (2.5 ish)
transmitted by blood, injecting, piercings, tattoos

If get ACUTE - icteric and then resolves
If CARRIER - HbaAg is in circulation for more than 6 months; usually anicteric, but can lead to cirrhosis and hepatocellular carcinoma.

Pathogenesis: viral replication and immune mediated cytotoxicity + host chromosomal infections

40
Q

How to treat/prevent/control Hep B

A

Vaccine available
Give antiviral prophylaxis for transplants if they’ve had hep b in the past
Hep B carriers not allowed to be doctors (?)

Treat with antiviral therapy: adefovir, lamivudibem tenofovir, entecavir - won’t kill but will stop replication
Also give interferon

41
Q

How does Hep D work

A

ssRNA virus enveloped by HbsAg, needs it to survive.

Hep B vaccination is protective against it

42
Q

How does Hep C work

A

ssRNA enveloped flavivirus
transmitted with injecting, blood, tattoos, piercings, vertical route (mother to child) and sexual intercourse (lower risk)
40% route unknown
incubation period 6-12 weeks

Majority of people don’t know they have the disease -75% present with a bit of abdominal pain and LFTs that are only slightly off.
20% are icteric but resolves on tis own.

40-50% of carriers can get chronic liver damage and of these 20% can get cirrhosis and potentially develop hepatocellular carcinoma

43
Q

How to treat Hep C

A

With antivirals - can eradicate infection as long as virus doesn’t integrate itself into the chromosome.

44
Q

What is an eclipse phase?

A

period from viral entry to release of infected virions

45
Q

Describe the herpesviridae family

A

Large dsDNA
Isohedral
Enveloped
All members morphologically similar under EM

46
Q

What are three classes of herpesviridae and what are they each known for? +give 2 examples of each

A

Alpha, beta and gammeherpesviridae
Alpha e.g. VZV and herpes simplex 1,2 known for causing blisters and having neuronal latency
Beta e.g. CMV and HP 6,7, known for only affecting immunocompromised
Gamma e.g. EBV and HP8, known for causing malignancies

47
Q

Lytic vs latent infection?

A

Lytic is when viruses are replicating, host cells are productively infective
Latent is when no more virions are made but cells still infected - can be reactivated

48
Q

Does a seropositive status indicate infection or immunity?

A

infection

49
Q

What antivirals are used to treat herpes virus?

A

Acyclovir, ganciclovir
(ends w CLOVIR)
doesn’t eradicate only controls latent infection

50
Q

Describe the structure of a varicella zoster virus (VZV)

A

Large dsDNA enveloped, isocahedral

an alphaherpesvirinae

51
Q

Where is latency of VZV?

A

In dorsal or cranial nerve ganglia

Reactivation causes shingles

52
Q

What are potential complications of VZV/HZV?

A

Severe haemorrhagic varicella - problems clotting
Secondary bacterial infection causing pneumonia or rash
Encephalitis
Acute cerebellar ataxia (especially in kids - start walking funny and off balance)
Visceral inflammation (especially seen in immunocompromised): pneumonitis, hepatitis, meningoencephalitis

With shingles can also affect trigeminal nerve sensory area - can cause eye- 50% and cause loss of eye sight
(in opthalmic zoster - mandatory opthalmological assessment)

In elderly post-herpetic neuralgia can occur - pain that goes on and on

53
Q

When is the infectivity and incubation period for VZV

A

Incubation is 10-21 days after exposure

Infectivity is from 48hrs before rash developed to until all lesions are crusted over

54
Q

What memory cells remain after primary infection of VZV

A

VZV specific IgG and IgA

VZV specific CD4 and CD8 t-cells

55
Q

How is VZV transmitted?

A

Respiratory route before rash
Skin lesions also infective
Shingles spread by contact e.g. door handles

Maternal varicella in first 20 weeks gestation can result (2%) in fetal abnormalities
Maternal shingle is harmless to fetus
Perinatal infection can cause neonatal varicella (associated with high mortality of infant)

56
Q

What prophylaxis measures are there for VZV?

A

Varivax vaccine - administer within 72 hours (but live vaccine so not for immunicompromised)

Varicella zoster immunoglobulin - administer within 7 days of significant contact e.g. pregnant, immunosuppressed, or neonate of a seronegative mother

57
Q

How to treat VZV

A

None given in uncomplicated childhood chicken pox
Give anti-virals in adults and immunocompromised
- Aciclovir (can be IV), valacivlovir, famciclovir
- if given orally give with amino acid valine to increase its absorption in GI tract

Need more to treat VZV than HZV

58
Q

What vaccines are there for VZV/HZV?

A

Oka varicella vaccine

  • live vaccine
  • may still develop chicken pox but will be less severe
  • can cause rash

Zoster vaccine

  • recommended when over 70
  • reduces risk of shingles and post-herpetic neuralgia
59
Q

What is bronchiolitis?

A

Inflammation of the bronchioles - smallest airways of the lungs - become inflamed and infected

60
Q

What causes bronchiolitis?

A

Most commonly RSV - respiratory synctium virus

61
Q

Who gets bronchiolitis?

A

90% of children 0-2.
Peaks at 2-5 months
Rare in first month of life and after 2 years
Very low mortality 0.002%

Can also get infected by RSV post hematopoeictic stem cell transplantation - from URTI to LRTI (50% nosocomially acquired)

62
Q

What lines respiratory airways?

A

Cilliated psudostratified columnar epithelial cells

63
Q

What lines the back of mouth and throat?

A

Mucosa - stratified squamous epithelium

64
Q

What is croup?

A

Laryngo-tracheo-Bronchitis

Presents with hoarseness, barking cough and stridor

65
Q

What is croup caused by?

A

Mainly parainfluenza viruses

66
Q

What are common viral causes of pneumonia?

A

Influenza virus
RSV
Adenoviruses

67
Q

What two viruses transmit with large droplets

A

RSV and the common cold

68
Q

Descrive the influenza virus structure

A

RNA capsid, enveloped with two main glycoprotein:
H - haemaglutinin - binds to cell it wants to enter at sialic acid receptor
N - neuroaminidase - helps virus cleave off and be released

Ion channel is M2: releases virus

69
Q

What diseases do coronaviruses lead to?

A

Mostly common cold or other benign respiratory infection. But can be more severe: SARS & MERS

70
Q

ebola is what kind of virus?

A

filovirus

ssRNA enveloped

71
Q

where in body does ebola effect?

A

liver, kidney, GI tract, respiratory system,

most die within few weeks from renal failure due to hypotensive shock

72
Q

lab findings of ebola

A

minimal abnormalities in early stages
low thrombocytopaenia
AST>ALT
hypo all salts ca, k, na, mg

73
Q

what is vaccine for ebola called?

A

rVSV-EBOV

74
Q

what type of virus is Zika?

A

flavivirus