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MICRO > Ch4: Skin, Musculoskeletal, Blood, and Lymph Part II > Flashcards

Ch4: Skin, Musculoskeletal, Blood, and Lymph Part II Flashcards

1
Q

Infections of joint and bone include? 4

A
  1. Parovirus B19: Developed countries (Slapped cheek)
  2. Rubella: Nonvaccinated adults
  3. Hep B: HIV-1 and HTLV-1
  4. Alphavirus
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2
Q

5 classic childhood viral rashes?

A
  1. Measles: Rubeola
  2. German measles: Rubella
  3. Roseola
  4. Fifth disease
  5. Chickenpox: Varicella zoster
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3
Q

5 herpes virus of skin?

A
  1. Herpes simplexes 1 and 2
  2. Varicella zoster
  3. Human herpes virus 6, 7, 8
  4. EBV
  5. CMV
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4
Q

4 families of viruses of skin?

A
  1. Herpes
  2. HPV
  3. Coxsackie
  4. Poxviruses
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5
Q

3 subfamilies of herpesvirus?
Which has short growth cycle?
Which has long?

A

Alpha: Short
Beta: Long
Gamma

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6
Q

Members of alpha herpes family? 3

A

HSV-1
HSV-2
Varcicella Zoster

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7
Q

Members of gamma herpes family? 2

A

EBV: HSV-4

Kaposi’ sarcoma: HHV-8

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8
Q

Members of beta herpes family? 3

A

CMV (HHV-5)
HHV-6
HHV-7

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9
Q 
In terms of herpes
Size?
Envelope presence?
Genome shape? 
Genome type? 
Shape of capsule?
A 
Large
Enveloped
Linear
DsDNA
Icosadeltahedral
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10
Q

Since herpes have a capsule, they have a tegument which contains what?

A

Enzymes for replication

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11
Q

What determines what cell/tissue, the herpes virus attacks?

A

Receptors

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12
Q

What are the viral adhesins of herpesvirus?

A

Envelope glycoproteins

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13
Q

What is the primary manifestation of herpesvirus in humans?

A

Common infections but benign in children

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14
Q

What is the immune response of herpesvirus?

A

CMI

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15
Q

What is the primary treatment of herpesvirus?

A

Targeting viral DNA polymerase

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16
Q

What main feature do all herpesviruses have?

A

Latency

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17
Q

How do viruses do latency? (2)

A
  1. Make non-encoding transcripts that prevent apoptosis

2. Express proteins during latency

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18
Q

What is state of herpesvirus genomes during latency?

A

Circular, episomal form separate from host genome

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19
Q

How are herpesviruses spread? 3

A

Respiratory droplets
Oral mucosa
DIrect contact

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20
Q

What herpesviruses can be be spread without symptoms?

A 
HSV 1-2
EBV 4
CMV 5
HHV-6
HHV-7
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21
Q

When is VZV transmitted?

A

Only when patient has varicella or zoster

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22
Q

What is required for HSV spreading?

A

Direct contact

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23
Q

Most herpesviruses are diagnosed how?

A

Clinical symptoms

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24
Q

What is used in confirming acute or previous herpesvirus infection?

A

Serology

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25
Q

PCR is used to test what herpesvirus?

1-6

A 
HSV 1-2
VZV 3
EBV 4
CMV 5
HHV-6
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26
Q

How to detect VZV in ski nlesions?

A

Ab testing

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27
Q

What herpesviruses cause both intranuclear and cytoplasmic inclusions?

A

CMV 5

HHV-6

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28
Q

What herpesviruses result in only intranuclear inclusions?

A

HSV 1-2

VZV 3

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29
Q

HSV 1-2 infection
Can infect what cell types?
Where is it lytic? (2)
Where is it latent?

A

Most cell types
Mucoepithelial and fibroblasts
Neurons

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30
Q 
Where does HSV-1,2 
initially attach? 
What gives it a tight binding? (2)
What does gC do? 
What does gE and GI do?
A

Heparin sulfate proteoglycans

Nectin-1alpha and HVEM

Binds to and depletes C3 from seru

Complex with Fc on IgG

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31
Q

Which is worse for HSV, 1-2

Primary eruption or recurrence?

A

Primary eruption

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32
Q

What happens in primary eruption of HSV?

A

Vesicle that erupts into a wet ulcer with pain and itching an dmalaise and fever.

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33
Q

What happens in recurrence of HSV?

A

Lesions with some local symptoms

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34
Q

Where does the HSV remain latent?

A

Trigeminal or sacral nerve

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35
Q

First episode of HSV-1 has what two features?

A

Gingivostomatitis

Pharyngitis

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36
Q

How do primary lesions look in HSV?

A

Dewdrop on rose petal

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37
Q

First episode primary genital herpes lasts how long?

A

Longer: 10-12 days

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38
Q

First episodes of genital herpes caused by HSV-2 in patients who already had HSV-1 are different how? 2

A
  1. Less frequent systemic symptoms

2. Faster healing

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39
Q

Herpetic Whitlow signs include what? (3)

A

Edema
Erythema
Localized tenderness at finger

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40
Q

Herpes gladiatorum is seen in who?
Why?
Where do they have herpes lesions?

A

Wrestlers
Trauma to skin transmission
Thorax, ears, face, hands

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41
Q

In patients with eczema, how does HSV present?

A

Eczema herpeticum

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42
Q

Reactivation triggers of HSV? (5)

A
  1. Fever
  2. Nerve injury
  3. UV
  4. Stress
  5. Hormone changes
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43
Q

HSV Reactivation sees what changes in immune response?

A

Shift from HSV-specific T cells to Th2 cells

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44
Q

What is different about location of lesions in recurrence of HSV?

A

Only one one side of body

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45
Q

Innate response to HSV?
CMI response to HSV?
How does HSV counteract? 2

A

IFN and NK cells limit progression
CMI kills infected cells

  1. Blocks IFN
  2. Blocks TAP proteins –> No MHC Class I
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46
Q

Incubation period of HSV 1-2?

A

1-26 but usually 6-8

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47
Q

How to stain for HSV? (3)

A
  1. Wright
  2. Giemsa (Tzanck preparation)
  3. Pap
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48
Q

Things seen upon HSV staining? 3

A
  1. Cowdry type A acidophilic intranuclear inclusions
  2. Syncytia
  3. Giant cells
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49
Q

What can you not separate HSV from upon staining?

A

VZV

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50
Q

Treatment of HSV?

A

Acyclovir

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51
Q

VZV is broken into what two parts?

A 
Varicella = Primary
Zoster = Recurrence
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52
Q

What keeps VZV in latency?

A

T cell response

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53
Q

What allows zoster to reoccur?

A

T cells aging leading to shingles

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54
Q

How does VZV infect and remain latent in body?

A

Droplets inhaled –> Gets in lymphatics (Primary viremeia) –> Goes to secondary lymph organs –> Gets in blood (Secondary viremia) –> Goes to skin –> Goes into latency in neurons

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55
Q

Rash is described how in VZV?

A

Cropping rash that are at one location for one stage in disease

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56
Q

How is VZV described?
How long does the dermal rash last?
Where does the rash occur most? 2

A

Self-limiting infection
3-5 days of cropping
Trunk and SCALP

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57
Q

How is VZV infection different in adults for first time?

A

More serious: Pneumonia and encephalitis

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58
Q

How long does VSV incubation last?

A

10-21 days

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59
Q

Reactivation of VZV results in what?

A

Zoster or Shingles

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60
Q

Where does Zoster/Shingles occur?

A

Entire dermotome due to virus at that nerve root spreading down it.

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61
Q

What dermatomes are most involved in zoster/shingles?

A

Thoracic and lumbar

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62
Q

Herpes zoster goes where if 1st or 2nd branch of 5th cranial nerve is affected?

A

Eyelids

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63
Q

How does someone know a shingles attack is coming?

What happens after?

A

Pain in dermotome 2-3 days before

Chronic debilitating pain

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64
Q

Zoster/shingles last how long?

A

10-15 days

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65
Q

Zoster/shingles is seen in what % of population?

A

Over 45 years old

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66
Q

Immune response to VSV? 2

Evasion? 3

A
  1. CMI
  2. TLR-2 of innate
  3. FcRgammaII receptor
  4. Inhibition of MHC-I
  5. Decreased IFN-gamma
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67
Q

Route of transmission of VZV?

A

Respiratory

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68
Q

Latency of VZV?

A

Sensory neuronal cells (trigeminal, dorsal root, cranial ganglia)

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69
Q

How is VZV different during latency from other herpes?

A

Expresses different RNA transcripts during latency

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70
Q

How do you diagnose VZV?

A

Same as you would HSV 1-2
Stains
PCR

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71
Q

How do you treat adult zoster infections? (3)

A
  1. Acyclovir (DNA Poly inhibitors)
  2. Pain killers
  3. Plasma
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72
Q

How do you treat someone with chickenpox? 2

A
  1. Good hygiene

2. Acetaminophen

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73
Q

The vaccine for VSV is in what form?

A

Live attenuated Oka strain

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74
Q

The VSV vaccine has what immune reaction?

A

T cell immunity

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75
Q

Zoster vaccine is different from VSV vaccine how?

A

High titer version of Oka

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76
Q

What is common side effect of VSV vaccine?

What is the risk factor for it?

A

Rash

Immunosuppressed

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77
Q

HHV-6 and HHV-7 infect what type of cells?
What do they cause?
What patients do they reactivate in?

A

T cells

Exanthema subitum/roseola infantum

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78
Q

Two types of HHV-6?

A

HHV-6A and HHV-6B

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79
Q

HHV-6 lives where?
Infects what type of T Cells?
HHV-6A likes what type of cells?
HHV-6B likes what type of cells

A

CNS

CD4

Neural cells

Peripheral Blood Mononuclear cells

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80
Q

HHV-6 is in what type of form in WBC’s?

Infection in these cells appears how?

A

Latent

ballooning cells with intranuclear inclusions

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81
Q

What percentage of adults are seropositive for HHV-6?

Why do moms pass on HHV-6 to their kids so easily?

A

95%

Mom’s antibodies decline and allow kids to get infected

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82
Q

HHV-7 infects what cells?

A

CD4 T cells
Salivary gland cells
Lung and skin cells

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83
Q

Where is HHV-7 shed the most?

A

In saliva

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84
Q

How does HHV-7 combat immune response?

A

Induces degradation of MHC I

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85
Q

What is the main cause of roseola?

Subset of roseola cause?

A

HHV-6B

HHV-7

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86
Q

Primary manifestation of HHV6 and HHV7?

A

High fever (several days) followed by a rash (1-3) days

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87
Q

How to diagnose HHV6 and 7?

A

Culture, PCR, serology

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88
Q

How to detect acute HHV6 in children?

A

Compare acute and latent serum

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89
Q

HHV-6 is sensitive to what in vitro?

A

Ganciclovir, foscarnet, cidofovir

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90
Q

HHV6, HHV7 and CMV are not sensitive to what famous anti-viral?

A

Acyclovir

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91
Q

Kaposi’s sarcoma is a tumor arising where?

A

Multiple locations in blood an dlymph

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92
Q

What virus is Kaposi’s sarcoma?
What cells are infected?
Two main changes that will cause tumor?

A

HHV-8
Endothelial cells
1. Spindle shaped proliferating cells
2. Angiogenesis

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93
Q

Nuclecapsid contains what two things in measles/Rubeola?

A

Helical symmetry

-ssRNA

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94
Q

Envelope contains what two things in measles/Rubeola?

A

Fusion Protein F

Attachment Protein Hemagglutinin H

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95
Q

What enzyme is NOT found in measles virus?

A

Neuraminidase

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96
Q

What is the diagnostic progression of measles? 3

A

Cough, Coryza, Conjunctivitis –> Koplik’s spots –> Rash

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97
Q

What is the path of measles pathogenesis?

A

Inhaled –> Replicates in RT –> Spreads by lymph –> Viremia –> Conjunctiva + RT + UT + BV’s + lymph + CNS –> Endothelial cells infected –> Rash –> Usually recover

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98
Q

What is a fatal manifestation of measles/rubeola?

What causes it? 2

A

Subacute sclerosing panencephalitis

  1. Host: Defective immunity and Ab’s
  2. Virus: Defective virus that can’t replicate
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99
Q

Immune response to measles?

A

CMI

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100
Q

Route of measles transmission?

A

Respiratory droplets

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101
Q

When is measles most contagious?

A

Late prodromal phase: Peak of CCCP peak

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102
Q

Incubation period of measles?

A

9-11 days

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103
Q

What is historically best test for diagnosing measles?

A

Hemagglutination inhibition test

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104
Q

What’s diagnostic in serum for measles?

A

Serum titer 4X increase in measles Ab

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105
Q

Vaccine type for measles?

A

Live attenuated

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106
Q

Treatment for measles? 3

A
  1. Treat secondary bacterial infections
  2. Antipyretics
  3. Fluids
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107
Q 
German measles/rubella has what main clinical manifestation? 
What demographic is it significant in? 
Type of virus? 
Envelope presence? 
Genome type?
A

Lacey rash

Pregnant women

Togavirus

Enveloped +ssRNA

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108
Q

Pathogenesis of Rubella?

A

URT infection –> Lymph –> Viremia –> Rash

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109
Q

What is the important protein in Rubella for attachment, fusion, hemagglutination and neutralization

A

E1

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110
Q

How many viremias occur in Measles and german measles?

A

Two

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111
Q

Rubella/German measles virus is seen in which cells first

A

Leukocytes

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112
Q

What determines severity of Rubella/German measles?

A

Age

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113
Q

How does Rubella/German measles rash change over 3 days?

A

Day 1: Starts on forehead then spreads down and back

Day 3: Becomes faint but disappears how it appeared

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114
Q

What is the problem if a fetus gets Rubella/German measles?

A

High risk for serious sequelae

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115
Q

Immune response to Rubella? 3

A
  1. Ab’s limit viremia
  2. Type III HS results in rash
  3. CMI clean up
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116
Q

Rubella pathogenesis transmission?

A

Droplets

117
Q

When are patients most contagious with Rubella/German measles?

A

While rash erupts

118
Q

Incubation of rubella?

A

14-21 days

119
Q

Best lab diagnosis for Rubella/German measles?

A

Serology

120
Q

Vaccine for Rubella/German measles?

A

Live attenuated MMR

121
Q

Rubella vaccine may have what side effects

A

Viremia –> Type III HS –> fever, arthritis

122
Q

Complications in Rubella/German measles vaccine is seen in who?

A

Women older than 25

123
Q

What is the smallest DNA virus?

A

Parovirus

124
Q

Does Parovirus have a envelope?
Shape?
Genome shape?
Genome type?

A

No
Icosahedral
Linear
ssDNA

125
Q

Parovirus B19 replicates where?

Which causes what? (2)

A

URT

Viremia and spread to bone marrow

126
Q

What does parovirus B19 depend on for replication?
Specifically?
What seems to be spared?
Is the infection cytotoxic?

A

Active replicating cells
Bone marrow blood cells
Pluripotent stem cells
Yes

127
Q

What are required for Parovirus B19 to replicate?

A

Replicating factors of S phase

Cellular DNA polymerase

128
Q

What acts as primer for parovirus B19?
Where is assembly?
How is the virus released?

A

Inverted repeats
Nucleus
Cell lysis

129
Q

Target cell receptor for parovirus B19?

A

Blood Group P antigen (globoside)

130
Q

2 phases of Parovirus B 19?

A

Lytic infection phase

Noninfectious immunologic phase

131
Q

Things happening during Parovirus B10 lytic phase? 3

A
  1. Hb and RB count drops
  2. Virus in throat and blood
  3. Flu like symptoms
132
Q

Things happening during noninfectious immunologic phase of parovirus b19? 3

A
  1. Hb and RB count drops
  2. Virus-specific IgG Ab present
  3. Rash/arthralgia (Type III HS)
133
Q

Primary manifestation of Parovirus B19?

A

Slapped cheek rash

134
Q

Parovirus B19 can cause what in patients with anemia?

A

Aplastic crisis

135
Q

Intrauterine infection with parovirus b19 results in what?

A

Abortion (anemia + CHF)

136
Q

Immunodeficient patients develop what with parovirus b19?

A

Bone marrow suppression

137
Q

Immune response to parovirus b19?

A

Ab’s stop viremia

138
Q

Route of transmission for parovirus b19?

A

Respiratory

139
Q

Diagnosis for parovirus b19?

A

Clinical

ELISA or PCR

140
Q

In most people how do you treat parovirus b19?

A

You don’t. it’s self-limiting

141
Q

Coxsackie A and B are members of what family?
Envelope presence?
Type of genome?
Shape of genome? (2)

A

Picornaviridae
No
+ ssRNA
Linear and nonsegmented

142
Q

Coxsackie A produces what?

A

Vesicular lesions

143
Q

Enterovirus pathogenesis?

A

Enters through mouth –> Replicates in oropharynx –> Primary viremiain blood –> Goes to target tissue –> Secondary viremia

144
Q

What is herpangina?
Who is it seen in?
How many lesions?

A

Vesicular ulcerated lesions around soft palate and uvula
Children under 10
1-12 lesions

145
Q

Hand/foot and mouth disease is caused by what?

A

Coxackie A16

146
Q

What is seen in Hand/foot and mouth disease? 2

A
  1. Tender, papules and vesicles on hands, feet, mouth, and tongue surrounded by erythema
  2. Fever
147
Q

HSV gangiostomatitis occurs where?

A

Anterior oral cavity: Inner lips, buccal mucosa, tongue

148
Q

What is seen in HSV and not herpangina?

A
  1. Gingivitis
  2. Systemic toxicity
  3. Cervical lymphadenitis
149
Q

Aphthous stomatitis is what?

A

Recurrent ulcers on lips, tongue, buccal mucosa of older children and adults

150
Q

3 manifestations of Coxsackie B?

A

Pleurodynia
Myocarditis
Pericarditis

151
Q

What is Pleurodynia also known as?
What are the symptoms? (2)
How long does it last?
Where is it tender?

A

Bornhom disease or Devil’s grip

  1. Fever
  2. One sided low thoracic pleuritic chest pain

2 weeks

Involved side muscles

152
Q

Myocarditis coxsackie B is life threatening when?

A

In children

153
Q

HPV has what genome shape?
What genome type?
Envelope?
Shape?

A

Circular

DsDNA

Naked

Icosahedral

154
Q

Does HPV genome integrate into host?

How many regions does HPV genome have?

A

No

3 regions

155
Q

What are most important proteins in HPV?

A

E5, E6, E7

156
Q

E5 in HPV does what? (2)

A
  1. Prevents acidification of endosomes

2. Stimulates EGF-R

157
Q

E6 in HPV does what?

A

Binds and destroys P53:

158
Q

E7 in HPV does what?

A

Binds and inhibits Rb

159
Q

How does HPV replication rates differ by location?

A

In basal epidermis –> Little to no replication

As you move to surface –> More replication

160
Q

Most of the time what do you get from EPV on skin?

A

Wart

161
Q

Upregulated E6 and E7 can cause what?

A

Benign mass or invasive cancer

162
Q

Does HPV spread?

A

No, remains local

163
Q

Plantar warts are found where?
Why is their growth different?
Are they painful?
Are most warts plainful?

A

Sole of feet

Weight compression forces them to grow inward

Yes

No

164
Q

How do patients with HPV caused Benign head and neck tumors present?

A
  1. Hoarseness of strange cry
  2. Respiratory distress
  3. Airway obstruction
165
Q

What forms of HPV cause laryngeal tumors that can kill children?

A

6 and 11

166
Q

HPV manifestations on the cervix?

A

Warts after sexual contact

167
Q

Main types that cause cervical growth in HPV?

A

16, 18, 31, 45

168
Q

What is special about HPV 16 and 18?

A

Can get in our genome

169
Q

Immune response to HPV?

A

Attack the L1 protein of the virus

170
Q

Route of transmission of HPV? 4

A

Direct contact: abrasions, fomites, sex, birth

171
Q

Incubation of HPV?

A

Weeks to years

172
Q

Diagnosis of HPV?

A

Koilocytes (Enlarged keratinocytes with clear haloes around shrunken nuclei)

173
Q

Vaccine for HPV?

A

Inactivated quadrivalent 6, 11, 16, 1

174
Q

HPV’s status in permissive cells?

Non-permissive cells?

A

Lytic

Chronic latent and transforming

175
Q

Besides cervical cancer what can HPV 16 and 18 also cause?

A

Oropharyngeal cancer

176
Q

HPV treatment?

A

Remove clinical manifestations (freeze, burn, chemicals, duct tape)

177
Q 
Smallpox/Variola replicates where? 
Family of viruses? 
Genome shape?
Genome type? 
Envelope?
A 
Cytoplasm
Orthopoxvirus
Linear
DsDNA
Enveloped
178
Q

How does poxvirus leave the cell?

A

Disruption of exocytosis

179
Q

How does smallpox spread?

A

Virus is inhaled –> Multiplies in URT –> Gets in lymph –> Nodes –> Goes systemic + hemorrhages in BV’s –> Rash

180
Q

4 main clinical types of variola/smallpox?

A

Ordinary small pox
Vaccine-modified small pox
Flat smallpox
Hemorrhagic smallpox

181
Q

Ordinary smallpox is what % of cases?
Symptoms?
What does mortality depend on?

A

90%
Fever and rash
Extent of rash

182
Q

Vaccine-modified smallpox produces what?

A

Mild prodrome with a few skin lesions

183
Q

Flat smallpox sees what?

A

Slow focal lesions with overall infection and 50% death rate

184
Q

Hemorrhagic smallpox sees what?

A

Bleeding into skin and mucous membranes –> Death in a week

185
Q

Where are smallpox lesions seen most?

Where are chickenpox lesions seen most?

A

Palms, soles, and Face (EXTREMITIES)

Torso

186
Q

Route of transmission of smallpox? (2)

A
  1. Skin

2. RT mucosa

187
Q

Incubation period of smallpox?

A

5 to 17 days

188
Q

Diagnosis of smallpox by histo?

A

Rounded and fused cells

Pock morphology

189
Q

Vaccine for smallpox is important why?

A

1st live vaccine

190
Q

What are two of 11 pox viruses that are not zoonoses?

Which zoonose can be transferred by humans

A

Variola
Molluscum contagiosum

Monkeypox

191
Q

Reservoir host of monkeypox?

Most important symptom?

A

Rodents

Lymphadenopathy of submandib, cervical and sublingual

192
Q 
Cowpox is acquired how? 
Where are lesions? (2)
Skin lesions eventually form what? 
Is lesion painful?
Initial symptoms?
A 
Contact with cows and other animals
Hands and face
Black crust
Yes
Flu like
193
Q

Molluscum contagiosum causes what type of lesion?
How is it transmitted?
What do the lesions become?
Where are they seen?

A

Wart-like

Direct contact

Umbilicated nodules with central caseous plug

Trunk and genitalia

194
Q

Molluscum contagiosum incubation period?
Treatment? (2)
Diagnosed how?

A

2-8 weeks

Curettage or liquid nitrogen

Clinical appearance

195
Q

Epstein-Barr virus?
target tissue? (2)
Target cell? (2)
Target cell receptor? (2)

A

Oropharynx + salivary gland

B cells + Epithelial cells

C3d receptor + MHC II

196
Q

At peak of infection, how many B cells have EBV?

A

20%

197
Q

Why is good immune response needed for EBV?

What is the consequence?

A

Have to shutdown proliferation of B cells

Cause infectious mononucleosis

198
Q

Why is there an increase in EBV infection with age of seroconversion?

A

Differences in immune response of different age groups (Young better than old)

199
Q

EBV pathogenesis?

A

EBV in saliva –> B cells –> B cells proliferate –> T cells activated -

200
Q

How is EBV mono spread?

A

Intimate contact

201
Q

How does the imune system respond to EBV?

A

CD8 and CD4 T cells and NK cells attack B cells

202
Q

The killing of lymphocytes by the immune system is done by who?

A

CD8 T cells

203
Q

CD8 t cells also are responsible for the symptoms of mono why?

A

Release cytokines

204
Q

What is the humoral response to EBV?

A

Ab’s against EBV antigens VCA and EA

205
Q

When does the Ab response to latency EBV antigens occur?

What are these?

A

In convalescence

EBNA1-3, EBNALP

206
Q

Diagnosis of EBV? (7)

A
  1. Clinical symptoms
  2. Palatal petechiae
  3. Atypical lymphocytes
  4. Heterophile Ab
  5. Anti-EBV Ab’s
  6. IgM to VCA
  7. IgG to VCA and EBNA
207
Q

Primary treatment of EBV?

A

Treat symptoms

208
Q

What cells are seen in EBV in histo?

A

Downey cells

209
Q

When do you see all but the Anti-EBNA Ab together?

A

Acute primary

210
Q

When do you see Anti-EBNA?

A

In latency

211
Q 
CMV is of what family of viruses?
Envelope? 
Shape of genome?
Genome type? 
Size?
A

Herpesviridae

Enveloped

Linear

dsDNA

Largest herpes virus

212
Q

Target tissue of CMV? (5)

A
  1. Salivary gland
  2. Kidney tubules
  3. Cervix
  4. Testes
  5. Epididymis
213
Q

How does CMV mess with immune response?

A
  1. Interfere with MHC-1

2. Induce FC receptors

214
Q

Target cell type of CMV?

A

Epithelial

215
Q

Target cell receptor of CMV?

A

Heparan sulfate proteoglycans

216
Q

CMV appears how clinically in most people?

A

Silent

217
Q

Primary infection with CMV In young adult can produce what?

A

Mono with fever, lymphadenopathy

218
Q

What % of mono is EBV?

What % is CMV?

A

79%

21%

219
Q

How do you determine EBV vs. CMV?

A

EBV = Heterophile ab

220
Q

CMV result in normal person?
Seronegative mother’s baby?
Immunosuppressed?

A
  1. Silent or mono

Cytomegalic inclusion disease

Multisite symptomatic disease

221
Q

When is CMV DNA monitored in whole blood?

A

Transplant patients

222
Q

Infected specimens with CMV show what on histo?

A

Large cells with basophilic intranuclear inclusions called Owl’s Eye

223
Q

Immune response to CMV?

A

Since CMV goes latent in blood cells, CMI takes forever to get rid of it

224
Q

Route of transmission for CMV?

A

Saliva, sex, blood, transplant

225
Q

Latency of CMV is in what cells? (3)

A

monocytes
macrophages
CD34 cells

226
Q

Primary treatment of CMV?

A

Anti-virals

227
Q

HIV has what adherence infusion proteins? 2

A
  1. TM gp41

2. SU gp120

228
Q

HIV-1 has what 4 groups?

A

M, N, O, P

229
Q

M group of HIV-1 contains what subtypes?
Which are in North America?
Which are in Africa?

A

A-K
B
A and C

230
Q

HIV-2 has what subtypes?

How does it compare to HIV-1?

A

A-F

Less aggressive

231
Q

How does HIV attach?

A

Gp120 and Gp41 binds to Primary CD4 receptor but also needs either CCR5 co-receptor on monocytes or CXCR4 on T cells

232
Q

Penetration of HIV is done how?

A

Bind to chemokine receptor –> gp41 has change

233
Q

Early phase of genome replication for HIV involves what?

A

Reverse transcriptase synthesizes complementary -cDNA copye of genome

234
Q

What else does RT do for HIV?

A

Serves as ribonuclease H –> Degrades RNA + Finishes dsDNA

235
Q

What happens after HIV’s dsDNA is made?

A

Put into genome of cell

236
Q

Late phase of HIV expression sees what?

What does this require?

A

Transcription by host RNA Polymerase II

Activation of cell and ability of host TF’s

237
Q

Products of gag, gag-pol and env are what?

A

Polyproteins

238
Q

How is HIV assembled?

A

Gag and gag-pol proteins are acetylated and bind to PM glycoproteins –> 2 RNA molecules with tRNA then complex –> Budding

239
Q

After envelopment, what happens to HIV?

A

Protease cleaves gag and gag-pol –> Release RT

240
Q

Major determinant of where HIV goes in tissues is what?

A

CD4

241
Q

HIV-1 will stick to what in epithelium?
Using what?
What will these cells then do?

A

Dendritic cells
Lectin DC-SIGN
Deliver HIV to T cells in lymph nodes

242
Q

HIV replicates where in the body?

A

Lymph nodes

243
Q

Acute phase of HIV lasts how long?

How much virus made daily?

A

First 2-4 weeks

10^10 virions

244
Q

What is acute retroviral syndrome during HIV acute phase?

A

Flu-like symptoms with a rash of the trunk

245
Q

What does HIV do during latency?

What cells is it latent in?

A

Replicate in lymph nodes –> Destroys lymph nodes

Macrophages and resting T cells

246
Q

What is AIDS related complex? (4)

A

Chronic lymphadenopathy and fever, weight loss, malaise

247
Q

What is seen in late phase?
At what level do you see symptoms?
At what level do you see opportunistic infections?

A

Viral levels increase with decrease in CD4

CD4 450/ml

CD4 350/ml

248
Q

Immune response has what effect on HIV/AIDS?

A

Restricts replication

249
Q

What cell is in dire need for good immune response against HIV?
What does it need?

A

CD8

CD4 activation

250
Q

Describe the change in virus levels in HIV and AIDS

A

Initial burst during HIV –.> Drops to almost nothing during latency –> Slowly increases during AIDS phase due to loss of T cells

251
Q

Describe the change in CD4 and T cell count in HIV and AIDS?

A

Slow steady decline in both from start to finish

252
Q

Describe change in Anti-HIV-1 antibody?

A

Initial big increase due to immune response –> But immune cells start dying –> Don’t produce enough Ab

253
Q

Below what blood level do you see really bad AIDS problems?

A

Below 200

254
Q

Transmission of HIV?

A

Bodily fluids

255
Q

What are sources of infected lymphocytes and monocytes in HIV?

A

Ulcers and discharge

256
Q

Why is RT-PCR good in HIV?

A

Determine viral load (higher it is, poorer the prognosis)

257
Q

What is the Rule Out test for HIV?

A

ELISA: Looks for anti-HIV antibodies

258
Q

What is the Rule IN test for HIV?

A

Western blotting

259
Q

How does CD4/8 ratio give prognosis in HIV?

A

Higher CD8 numbers = better

260
Q

Treatment for HIV/AIDS?

A
  1. Nucleoside analogues
  2. Non-nucleoside analogues
  3. Protease and integrase inhibitors
261
Q

What is HAART?

What does it involve?

A

High active anti-retroviral therapy

2 NRTI, 1 NNRTI/Protease inhibitor

262
Q

Side effects of HAART?

A

Kills mitochondria and alters fat distribution

263
Q

Arboviruses multiply where?

A

Arthropod vector

264
Q

Arborviruses have what symptoms? 2

What can it lead to?

A

Silent or Flu-like

Encephalitis

265
Q

Togaviruses and Flaviviruses have an envelope?
Shape?
Genome type?

A

Yes
Icosahedral
+ssRNA

266
Q

Vector-borne togaviruses belong to what genera?

A

Alphavirus

267
Q

Humoral response to alpha and togaviruses?

CMI response?

A

AB block prevents secondary viremia

Interferon release

268
Q

Dengue fever is also known as?
What is the virus?
Where does it replicate? (2)

A

Break-bone fever

Flavivirus

Monocytes and vascular endothelium

269
Q

When is dengue fever really serious?

A

Second time you get it with different antigen

270
Q

Treatment for dengue fever?

A

none

271
Q

Incubation of dengue fever?

Symptoms?

A

4-8 days

Flu + rash

272
Q

Serious complication of Dengue Fever?

When does it occur?

A

Dengue Hemorrhagic fever/Dengue shock syndrome

When someone gets a second version of the dengue fever (different antigens)

273
Q

Arenaviruses have an envelope?
Genome type?
Appears how on EM?

A

Yes
2 -ssRNA circles
Sandy appearance in ribosomes

274
Q

Lassa Fever replicates how?
Where is it seen?
transmission?

A

Binds to alpha-dystroglycan on mammalian cells
West Africa
Rodents, some humans

275
Q

Incubation in lassa fever?
Symptom?
What can it cause?

A

5-10 days
Fever
Hemorrhaging due to capillary damage –> 50% fatality

276
Q

Pathogenesis of arenaviruses?

A

Infect macrophages –> Release of mediators –> Vascular damage

277
Q

Treatment of arenaviruses?

A

Ribavirin

278
Q

Filoviruses shape?
Envelope?
Genome type?

A

Filamentous
Enveloped
-ssRNA

279
Q

Pathogenesis of filoviruses?

A

Tissue necrosis of parenchymal cells –> Vascular injury

280
Q

Manifestation of filoviruses?

A

Flu like –> Rash –> Fatal hemorrhaging fevers

281
Q

Diagnosis of filoviruses? (2)

A

Large eosinophilic cytoplasmic inclusion bodies

Detect viral Ag by immuno or ELISA

282
Q

Treatment for filoviruses?

A

Quarantine

283
Q

Ebola has what 4 subtypes?

A

Zaire, Sudan, Ivory Coast, Reston

284
Q

How does Ebola and Marburg enter body?

A

Mucus membranes of abraded skin

285
Q

Incubation for Ebola?

Incubation for Marburg?

A

2-21

5-10

286
Q

4 symptoms of Ebola and Marburg?

A

Fever, hemorrhaging, rash, Disseminated intravascular coagulation

287
Q

Reservoir for Marburg?

A

Tropical rainforest fruit bat

288
Q

Transmission of marburg and ebola? 2

A

Syringes and semen

289
Q

Diagnosis of marburg and ebola?

A

Detect Ag

MICRO (22 decks)

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