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Virology > Review 2 > Flashcards

Review 2 Flashcards

1
Q

What are antivirals used for in influenza?

A

treatment: reduce illness duration
prophylaxis: 70% effective in preventing flu

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2
Q

How do adamantanes work?

A

They block uncoating (block M2 channels from allowing pH to drop)

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3
Q

What do adamantanes work on

A

just influenza A

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4
Q

how do Neuraminidase inhibitors work?

A

They block budding of the influenza virus from the infected cell.

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5
Q

What do neuraminidase inhibitors work on

A

Influenza A and B

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6
Q

What are the names of adamantanes and Neuraminidase inhibitors

A

adamantanes - amantadine, rimantadine

neuraminidase inhibitors - oseltamivir, zanamavir

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7
Q

How is noro spread?

A

Fecal-oral

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8
Q

What is an important receptor for noro?

A

The H antigen which is a precursor to A, B, and O blood types on RBC’s

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9
Q

Who can resist noro?

A

non-secretors of H antigen (it’s not on their epithelial cells).

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10
Q

Where does noro replicate?

A

in the jejunum

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11
Q

What are the sx of noro?

A

vomiting

diarrhea

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12
Q

noro immunity?

A

none. people can get reinfected over and over again. sometimes within the same month

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13
Q

what types of populations is noro associated with?

A

closed populations like cruise ships, nursing homes

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14
Q

what makes noro selective for these populations

A
  1. little host immunity
  2. efficient transmission by food
  3. very stable virus (not killes by soap, EtOh, etc.)
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15
Q

How is rotavirus spread?

A

fecal oral

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16
Q

Who gets rotavirus?

A

6 mos - 2 years

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17
Q

what are the sx

A

vomiting and diarrhea

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18
Q

immunity to rota?

A

sort of. people usually will become immune and just have subsequent sub-clinical infections where they still shed virus and all.

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19
Q

Who is rota a big problem for?

A

developing world?

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20
Q

How is it similar to influenza A

A
  1. segmented genome

2. antigenic variations (antigenic shift and drift) just like flu

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21
Q

how does polio spread

A

fecal-oral

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22
Q

describe the pathogenesis of polio

A

gets in through the GI lumen -> GI lymphatics ->primary viremia (circulating in the blood) -> replication in viscera (organs) -> secondary viremia -> spreads to the CNS

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23
Q

What cells in the CNS does polio infect

A

motor neurons in the ventral horn

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24
Q

What does polio do to these cells?

A

causes cell death

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25
Q

What is the rate of inapparent and abortive polio?

A

95%

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26
Q

polio leading to aseptic meningitis?

A

4%

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27
Q

rate of paralytic polio?

A

1%

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28
Q

What are the advantages to the inactivated polio vaccine

A
  1. no backmutation

2. easy to combine with other vaccines

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29
Q

What are the downsides of IPV

A
  1. injection
  2. no mucosal immunity
  3. expensive
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30
Q

What are the advantages to the oral polio vaccine

A
  1. mucosal immunity
  2. long lasting immunity
  3. ease of administration
  4. cheap
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31
Q

What are the downsides to OPV?

A
  1. BACK MUTATION, FOOLS!!!

2. Need cold chain for transport

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32
Q

How does measles spread?

A

respiratory spread

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33
Q

Describe measles pathogenesis

A

infection of respiratory epithelium -> primary viremia -> replication in reticuloendothelial cells (liver, spleen, monos) -> widespread disseminated replication

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34
Q

What are the classic measles sx

A
  1. cough
  2. coryza
  3. conjunctivitis
  4. koplik’s spot

THEN rash

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35
Q

Immunity to natural measles infection?

A

life-long

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36
Q

complications from measles

A

respiratory: pneumonia
CNS: encephalitis, subacute sclerosing panencephalitis)
GI: gastroenteritis, hepatitis

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37
Q

Describe importance and presentaiton of koplik’s spots

A
  1. they precede the rash

2. they are blue-shite spots w/ surrounding erythema

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38
Q

How does the measles rash spread?

A

goes from the face downward. rash present on palms and soles. It is a flat rash.

the macules will become confluent with time

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39
Q

What are the fecal-oral hepatitides

A

A and E

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40
Q

What are the blood-borne hepatitides

A

B, D, and C

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41
Q

What hepatitides incubate for 2-7 weeks?

A

A and E

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42
Q

What hepatitides incubates for 2-23 weeks

A

C

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43
Q

What hepatitides incubate for 4-25 weeks?

A

B and D

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44
Q

What hepatitides cause chronic hepatitis

A

B/D, and C

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45
Q

Which hepatitides have vaccines?

A

B, A, E (not in the US)

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46
Q

What is it that actually causes hepatic damage in Hepatitis?

A

The CTL response damages the liver

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47
Q

What lab tests do we use for viral hepatitis?

A

AST and ALT show elevation with hepatic injury

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48
Q

What will present after abnormal LFTs?

A

bilirubin levels will be more elevated later. esp, during acute infection

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49
Q

What do we use for Hep A-D for Acute tests

A

A - IgM anti-HAV
D - IgM anti-HDV
C - Anti-HCV

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50
Q

What do we use for for chronic tests?

A

D IgG and IgM anti-HDV.

C - anti-HCV+ and the rising and falling of liver enzymes

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51
Q

What is the progression of sx of hepatitis after the asymptomatic incubation period?

A

1-2 weeks of fever, fatigue, nausea, abdominal pain
then later there will be dark urine, clay-coloured stool. Then 1-5 days later there will start to be jaundice, enlarged/tender liver. 1-4 months later there will be recovery OR chronic infection

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52
Q

What is the risk of chronic Hep B for adults?

A

~1% due to the good immune response. Low risk of cancer

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53
Q

What is the risk of chronic hep B for kids at birth?

A

90% due to bad immune response. The risk of cancer is high for these little tikes

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54
Q

What is the rate of chronic infection going into a nonreplicative phase?

A

10%per year of chronic infections will enter a nonreplicative phase which carries a low rate of transmission and little/no liver injury. Mostly asymptomatic

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55
Q

what occurs during the replicative phase of chronic infection

A

there is abundant virus. High rate of transmission and ongoing liver injury

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56
Q

What is the first thing that you see in Acute HepB

A

HB surface Ag. It spill out in larger numbers than needed for viral replication. you will then see a huge

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57
Q

What is made after this?

A

HB e Antigen. This is a protein cleaved from the core cassette

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58
Q

What is the first antibody response that you see with HepB?

A

IgM directed against the HB core antigen

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59
Q

What happens after the IgM against core antigen?

A

you get IgG against Core antigen AND eventually the anti-HB e antigen antibodies

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60
Q

When does someone have longstanding HB immunity?

A

When there is antibody against the HB surface antigen (anti-HBs)

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61
Q

What happens during chronic HepB infection?

A

you get the same HBsAg test positive and then the IgM anti-HBc and class-switch to IgG. BUT you never end up with the nice anti-HBsAg response

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62
Q

What tests are positive for acute HBV?

A

HBsAg, HBeAg, IgM anti-HBc

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63
Q

What tests are positive for Recovered HBV?

A

IgG anti-HBe, IgG anti-HBc, IgG anti-HBs (this is the important one)

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64
Q

What tests are positive for chronic infection?

A

IgG anti-HBc, HBsAg, HBeAg (could be + if ongoing damage or - if in a latent phase), anti-HBeAg (variable)

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65
Q

What tests are positive for vaccinated individuals

A

anti-HBs

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66
Q

Why is HDV dependent on HBV?

A

It uses the HBV capsid protein

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67
Q

What does HDV do during acute HBV infection?

A

This co-infection is pretty bad and will lead to increased risk of fulminant hepatitis. It will clear though if HepB clears

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68
Q

What happend if you’ve got HDV with chronic HBV?

A

It will lead to fuliminant hepatitis. Increased progression towards hepatocellular cancer.

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69
Q

How often does Hep C become chronic in adults?

A

85% of the time. very few people will actually clear this

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70
Q

What makes it unique in it’s chronic progression?

A

intermittent spikes of replication due to the antigenic variation

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71
Q

How does the liver get damaged?

A

Immune response. Can lead to cirrhosis

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72
Q

What is the annual risk of hepatocellular cancer with chronic HCV?

A

1-4%

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73
Q

What unites all arboviruses?

A

the route of transmission through an arthropod vector.

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74
Q

What are the 2 main classifications of arboviruses?

A
  1. encephalitic viruses

2. hemorrhagic fever viruses

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75
Q

What are the 4 encephalitic arboviruses?

A
  1. WNV
  2. EEE
  3. WEE
  4. SLE
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76
Q

Humans are usually what type of hosts for the encephalitic arboviruses?

A

incidental

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77
Q

What is the mosquito vector for WNV?

A

Culex mosquitoes

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78
Q

Where do these mosquitoes get WNV?

A

birds

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79
Q

Describe the pathogenesis of WNV

A

goes to blood -> replicates in lymphatics -> viremia -> infects the brain

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80
Q

What percentge are asymptomatic?

A

75%

81
Q

Describe West Nile Fever

A

Fever, myalgias, fatigue, headache

82
Q

Describe WNV neuroinvasive disease

A

meningitis, encephalitis, WNV “poliomyelitis” (infection of anterior horn cells leading to flaccid paralysis)

83
Q

Can humans be reservoirs of WNV?

A

No

84
Q

What makes dengue and its vector and lifecycle unique among the arboviruses

A

Humans and Aedes mosquitos are the only reservoirs

85
Q

What is dengue fever also called?

A

breakbone fever

86
Q

What are the sx of the dengue fever?

A

musculoskeletal pain, fever

87
Q

What are the sx of dengue hemorrhagiv fever?

A

bleeding of skin, gums, GI, etc.

88
Q

What are the lab results of DHF

A

decreased platelets which is a sign of leaky capillaries. Also, this causes hematoconcentration and increased Hematocrit

89
Q

Describe the Dengue Shock Syndrome

A

DHF plus circulatory failure

90
Q

Describe the pathogenesis of dengue

A

infection in the blood -> infection of macrophages -> ??something?? -> suppression of hematopoeisis -> widespread replication

91
Q

How many serotypes of Dengue are there?

A

4

92
Q

What does infection with 1st cause?

A

Dengue Fever

93
Q

What can infection with the subsequent serotypes cause?

A

DHF

94
Q

What is the theory for this DHF after multiple serotype infection?

A

the cross-reactive antibodies against each serotype will actually latch onto the new strain and attract macrophages, BUT this just enhances the infection of these macrophages. antibody-dependent enhancement

95
Q

What is the vector for yellow fever?

A

Aedes

96
Q

What are the reservoirs for yellow fever?

A

humans and monkeys

97
Q

Describe the pathogenesis of YF

A

blood infection -> infection of macrophages -> viremia -> suppression of hematopoiesis

98
Q

What is the first manifestation of yellow fever?

A

Flu-like sx for 3 days which will resolve and all will be well for 24 hours

99
Q

What can happen after the first initial yellow fever and nice 24 hours period?

A

high fever, abdominal pain, vomiting

100
Q

What does this high fever sx lead to in yellow fever?

A

hepatitis -> jaundice -> hemmorrhagic manifestations (renal failure, intravascular pressure fall)

101
Q

What is the ultimate end of this hemorrhagic yellow fever presentation?

A

coma, death (~50% of cases)

102
Q

What type of a vaccine is there for yellow fever?

A

a live attenuated vaccine

103
Q

What type of genome do herpes viruses have?

A

Double stranded DNA

104
Q

Where does the herpes genome replicate?

A

In the host cell nucleus

105
Q

What is the disease presentation of herpesviruses?

A

primary infection -> latency -> reactivation

106
Q

What is the most common type of herpes for oral contact?

A

HSV-1 much more than HSV-2

107
Q

What is the most common type of herpes for sexual contact?

A

HSV-2 is much more than HSV-1

108
Q

Describe the pathogenesis of HSV

A

primary infection in epithelial cells -> axonal transport ->latent in sensory neurons -> reactivation and axonal transport ->recurrent infection in epithelial cells -> sx maybe… you can still shed it without being aware

109
Q

What is the classic dermatological presentation of HSV?

A

painful, clustered vesicle -> ulcerations -> crusting and resolution

110
Q

How is chickenpox spread?

A

respiratory

111
Q

How is VZV spread when someone has shingles?

A

contact spread (although this is very uncommon)

112
Q

Describe the pathogenesis of VZV

A

primary infection in nasopharynx -> (fever) viremia -> infection in other sites (most importantly SKIN and sensory neurons) -> latent in sensory neuron -> reactivation and axonal transport -> replication in skin across a dermatome

113
Q

describe the dermatological presentation of primary VZV (chickenpox)?

A

Fever with maculopapules, vesicles and crusted lesions together. These start on the trunk. It is often described as a dewdrop on a rose petal because it is a raised lesion

114
Q

What does reactivation VZV look like?

A

painful vesicular rash in a dermatomal distribution

115
Q

What is the vaccination for VZ

A

an attenuated viral vaccine

116
Q

What is the difference between the chickenpox vaccine and the zostavax?

A

same thing just a 4x greater dose

117
Q

How is EBV transmitted?

A

in saliva (kissing disease)

118
Q

Describe pathogenesis of EBV

A

primary infection in oropharynx -> viremia -> infection of B-cells -> latent in B-cells -> reactivation

119
Q

Describe severity of primary infection

A

it is usually mild or even asymptomatic in children

120
Q

Describe the clinical presentation of mononucleosis esp. in adolescent and adults

A

low-grade fever, pharyngitis, lymphadenopathy. ALSO, you see atypical lymphcytosis (i.e. a giant CD8 response). Serious malaise and fatigue

121
Q

What is the reactivation illnesses associated with EBV?

A
  1. lymphoproliferative diseases
  2. burkitt’s lymphoma
  3. nasoopharyngeal carcinoma
122
Q

What is the diagnostic test for acute EBV?

A

you test for heterophile antibodies which patients will make when infected

123
Q

How does one test for heterophile antibodies?

A

you do an agglutination assay with RBC’s from sheep, horses, or cows that will show agglutination with the heterophile antibodies of humans. MONOSPOT TEST

124
Q

Are people with latent EBV (also EBV-associated malignancies) going to test positive?

A

no on the heterophile antibody test

125
Q

How does CMV present?

A

CMV is exactly like EBV and is another cause of mononucleosis

126
Q

How does one distinguish CMV from EBV?

A

CMV is NEGATIVE on the monospot test (no heterophile antibodies)

127
Q

When does CMV reactivate?

A

in transplant patients you see the following: GI inflammation, pneumonia, and disseminated disease
In HIV patients: retinitis (the leading cause)

128
Q

What is HHV-6

A

6th disease AKA exanthem subitum or roseola

129
Q

How does HHV-6 present?

A

Fever (maybe seizures) followed by a generalized rash

130
Q

What is HHV-8

A

Kaposi’s sarcoma (but only on reactivation)

131
Q

What is the mechanism of acyclovir?

A

It is a nucleoside analogue. It is phosphorylated by a viral thymidine kinase where it is then incorporated into the DNA. Then because it has no 3’ OH, it STOPS DNA synthesis

132
Q

What is the oral form of acyclovir?

A

valacyclovir

133
Q

What is a/vala-cyclovir good for?

A

HSV, VZV

134
Q

How does Ganciclovir work?

A

Same way as acyclovir (nucleoside analogue), it just targets infected cells a bit better.

135
Q

What is the oral form of ganciclovir?

A

valganciclovir

136
Q

What is gan/valgan-ciclovir good for?

A

CMV

137
Q

How does foscarnet/cidofovir work?

A

It inhibits viral DNA polymerase (not involved with the thymidine kinase)

138
Q

When does one use foscarnet/cidofovir?

A

After failing acyclovir or ganciclovir

139
Q

How does one acquire HIV?

A

Sexual contact

140
Q

What 3 things determine the risk of transmission to a partner?

A
  1. type of sex - anal sex>vaginal sex> oral sex
  2. level of viruses - higher viral load in source partner increases risk of transmission
  3. ulceration - presence of herpes in either partner will increase risk of transmission
141
Q

What is the risk of HIV transmission mother to child without meds?

A

1 in 3

142
Q

What is the risk of HIV transmission MTC with meds

A

<1%

143
Q

What are other ways of getting HIV

A

IDU, medical use of blood products is now very very low

144
Q

what is the first step in HIV life cycle and what are the necessary proteins?

A

It is entry
gp120 is a docking protein
gp41 is a fusion protein

145
Q

What are the cell proteins that interact with gp120.

A

CD4 (1st) and CCR5… later in infection there is CXCR4 tropism

146
Q

What does reverse transcriptase do?

A

It will take the RNA from HIV and convert it to dsDNA getting it ready for it’s big proviral debut

147
Q

What does integrase do?

A

It will take the DNA made from the RT and splice it into the latent provirus

148
Q

What happens when the T cell is activated?

A

There is more proliferation and the virions will then assemble at the cell membrane.

149
Q

What does the protease do?

A

It will help to mature the virions

150
Q

Can you remember the natural history of HIV infection withe CD4’s and viral load?

A

YES

151
Q

What happens between 400 and 200 CD4’s

A

TB, zoster, oral candidiasis

152
Q

What happens between 100 and 200 CD4’s

A

PCP, esophageal candidiasis, mucocutaneous herpes

153
Q

What happens between 100 and 50

A

Toxo, cryptococcosis, MAC, CMV

154
Q

what happens at below 50

A

cryptosporidiosis, PML

155
Q

What shows up in a test for acute first, p24 or HIV viral load?

A

viral load

156
Q

What does HIV RNA help with

A
  1. predicts rate of progression

2. measures efficacy of ART’s

157
Q

How does one do resistance testing?

A

Sequencing of the HIV RNA for mutation associated with resistance to ARTs

158
Q

What drugs target GP41

A

fusion inhibitors

159
Q

drugs that targe CCR5?

A

CCR5 antagonists

160
Q

Drugs that target Reverse Transcriptase?

A
  1. nucleoside RT inhibitors

2. non-nucleoside RT inhibitors

161
Q

Drugs that target integrase?

A

integrase strand transfer inhibitors

162
Q

Drugs that inhibit the protease?

A

protease inhibitors

163
Q

How do NRTI’s work?

A

incorporate into nascent viral DNA blocking the elongation of that DNA

164
Q

How do NNRTI’s work?

A

Bind outside the active site of the RT and allosterically inhibit RT

165
Q

How do PI’s work?

A

They are structural analogues of the protease substrate and thus block the actual stuff

166
Q

How do integrase strand-transfer inhibitors work?

A

bind integrase at the catalytic site, blocking the integration of the proviral DNA into the host DNA

167
Q

How do fusion inhibitors work?

A

Block gp41 from achieving the conformation needed for fusion

168
Q

CCR5 antagonsist

A

binds the CCR5 stopping the interaction with gp120

169
Q

Who is ART recommended for?

A

All HIV infected. Even more so with lower CD4’s

170
Q

What else is ART advocated for?

A

PReP

171
Q

What is the formula for starting HIV therapy

A

2 NRTI’s plus your choice of one of the following:
NNRTI
boosted PI
integrase strand transfer inhibitor

172
Q

What is a boosted PI?

A

It is a PI given with a little bit of ritonivir. The ritonivir will stop the liver from getting rid of the PI and thus make sure there is more in the body.

173
Q

What are things included in the enterovirus group

A

SO MANY. but among the most important are poliovirus and coxsackieviruses

174
Q

What causes polio

A

poliovirus 1-3

175
Q

What does Coxsackievirus A cause

A

hand-foot-mouth disease, herpangina

176
Q

What does coxsackievirus B cause

A

myocarditis and pericarditis

177
Q

How does mumps spread?

A

droplet respiratory

178
Q

Where does mumps infect and what are the sx?

A

parotid glands with swelling and pain with resolution in 7-10 days

179
Q

what are some mumps complications?

A

complications are orchitis/oophoritis. aseptic meningitis, encephalitis. pancreatitis. Rarely there will be hearing loss in children. Fetal loss in the 1st trimester.

180
Q

Can mumps be prevented?

A

Yes with a great vaccine

181
Q

How does one get adenoviruses?

A

respiratory, fecal-oral, and fomite

182
Q

What is the adenovirus fate?

A

generally self-limited and respiratory manifestations

183
Q

Where else can adenovirus present?

A

ocular infections

184
Q

Describe the ocular infections of adenovirus infections.

A

pharyngoconjunctival fever, epidemic keratoconjuncitivits

185
Q

Describe the fecal-oral presentation of adenoviruses

A

self-limited, acute, watery diarrhea

186
Q

What about adenovirus in the immunocompromised?

A

there can be reactivation illness or new infection

187
Q

What will happen with adeno in HSCT patient?

A

usually within 100 days of transplant, you will find:

  1. hemorrhagic cystitis
  2. enteritis
  3. pneumonitis
  4. hepatitis with viremia
188
Q

Where does adenovirus play for solid organ transplant?

A

It will infect the transplant organ

189
Q

How is parvovirus B19 spread?

A

respiratory AND vertical transmission

190
Q

What is the common name of the Parvo B19 and how does it present

A

“Slapped cheek disease” or 5th disease. It will present with fever and arthropathy: self-limited symmetric swelling and pain of joints in hands and feet.

191
Q

What is the lab finding with Parvovirus B19 slash where does it replicate?

A

ANEMIA!!!! It replicates in the erythroblast.

192
Q

What populations do we worry about with parvo and why?

A
  1. people with underlying hemolytic disease
    - this can put them into transient aplastic crisis
  2. pregnant ladies
    - usually ok, BUT small chance for reduced fetal RBC’s, fetal death, fetal hydrops
  3. immuncompromised
    - pur red cell aplasia possible
193
Q

What are the 3 main types of infections in terms of infection control.

A
  1. contact
  2. airborne
  3. droplet-borne
194
Q

describe contact diseases and give the 6 or 7 examples

A

Direct person-to-person spread OR contact with a contaminated intermediate object (such as equipment, furniture, etc.

  1. MRSA
  2. Van-resistant enterococcus
  3. C. Diff
  4. rotavirus
  5. RSV
  6. HSV
  7. lice/scabies
195
Q

What are the precautions taken for contact?

A
  1. Hand hygiene before gloves
  2. Gown
  3. gloves
  4. Dedicated equipment (e.g. stethoscopes)
  5. Single room sometimes
196
Q

describe droplet diseases and give the 5 examples

A

Large droplets generated during coughing, sneezing, talking.

Propelled a short distance (< 3 feet) and land on eyes, nasal mucosa, or mouth of susceptible individual.

197
Q

What are the droplet precautions?

A
  1. Surgical mask within 3 feet of patient
  2. Hand hygiene
  3. Single room sometimes
198
Q

describe airborne diseases and give the 5 examples

A

Small droplet nuclei, skin squames, or dust particles that contain microorganisms are transmitted by air currents over long distances.

Deposited in the lower airways of a susceptible host

  1. Tuberculosis
  2. Varicella
  3. measles
  4. smallpox
  5. Aspergillus
  6. Legionella
199
Q

What are the airborne precautions?

A
  1. Isolation room with negative pressure airflow
  2. respirator
  3. Visitation Restriction
  4. NO VISITATION FOR Non-immune individuals

Virology (9 decks)

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