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Flashcards in virology review Deck (253):
1

viruses are composed of

1. nucleic acid
2. protein capsid
3. some have lipid envelope
4. genome (DNA or RNA, a very few have both)

2

viruses depend on what for replication?

host cells

3

what are the structural characteristics of viruses?

1. nucleic acid (ss (+/-) or ds RNA or DNA, and # of segments)
2. capsid structure (icosahedral, helical or complex)
3. presence or absence of an envelope

4

different types of nucleic acid present in a virus

1. ss +/- RNA
2. ds RNA
3. ss or ds DNA

5

what are the targets of Abs against viruses, and why?

viral receptors for host cells, because they're exposed

6

segmented nucleic acids allows for -----? what are two viruses for which this is important?

reassortment.
important for: influenza A and rotavirus

7

are enveloped or nonenveloped viruses more stable?

nonenveloped

8

what is a structural similarity of most GI viruses? Why?

most are nonenveloped because they have to survive bile salts/stomach acid, so they have to be more stable. (ie noravirus and rotavirus)

9

unlike - ssRNA, +ssRNA is...

weakly infectious as is if it gets into the right part of the cell

10

all viruses have to make _____ at some point during their life cycle in order to make proteins

mRNA

11

- ss RNA needs to do what in order to become infectious?

needs to make + strand copies ---> mRNA

12

all RNA viruses, except retroviruses ENCODE for what one thing that humans don't have

RNA-dependent RNA polymerase, which humans don't have

13

unlike other RNA viruses, Retroviruses ENCODE

RNA-dependent DNA polymerase (aka reverse transcriptase)

14

unlike + ssRNA viruses which can encode RNA-dependent RNA polymerase, -ssRNA viruses have to...

bring a polymerase to copy the RNA

15

how do we detect viral infections? (3 methods)

1. serology (Igm/IgG)
2. viral replication in cell culture with euk. cells (not very common now)
3. look for components of a virion using immunological methods (looks for prots) or PCR (nucleic acid)

16

what does serology look for/tell us about viruses?

Abs-- IgM vs IgG tells us whether the ifxn is acute vs chronic. you usually have to take the serology two times and compare them-- a 4 fold increase in IgG indicates an ifxn

17

how can components of a virion be detected?

1. protein is detected by immunological methods (ie rapid influenza test)
2. PCR shows viral nucleic acids

18

3 patterns of viral ifxns

1. acute: the amount of virus in the host increases, decreases and then is gone from the body
2. Latent: the virus is present in the host (and can be integrated into the genome) but not replicating
3. chronic: a persistent ifxn with ongoing viral replication. there's no latent integration of the virus into the host

* some viruses move back and forth

19

what is acute viral ifxn, and what are 7 examples of viruses that cause it?

acute: the amount of virus in the host increases, decreases and then is gone from the body
1. influenza
2. rotavirus
3. norovirus
4. polio
5. arbovirus
6. arboviruses
7. Hep A, E

20

what is latent viral ifxn and 2 examples?

Latent: the virus is present in the host (and can be integrated into the genome) but not replicating
1. Herpes simplex virus (HSV)
2. HIV

21

what is chronic viral ifxn? 2 examples?

chronic: a persistent ifxn with ongoing viral replication. there's no latent integration of the virus into the host
1. Hep B
2. Hep C

22

3 body sites of the upper respiratory tract (URT), and common manifestation of illnesses associated with them

1. nasal cavity: common cold
2. pharynx: pharyngitis
3. larynx: laryngitis and croup

23

4 body sites of the lower respiratory tract (LRT), and common manifestation of illnesses associated with them

1. trachea: tracheitis
2. bronchi: bronchitis
3. bronchioles: bronchiolitis
4. alveoli: pneumonia

24

4 respiratory viruses and main site of ifxn?

1. rhinovirus- nasal cavity (common cold)/some pharynx (pharyngitis)
2. parainfluenza- some LRTI but mainly URTI-- larynx, (laryngitis & croup), pharynx (pharingitis) and nasal cavity (common cold)
3. RSV (respiratory Suncytial virus)- URTI and LRTI but mainly Bronchioles (bronchiolitis) and nasal cavity (common cold)
4. Influenza- URTI and LRTI but mainly alveoli (pneumonia) and nasal cavity (common cold)

25

manifestations of rhinovirus

ifxn of nasal cavity (common cold)/some pharynx (pharyngitis)

26

manifestations of parainfluenza

parainfluenza- some LRTI but mainly URTI-- larynx, (laryngitis & croup), pharynx (pharingitis) and nasal cavity (common cold)

27

manifestations of RSV in children under 2 yo? in adults?

2 yo: bronchiolitis
adults: common cold

28

RSV is spread via

droplet

29

pathogenesis of RSV leading to bronchiolitis in children < 2yo

1. LRTI ifxn ---> bronchiolar (part without cartilage) inflammation ---> bronchiolar narrowing due to edema/etc. ---> wheezing on expiration, decreased O2 exchange/gas trapping ----> recovery

30

how protective is the immune system for repeated infections from RSV?

not good! You can get infected again because immunity is so bad. the manifestation generally decreases though (ie common cold in adults)

31

sources of influenza

1. birds (inf. A)
2. pigs (inf. A)
3. humans (inf A, B and C)

32

how is influenza spread

1. droplets (cough/sneeze)
2. animals ( inf A)

33

hosts for inf.
A:
B:
C:

hosts for inf.
A: mammals and birds
B: humans (and seals)
C: humans

34

disease for inf.
A:
B:
C:

disease for inf.
A: mild-severe
B: mild, rarely severe
C: very mild, generally in children

35

antigenic variation and outbreak associated with it in inf
A:
B:
c:

antigenic variation in inf
A: shift and drift (pandemics and epidemics respectively)
B: drift (epidemics)
c: NA

36

vaccines for inf:
A:
B:
C:

vaccines for inf:
A: yes
B: yes- included in vaccine for A
C: no bc the manifestations are so mild

37

antigenic drift in influenza is caused by... and leads to...

point mutations in H (hemaglutinnin) and N (neuraminidase) proteins-- so that they start to escape the immune response so hat there's more outbreak on the population level
... leads to epidemics, mild/regional outbreaks

38

antigenic shift is caused by... and leads to...

caused by: introduction of a new Ag type into the human population so there's pretty much no immunity in the pop
leads to: lg, explosive outbreaks, pandemics

39

what leads to Anigenic shifts in Influenza A

reassortment --- RNA of 2 different inf viruses (often 1 from a bird and one from a pig and/or human) mixes, and then is transmitted to a human

40

antivirals are used for what 2 things related to infuenza?

1. treatment (decrease duration of symptoms)-- most effective within 48 hours of onset
2. prophylaxis: 70% effective for household members, etc

41

because resistance to the influenza antivirals is common and varies with the strain (subtype), before treating someone you should...

look at what the CDC recommends

42

two types of adamantases

1. amantadine and rimantadine

43

two classes of drugs used to txt influenza

1. adamantases
2. neuraminidase inhibitors

44

2 types of neuraminidase inhibitors

1. olseltamivir
2. zanamavir

45

mechanism of how adamantases blocks spread of influenza A

it prevents the influx of H+ into the endosome via the M2 channels, so the virus isn't uncoated/can't be released into the cytoplasm

46

mechanism of how neuraminidase inhibitors prevent the spread of influenza A and B

it blocks the release of the virus from the cell because it prevents neuraminidase from cleaving sialic acid

47

Norovirus is spread via

the fecal-oral route/food

48

what are "norovirus "non-secreters"

people who don't have H antigen on their epithelial cells and so they can't be bound by norovirus/they can resist ifxn

49

pathogenesis of norovirus

1. pathogen gets into gi tract (usually via contaminated food)
2. binds H Ag on host cells
3. replicates in the jejunum
4. leads to vomiting and diarrhea
5. recovery with little/no immunity from future ifxn

50

what is norovirus?

viruses that cause gastraoenteritis

51

what is the H antigen?

a carb structure found on many types of cells that is the precursor to O, B and A Ag on RBCs. It is the receptor for the norovirus

52

norovirus is aka

the cruise ship virus-- bc it's associated with outbreaks in closed pops that are difficult to stop.

53

why is it so difficult to stop the transmission of norovirus

1. little host immunity
2. efficient transmission (food borne)
3. very stable virus, not inactivated by soap, EtOH, ammonia based products-- you need bleach

54

rotavirus is primarily found in people of what age

young children (6 mo-2 yo)

55

how is the rotavirus spread?

fecal-oral

56

pathogenesis of the rotavirus?

1. fecal-oral spread
2. vomiting/diarrhea
3. dehydration, recovery with hydration
4. subsequent infections are subclinical (asymp)-- but still shedding virus

57

if not treated, rotavirus can lead to

significant morbidity and death due to severe dehydration

58

the significance and epidemiology of rotavirus

1. it's a major cause of endemic diarrhea in childrenworld-wide (particularly where vaccine isn't used)
2. significant cause of morbidity/mortality in developing nations
3. Antigenic variations using same mech as influenza A (reassortment bc rotavirus is segmented and there are animal and human versions)
4. safe and effective oral vaccines available

59

how is polio spread?

fecal-oral

60

pathogenesis of polio?

1. lands in the GI lumen
2. enters GI lymphatics (GALT), and moves back and forth between GI lumen and GALT
3. primary viremia-- low levels of viral load in blood
4. Replication in viscera
5. secondary viremia- with higher levels of virus in blood
6. CNS ifxn

61

4 different manifestations of polio

1. inapparent/asymptomatic
2. abortive polio (headache, fever, sore throat)
3. aseptic meningitis
4. paralytic polio (1%)- ifxn of motor neurons, cell death and paralysis. bulbar ifxn: medulla oblongata controls resp-- respiratory paralysis

62

two types of polio vaccines?

1. Inactivated Polio Vaccine (Salk Virus)
2. Oral Polio Vaccine (Sabin)

63

how is the inactivated Polio Vaccine prepared (salk)? how about the oral polio vaccine (sabin)?

1. formalin inactivation
2. attenuated-- passed in cell culture repeatedly until it's no longer infectious

64

advantages of the inactivated polio vaccine (IPV) (3)

1. no vaccine assoc. poliomyelitis
2. humoral immunity
3. can be combined with other vaccines that are injected

65

disadvantages of the inactivated polio vaccine (salk) (3)

1. injection-- painful and inconvenient
2. no mucosal immunity
3. expense

66

advantages of OPV (oral polio vaccine) (4)

1. humoral and mucosal immunity
2. duration of immunity
3. ease of administration
4. cheap

67

disadvantages of the oral polio vaccine (OPV) (2)

1. can mutate to virulent form through point mutations in the genome
2. cold chain transport

68

what is the most infectious virus that we know about?

measles

69

the pathogenesis of measles (5)

1. infects the respiratory epithelium
2. primary viremia
3. replication in the reticulo-endothelial system (RES)
4. secondary viremia
5. widespread replication

70

what is primary viremia

the viral load in the blood after the initial ifxn at site of infxn-- usually lower

71

what is secondary viremia?

the viral load in the blood after it already replicated in different organs -- usually higher than primary viremia

72

3 "c's" of classic measles

cough, coryza, conjunctivitis

73

classic measles presentation

cough, coryza (runny nose), conjunctivitis, koplik's spots, then rash and life-long immunity

74

complications of measles (5 in 3 different body parts)

1. respiratory: pneumonia
2. CNS: encephalitis, SSPE (subacute pan encephalitis)
3. GI: gastroenteritis, hepatitis

75

when does Koplik's spots appear in the relation to the measles rash? and what does it look like?

it precedes the rash, it's blue-white spots with surrounding erythema on the hard palate and inside of the cheek

76

what does the measles rash look like? where does it start and how does it spread?

1. it's macules that become confluent over time (spread into each other)
2. it starts on the face and moves downward to the trunk, includes the palms and soles

77

Hepatitis A is very similar to...

hepatitis E

78

Hep A
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:

Hep A
spread: fecal-oral
incubation wks: 2-7
acute hepatitis: decreased in children
chronic hepatitis: no
hepatic cancer: no
vaccine: yes

79

Hep E
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:

Hep E
spread: fecal-oral
incubation wks: 2-7 wks
acute hepatitis: increased with pregnancy
chronic hepatitis: no
hepatic cancer: no
vaccine: yes, but not in the US-- it's produced in china and used primarily in east asia where hep E is common

80

Hep B
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:

Hep B
spread: percutaneous, sex, vertical
incubation wks: 4-25 wks
acute hepatitis: yes
chronic hepatitis: approx 5%
hepatic cancer: yes
vaccine: yes

81

Hep D
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:

Hep D
spread: percutaneous, sex, vertical
incubation wks: 4-25 wks
acute hepatitis: w/B
chronic hepatitis: increased w/B
hepatic cancer: increased w/B
vaccine: only for Hep B

82

Hep C
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:

Hep C
spread: percutaneous, sex, vertical
incubation wks: 2-23 wks
acute hepatitis: yes
chronic hepatitis: approx 80%
hepatic cancer: yes
vaccine: no

83

which hepatitis's are spread by fecal-oral transmission? Which ones are transmitted via percutaneous, sex or vertical exposures?

fecal oral: A and E
percutaneous, sex, vertical: B, D, C

84

we have vaccines for which viral hepatitis?

hep A, E (outside of the US), and B
- you don't need a vaccine for D, you can just get rid fo B

85

which for of hepatitis is completely dependent on the existence of another form of Hep?

hep D is dependent on the existence of Hep B

86

which forms of hepatitis are associated with hepatic cancer?

Hep B, D and C

87

which form of Hep is primarily associated with chronic hepatitis?

C

88

liver injury in viral hepatitis is caused by

the immune response-- Cytotoxic T lymphocytes (CTLs)-- histologically, you can see lg # of blue lymphocytes, and there are lg # of cells undergoing death by necrosis

89

what are 2 serum indicators of viral hepatitis? (2)

1. serum aspartate and alanine aminotransferases (AST and ALT) are elevated with hepatic injury
2. bilirubin levels are elevated slightly after

90

lab tests for viral hep A:
acute:
chronic:

lab tests for viral hep A:
acute: IgM anti-HAV
chronic: NA

91

lab tests for viral hep D:
acute:
chronic:

lab tests for viral hep D:
acute: IgM anti-HDV
chronic: IgG and IgM anti-HDV

92

lab tests for viral hep c:
acute:
chronic:

lab tests for viral hep c:
acute: anti-HCV Ab
chronic: anti-HCV +, HCV RNA and liver enzymes rise and fall

93

manifestations of acute viral hepatitis (5)

1. asymptomatic incubation-- variable length, relatively long
2. fever, fatigue, nausea, abdominal pain
3. 1-2 wks later: dark urine, clay colored stool bc liver stops being able to conjugate bilirubin
4. 1-5 days later: jaundice/icterus, enlarged/tender liver
5. 1-4 months later: recovery or chronic hep

94

adolescents and adults and Hep B-
route of transmission:
immune response:
chronic risk:
risk of cancer:

adolescents and adults and Hep B-
route of transmission: percutaneous, sex
immune response: good
chronic risk: 1%
risk of cancer: low

95

infants and Hep B-
route of transmission:
immune response:
chronic risk:
risk of cancer:

infants and Hep B-
route of transmission: perinatal/vertical
immune response: poor
chronic risk: 90%
risk of cancer: high

96

who gets chronic hepatitis B?

90% of perinatal ifxns, and 1% of adults/adolescents

97

two paths for chronic hep B infection

1) chronic infection ---> replicative phase (abundant virus) ---> high rate of transmission and ongoing liver injury/disease
2. chronic ifxn --> replicative phase (abundant virus) ---> 10%/yr go into a nonreplicative phase (scant virus) ---> low rate of transmission and little/no liver injury, and often asymptomatic

98

what happens during acute HBV if it leads to recovery
HBsAg (surface Ag):
IgM anti HBc (core):
IgG anti-HBc:
anti-HBs
HBeAg:
Anti-HBeAg:

what happens during acute HBV if it leads to recovery
HBsAg (surface Ag): sharp rise and drop -- peaks around wk 8
IgM anti HBc (core): rises after the rise of HBsAg, peaks around wk 24
IgG anti-HBc: class switch around wk 24-- then stays high
anti-HBs: window of nothing after HBsAG disappears before we see anti-HBs increase around wk 24
HBeAg: indicates replication. Stops around the class switch to IgG
Anti-HBeAg: can be found for a while

99

Chronic HBV
replicative phase:
nonreplicative phase:
HBeAg:
Anti-HBeAg:
HBsAg:
IgM anti-HBc:
IgG anti-HBc:

Chronic HBV
replicative phase: > 1000 HBV/ml-- high levels of virus detected in the blood
nonreplicative phase: < 1000 HBV/ml in blood, HBeAg fades during this period
HBeAg: persists during replication period
Anti-HBeAg: present during non-replicative phase
HBsAg: first thing to show up during replicative phase
IgM anti-HBc: follows the HBsAg, rises and falls with a class switch
IgG anti-HBc: class switch from IgM to IgG. IgG persists

100

if someone is susceptible to Hep B virus, they will be + for which of the following?
HBsAG
HBeAG
IgM a-HBc
IgG a-HBc
a-HBs
a-HBe

none!

101

if someone has acute Hep B virus, they will be + for which of the following?
HBsAG
HBeAG
IgM a-HBc
IgG a-HBc
a-HBs
a-HBe

HBsAg, HBeAG, IgM a-HBc

102

if someone has recovered from Hep B virus, they will be + for which of the following?
HBsAG
HBeAG
IgM a-HBc
IgG a-HBc
a-HBs
a-HBe

IgG a-HBc, a-HBs, a-HBe

103

if someone has chronic Hep B virus, they will be + for which of the following?
HBsAG
HBeAG
IgM a-HBc
IgG a-HBc
a-HBs
a-HBe

HBsAg, it might have + HBeAg, IgG a-HBc, a-HBe

104

if someone has been vaccinated for Hep B virus, they will be + for which of the following?
HBsAG
HBeAG
IgM a-HBc
IgG a-HBc
a-HBs
a-HBe

a-HBs

105

if you still have Hep B ifxn (acute or chronic) you will have what in your blood?

HBsAg

106

the biggest difference in serology between people with acute vs chronic Hep B

CLASS SWITCH AGAINST THE CORE PROTEIN
acute has IgM a-HBc
chronic has IgG a-HBc

107

Hepatitis D is dependent on what for survival? Why?

it's dependent on hepatitis B because it gets its capsid protein from HBV

108

coinfection of HDV and HBV usually leads to

acute hepatitis with recovery, but the risk of fulminant hepatitis is increased

109

superinfection of HBV with HDV usually leads to

acute exacerbation with fulminant hepatitis. this can also lead to chronic hepatitis with increased progression and hepatocellular cancer

110

manifestations of chronic hepatitis C

chronic ifxn ----> intermittent increase in replication (Ag variation) ---> immune response ----> liver damage, can cause cirrosis

the intermittent increase in replication can lead to hepatocellular cancer (annual risk of 1-4%)

111

how are arboviruses defined?

by transmission via arthropods

112

the two groups of arboviruses based on manifestations

1. encephalitis viruses
2. hemorrhagic fever viruses

113

Encephalitic Arbovirus manifestations

asymptomatic to severe encephalitis- fever and fusion

114

transmission of encephalitic arboviruses is between _____ by _____?

between vertebrates, by mosquito vectors

115

4 major encephalitic arboviruses

1. WNV
2. EEE
3. WEE
4. SLE

116

how do humans fit into the arbovirus lifecycle?

they're usually incidental hosts

117

what type of mosquito transmits WNV?

culex mosquito

118

pathogenesis of WNV

1. gets in blood from the bite
2. replicates in the lymphatic system
3. viremia
4. affects the brain

119

3 manifestations of WNV

1. asymptomatic- 75%
2. West Nile Fever (25%)- fever, HA, myalgias, fatigue
3. neuroinvasive disease (1%)- meningitis, encephalitis, WNV poliomyelitis

120

manifestations of West Nile Fever (25% of people with WNV)

ever, HA, myalgias, fatigue

121

manifestations of neuroinvasive disease from WNV (1%)

meningitis, encephalitis, WNV poliomyelitis

122

dengue virus is spread by what type of mosquito

aedes

123

Dengue fever is also known as

breakbone fever

124

Dengue virus enters your system through the...

blood (transmitted via mosquitos)

125

pathogenesis of Dengue (4 steps)

1. Enters blood (via Aedes mosquito)
2. infection of macrophages
3. ???
4. suppression of hematopoiesis in infected individual and widespread replication

126

symptoms of Dengue Fever (aka Breakbone fever)

fever, muskuloskeletal pain

127

symptoms of dengue Hemorrhagic fever (3)

1) spontaneous bleeding of the skin, gums, GI, etc
prolonged/heavy menses
2) decreased platelets
3) capillary leakage (loss of albumin)

128

symptoms of Dengue shock syndrome (4)

Dengue Hemorrhagic Fever (DHF) PLUS CIRCULATORY FAILURE
1) spontaneous bleeding of the skin, gums, GI, etc
prolonged/heavy menses
2) decreased platelets
3) capillary leakage (loss of albumin)
4) circulatory failure

129

3 different manifestations of Dengue Virus

1. Dengue Fever (breakbone fever)
2. Dengue Hemorrhagic Fever (DHF)
3. Dengue Shock Syndrome

130

How many serotypes are there of Dengue virus?

4

131

the initial infection with Dengue virus causes ?

Dengue Fever (breakbone fever). It DOES NOT CAUSE Dengue Hemorrhagic Fever! DHF!!

132

Can you get Dengue Hemorrhagic Fever (DHF) the first time you get dengue?

NO! you have to have been infected with dengue at least once before, and get infected with a different serotype to get DHF

133

why does an infection with a second serotype of dengue make the reaction to dengue worse?

bc weakly cross reactive ABs against different serotype of virus might increase infectivity of virus for macrophages

134

Yellow fever virus is usually hosted in what and transmitted by what?

hosted in primates and transmitted by the Aedes mosquito

135

Pathogenesis of the yellow fever virus

1. eners blood stream via the Aedes mosquito
2. Infection of macrophages
3. enters the bloodstream
4. suppression of hematopoiesis and widespread replication

136

the symptoms of Yellow Fever in the steps they present in (5)

1. fever
2. resolution
3. high fever and abdominal pain and vomiting
4. hepatitis which leads to jaundice (hence the "yellow" fever) and hemorrhagic manifestations
5. coma/death in 50% of those infected

137

is there a vaccine for yellow fever?

yes, vaccine with the attenuated virus

138

when is it recommended to get the yellow vaccine

if you're traveling in south america and africa

139

Human Herpes Virus genome:

dsDNA that replicates in the host cell nucleus

140

what is the normal cycle of infection for herpes (3 components)

1. primary infection
2. latency
3. reactivation

141

are the manifestations of primary human herpes virus and reactivation the same?

nope, they're different!

142

How is HSV-1 generally transmitted? HSV-2?

HSV-1 is transmitted from person to person orally
HSV-2 is transmitted from person to person sexually (via the genital mucosa)

143

pathogenesis of HSV

1. primary ifxn in epithelial cells
2. axonal transport to the nervous system
3. latent in sensory neuron (LAT transcript- latent associated transcript)
4. reactivation and axonal transport
5. recurrent ifxn in epithelial cells
6. +/- symptoms with release from host regardless

144

how does HSV move within the host?

axonal transport

145

where does HSV lay dormant?

in the sensory neurons (LAT transcript- latent associated transcript)

146

LAT transcript- what is it and what is it associated with?

Latent associated transcript

147

Oral and Genital HSV symptoms

painful clustered vesicles ----> ulcerations ---> crusting and resolution

148

oral herpes is associated with

cold sore, fever blisters

149

genital herpes in males is associated with

vesicular lesions on the shaft of the penis that ulcerate and crust over

150

2 ways that Varicella-Zoster Virus (VZV) is spread and and the presentation associated with each route of transmission

respiratory spread (chicken pox)
contact spread (uncommon-- shingles)

151

chicken pox (VZV) is spread by...

respiratory route

152

shingles (VZV) is spread via

contact

153

pathogenesis of VZV

1. primary infection in nasopharynx (respiratory droplets)
2. viremia
3. Ifxn of other sites including skin and sensory neurons
4. latent in sensory neurons
5. reactivation and axonal transport
6. replication in skin along a dermatome leading to vesicular lesions

154

what two viruses are latent in neurons?

HSV 1/2
VZV

155

primary VZV IFXN symptoms

chickenpox: fever with maculopapules, vesicles and crusted lesions together that start on the trunk (dewdrop on a rose petal)

156

where do chickenpox start?

on the trunk, and then spread outward to cover the entire body

157

VZV reactivation presents as

Herpes Zoster or shingles: painful vesicular rash in a dermotomal distribution

158

who is given the vaccination for VZV?

1. an attenuated viral vaccine is given to children to prevent primary ifxn
2. a larger dose of the same vaccine is given to older people to prevent reactivation ifxn-- vaccination of people who are already infected is an uncommon strategy

159

How is Epstein Barr virus (EBV) transmitted?

in saliva-- Kissing/sharing water bottles

160

pathogenesis of epstein barr virus (EBV)

1. primary infection in oropharynx
2. viremia
3. infection of B cells
4. latency in B cells
5. Reactivation in B cells

161

what is the site of latency for EBV?

B cells

162

what is aka the kissing disease?

EBV- Epstein Barr virus

163

sx of primary ifxn of EBV in children

mild or asymptomatic

164

sy of primary ifxn of EBV in adolescents and adults

mononucleosis- fever, pharyngitis, lympadenopathy and atypical lymphocytes (lg # of activated CD8 CTLs)

165

subsequent manifestations of reactivation of EBV

1. lymphoproliferative disease
2. Burkitt's lymphoma
3. nasopharyngeal carcinoma

166

what are heterophile abs and who makes them?

heterophile abs are human Abs that agglutinate (clump) RBCs from sheep, horses or cows. Pt with mononucleosis (EBV) make heterophile Abs

167

do pt with active EBV make heterophile Abs? What about Pts with latent EBV?

pt with active EBV do. Pts with latent EBV don't

168

how do you test for EBV ifxn?

the monospot test, which tests for heterophile Abs by seeing if sheep, horse or cow blood agglutinates when mixed with pt blood

169

The Herpes Viruses and their primary manifestation (6)

1. HSV-1- oral herpes
2. HSV-2- genital herpes
3. EBV- monomucleosis
4. CMV- heterophile negative mononucleosis
5. HHV-6 - sixth disease
6. HHV-8 - reactivation leads to Kaposi's sarcoma

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manifestations of CMV (cytomegaly virus) primary infxn

heterophile negative monomucleosis

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manifestations of CMV- cytomegalyvirus- reactivation in transplant pt

GI inflammation, pneumonia, disseminated dz

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manifestations of CMV- cytomegalyvirus- reactivation in HIV pt

retinitis (cotton, fluffy infiltrate at the back of the eye) and disseminated dz

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CMV is generally reactivated in what two types of pt

transplant pt and HIV pt

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manifestations of HHV-6 primary infection

sixth disease, exanthem subitum (childhood rash) or roseola. Fever +/- seizures followed by a generalized rash

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HHV-8 reactivation causes

Karosi's sarcoma (a sarcoma formerly seen in many pt with HIV but now rare bc of ARVs)

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What 2 antivirals are used for HSV and VZV? How do they work?

Acyclovir and Valacyclovir (oral) are both nucleoside analogues. This means that they are phosphorylated by the viral TK (thymidine kinase) enzyme and incorporated into the DNA, which stops DNA synthesis

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Acyclovir and Valacyclovir are both what types of antivirals? How do they work and what two viruses are they used for?

they are nucleoside analogues. This means that they are phosphorylated by the viral TK (thymidine kinase) enzyme and incorporated into the DNA, which stops DNA synthesis.
They are used for HSV and VZV

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why do acyclovir and valacyclovir stop viruses from replicating their genome, but not humans?

because they're phosphorylated by the viral Thymidine Kinase (TK), but not by the host

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what two antivirals are used to treat CMV, and how do they work?

Ganciclovir and Valganciclovir (oral) are both phosphorylated by viral kinase (UL97), incorporated into DNA by viral polymerase and then stop DNA synthesis

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what two antivirals are used for treatment of Herpes (HSV, VZV or CMV) if others prove unsuccessful because the strains of herpes are resistant? How do these work?

Foscarnet and Cidofovir inhibit viral DNA polymerase (no role for TK)

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What are Ganciclovir and Valganciclovir (oral) used for and how do they work?

they are used to txt CMV. They work by being are both phosphorylated by viral kinase (UL97), incorporated into DNA by viral polymerase and then stopping DNA synthesis

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what are Foscarnet and Cidofovir used for and how do they work?

txt of resistant strains of HSV, VZV or CMV. They inhibit viral DNA polymerase (no role for TK)

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why are Foscarnet and Cidofovir not used as a first line of defense agst herpes viruses?

because they cause renal toxicity

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How is HIV primarily acquired?

mainly by sexual transmission

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how does the level of virus in a source partner relate to the risk of transmission?

the higher the viral load, the more risk of transmission

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How do genital herpes affect transmission of HIV?

they increase the risk of transmission because it provides a way for the virus to move in/out

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rank oral sex, anal sex and vaginal sex from most risky for the transmission of HIV to the least risky

anal sex > vaginal > oral

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what is the risk of perinatal HIV transmission without ARV therapy? with ARV therapy?

without ARVs: 1/3
with ARVs: 1/100

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4 modes of transmission of HIV

sexual contact
perinatal transmission
IDU
medical use of blood/tissue

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what is the risk of HIV transmission from medical use of blood? organs?

risk from screened blood in the US is low (1/2,000,000), but many get it from organ transplants

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What viral particle allows HIV to dock on the host cells?

GP120

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what viral particle allows HIV to fuse with the host cell membrane?

gp41

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gp120 on HIV binds to what host cell receptors early in ifxn? What about later?

early: CD4 and CCR5
late: CXCR5

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life cycle of HIV (7 steps)

1. GP120 docks to host cell-- binds to CD4 or CCR5 early on in ifxn or CXCR4 late in ifxn
2. GP41 allows HIV to fuse to host cell
3. ssRNA is released from the capsid with reverse transcriptase
4. dsDNA is integrated into the genome at a random site
5. it's turned into a latent provirus
6. CD4 cells are activated, the virus starts replicating
7. the virus is assembled and a protease is included that is required for the maturation of the viral particle after budding

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symptoms of acute HIV ifxn

>70% of people: Fever, Fatigue
>50% of people: Rash, Myalgia/arthralgia, Pharyngitis, Night sweats
-Nausea, vomiting, diarrhea (30-60%)

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Pathogenesis of HIV

1. Mucosal exposure
2. Dendritic Cells are infected by HIV binding to CD4+
3. Transport to regional lymph nodes and rapid viral replication
Note: after this step, it is too late to treat with post-exposure prophylaxis
4. Blood stream invaded by virus-infected cells leads to widespread dissemination
5. Latent reservoir is established

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what two genetic factors alter one's susceptibility to HIV?

1. The CCR5 delta32 knockout will make the host immune to HIV
2. Various HLA types can lead to fast or slow progression

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levels of HIV, CD4 cells, anti-HIV antibody and anti-HIV CTL 2-6 weeks after ifxn (initial infection)

1. normal CD4’s
2. smoldering viral load
3. no anti-HIV antibodies
4. little CTL activity

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levels of HIV, CD4 cells, anti-HIV antibody and anti-HIV CTL 2-8 weeks after ifxn (acute phase)

1. Dip in CD4’s
2. Viral load in blood (viremia) is the highest it will ever be
3. Still no anti-HIV antibodies
4. Strong CTL activity

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levels of HIV, CD4 cells, anti-HIV antibody and anti-HIV CTL 6 months after ifxn

1. CD4 counts stabilize
2. Viral load stabilizes at VIRAL SET POINT determining how the disease will progress
3. Anti-HIV antibodies present (will screen positive for a rapid test)
4. CTL activity is reduced since the virus has become latent

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what opportunistic Ifxns are common when the CD4 count is between 400 and 300

400: herpes zoster- chickenpox reactivating as shingles
350: Tb- primary or reactivation, usually as a pneumonia
300: Oral candidiasis- due to overgrowth of oral Candida albicans, a yeast that's part of the normal flora, it presents a a whitish exudate in the mouth

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what is an independent predictor of future opportunistic ifxns in HIV pts?

oral candidiasis-- due to overgrowth of oral candida albicans-- presents as a whitish exudate in the mouth

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what opportunistic ifxn is common at a CD4 count of 200 and gives you the diagnosis of AIDS

pneumocystis carinii pneumonia

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what opportunistic ifxns are common around a cd4 count of 200 (3)

pneumocystis carinii pneumonia
esophageal candidiasis
mucocutaneous herpes

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what two opportunistic ifxns are common with a cd4 count arnd 100 (5)?

1. toxoplasmosis
2. cryptococcus
3. coccidioidomycosis
4. mycobacterium avium complex
5. CMV

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what are 2 opportunistic IFXNS are common around a CD4 count of 50?

1. cryptosporidius
2. PML

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If a person has an acute HIV ifxn, which of the following diagnostic tests will be positive?
ELISA for Ab
p24 Ag
Western Blot
HIV RNA (Viral Load)

maybe the p24 Ag, definitely the HIV viral load

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If a person has an established HIV ifxn, which of the following diagnostic tests will be positive?
ELISA for Ab
p24 Ag
Western Blot
HIV RNA (Viral Load)

all of them will be positive

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what is the p24 Ag?

a protein Ag produced by the HIV virus that can be tested for. It is sometimes found to be present in the acute stages of HIV, and always found in the established cases of HIV

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do 3rd and 4th generation ELISA tests detect Abs from HIV-1, HIV-2, or both?

both

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what does the 4th generation ELISA test test for? What is the benefit of this?

HIV-1 Abs, HIV-2 Abs and the p24 Ag. Because it also tests for the p24 Ag, it will become positive sooner than the otehr ELISA tests

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why is the measure of HIV RNA important?

the viral load predicts the rate of progression and predicts/measures the efficacy of anti-retroviral therapy

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what does the CD4 T-lymphocyte count tell us about HIV pts

the amount of immunosuppression

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how is resistance testing done in HIV pts?

by sequencing HIV RNA for mutations associated with resistance to anti-retrovirals

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what are the 5 targets of HIV drug therapy?

1. gp41 viral fusion protein
2. host CCR5 protein
3. reverse transcriptase
4. integrase
5. protease

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what is the mechanism for how Nucleoside reverse transcriptase inhibitors (NRTI) work?

they're incorporated into nascent viral DNA and then block the elongation of DNA

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what is the mechanism for how a non-nucleoside Reverse transcriptase Inhibitor (NNRTI) works?

it binds outside the active site of RT (reverse transcriptase) and allosterically inhibits the RT

218

how do protease inhibitors work?

it is a structural analogue of protease substrates that inhibit the protease from allowing the maturation of HIV after budding

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how do HIV fusion inhibitors work?

these are peptides of gp41 that block the conformational change in gp41 needed for fusion

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how do CCR5 antagonists work?

they bind CCR5, preventing interaction with gp120

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what are the 5 different types of HIV meds

1. NNRTIs (non-nucleoside rev. transcriptase inhibs)
2. NRTIs- Nucleoside rev. transcriptase inhibs
3. CCR5 antagonists
4. Fusion inhibitors
5. Protease inhibitors
6. Integrase strand-transfer Inhibitors

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how do Integrase Strand-Transfer Inhibitors work?

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

223

CDC guidelines recommend ART for who? what does the evidence suggest?

all infected ind to reduce the risk of disease progression. Data suggests the drugs seem to be most effective for those with lower CD4 counts

224

two reasons ART is recommended

1. to reduce the risk of disease progression in an individual
2. to reduce transmission

225

Initial therapy for HIV is:

2 NRTI plus one of the following:
-NNRTI
-Boosted protease inhibitor
-Integrase strand transfer inhibitor

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what is a "boosted" protease inhibitor

it's when a protease inhibitor is given with a low dose of ritonivir, which inhibits the hepatic metabolism of the protease inhibitor by cytochrome p450 so that the protease lasts longer in the blood

227

what is ritonivir?

it is a very weak protease inhibitor which, when given at very low doses can boost the effectiveness of other protease inhibitors by inhibiting the hepatic metabolism of the protease inhibitor by cytochrome p450 so that the protease lasts longer in the blood

228

what are enteroviruses?

a large group of viruses with multiple subgenera spread via fecal/oral system or respiratory spread that are an important cause of aseptic meningitis

229

which enterovirusal subgenera are responsible for polio?

polioviruses 1-3

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which enterovirusal subgenera are responsible for exanthems (skin rashes) and enanthem (lesions of the internal mucosal surfaces), typically in children, including: hand-foot-mouth disease (HFMD) and herpangina?

coxsackieviruses A

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which enterovirusal subgenera are responsible for myocarditis and pericarditis?

coxsackieviruses B

232

what is the most common cause of aseptic meningitis?

enteroviruses (polio, coxsackieviruses A and B)

233

are there any vaccines or antivirals for enteroviruses?

there are no antivirals, and polio is the only enterovirus with a vaccine

234

how is mumps spread?

respiratory route (droplets)

235

manifestation of the mumps?

ifxn of the parotid glands (possibly the submaxillary and salivary glands-- imagine the asymmetrically swollen faced child) with swelling and pain that resolves in 7-10 days

236

common complications of mumps include (2):

orchitis (swelling of the testes) and aseptic meningitis

237

rare complications with mumps

1. hearing loss (children)
2. encephalitis
3. fetal loss in first trimester
4. oophritis (swelling of ovaries)
5. pancreatitis

238

is there a vaccine for mumps?

yes and it's effective and safe

239

how are adenoviruses transmitted?

fecal-oral and fomite (ocular fluid) transmission

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manifestations of adenoviruses

1. self-limited respiratory manifestations
2. ocular ifxns: pharyngoconjunctival fever, epidemic keratoconjunctivits
3. self-limited, acute, watery diarrhea

241

what happens when immunocomp people get adenovirus

persistent virus can reactivate or new ifxn can occur

242

what are the manifestations of adenovirus in Hematopoieitic Stem Cell Transplant Pts (HSCT)

hemorrhagic cystitis, enteritis, pneumonitis, hepatitis with viremia

243

what two groups of people are particularly susceptible to adenoviruses?

HSCT- hematopioitic stem cell transplant pt
Solid organ transplant pt

244

Parvovirus B19 is transmitted via

respiratory and verticle transmission

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Parvovirus B19 commonly manifests in childhood as...

5th disease with fever and "slapped cheek rash", which then spreads to trunk, arms and legs

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parvovirus B19 in adults commonly manifests as

arthropathy: self-limited symetric swelling and pain of joints in hands and feet
Anemias (replicates in erythroblasts) leading to transient aplastic crisis with underlying hemolytic disease and pure red cell aplasia in immunocompromised

247

which disease is associated with slapped cheek rash?

parvovirus B19

248

primary ifxn with Parvovirus B19 in a pregnant women usually has what consequences for the fetus?

usually none, but it cal lead to reduced fetal RBC, fetal death and fetal hydrops (accumulation of fluid/edema in at least 2 fetal compartments)

249

where does Parvovirus B19 replicate? And what consequences does this have?

in erythroblasts-- which leads to anemia.
- transient aplastic crisis with underlying hemolytic disease
- pure red cell aplasia in immunocompromised

250

why does teh parvovirus B19 virus persist in the host?

bc there's a decreased host reponse, because the virus replicates in erythroblasts and causes anemia

251

which virus is - ssDNA, non-enveloped virus and what disease does it cause?

Parvovirus B19-- 5th dz and anemia

252

which virus has linear ds DNA with an icosahedral complex

adenovirus

253

which ds DNA viruses are enveloped? (3)

Herpesviruses (linear)
smallpox (linear)
Hepadnavirus (Hep B, circular)