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MICRO II > virology review > Flashcards

virology review Flashcards

1
Q

viruses are composed of

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

viruses depend on what for replication?

A

host cells

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3
Q

what are the structural characteristics of viruses?

A
  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
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4
Q

different types of nucleic acid present in a virus

A
  1. ss +/- RNA
  2. ds RNA
  3. ss or ds DNA
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5
Q

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

A

viral receptors for host cells, because they’re exposed

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6
Q

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

A

reassortment.

important for: influenza A and rotavirus

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7
Q

are enveloped or nonenveloped viruses more stable?

A

nonenveloped

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8
Q

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

A

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

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9
Q

unlike - ssRNA, +ssRNA is…

A

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

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10
Q

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

A

mRNA

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11
Q
  • ss RNA needs to do what in order to become infectious?
A

needs to make + strand copies —> mRNA

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12
Q

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

A

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

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13
Q

unlike other RNA viruses, Retroviruses ENCODE

A

RNA-dependent DNA polymerase (aka reverse transcriptase)

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14
Q

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

A

bring a polymerase to copy the RNA

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15
Q

how do we detect viral infections? (3 methods)

A
  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)
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16
Q

what does serology look for/tell us about viruses?

A

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

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17
Q

how can components of a virion be detected?

A
  1. protein is detected by immunological methods (ie rapid influenza test)
  2. PCR shows viral nucleic acids
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18
Q

3 patterns of viral ifxns

A
  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
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19
Q

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

A

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

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20
Q

what is latent viral ifxn and 2 examples?

A

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
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21
Q

what is chronic viral ifxn? 2 examples?

A

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

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22
Q

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

A
  1. nasal cavity: common cold
  2. pharynx: pharyngitis
  3. larynx: laryngitis and croup
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23
Q

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

A
  1. trachea: tracheitis
  2. bronchi: bronchitis
  3. bronchioles: bronchiolitis
  4. alveoli: pneumonia
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24
Q

4 respiratory viruses and main site of ifxn?

A
  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)
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25
Q

manifestations of rhinovirus

A

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

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26
Q

manifestations of parainfluenza

A

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

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27
Q

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

A

2 yo: bronchiolitis

adults: common cold

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28
Q

RSV is spread via

A

droplet

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29
Q

pathogenesis of RSV leading to bronchiolitis in children < 2yo

A
  1. LRTI ifxn —> bronchiolar (part without cartilage) inflammation —> bronchiolar narrowing due to edema/etc. —> wheezing on expiration, decreased O2 exchange/gas trapping —-> recovery
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30
Q

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

A

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

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31
Q

sources of influenza

A
  1. birds (inf. A)
  2. pigs (inf. A)
  3. humans (inf A, B and C)
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32
Q

how is influenza spread

A
  1. droplets (cough/sneeze)

2. animals ( inf A)

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33
Q

hosts for inf.
A:
B:
C:

A

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

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34
Q

disease for inf.
A:
B:
C:

A

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

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35
Q

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

A

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

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36
Q

vaccines for inf:
A:
B:
C:

A

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

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37
Q

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

A

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

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38
Q

antigenic shift is caused by… and leads to…

A

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

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39
Q

what leads to Anigenic shifts in Influenza A

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

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40
Q

antivirals are used for what 2 things related to infuenza?

A
  1. treatment (decrease duration of symptoms)– most effective within 48 hours of onset
  2. prophylaxis: 70% effective for household members, etc
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41
Q

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

A

look at what the CDC recommends

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42
Q

two types of adamantases

A
  1. amantadine and rimantadine
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43
Q

two classes of drugs used to txt influenza

A
  1. adamantases

2. neuraminidase inhibitors

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44
Q

2 types of neuraminidase inhibitors

A
  1. olseltamivir

2. zanamavir

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45
Q

mechanism of how adamantases blocks spread of influenza A

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

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46
Q

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

A

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

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47
Q

Norovirus is spread via

A

the fecal-oral route/food

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48
Q

what are “norovirus “non-secreters”

A

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

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49
Q

pathogenesis of norovirus

A
  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
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50
Q

what is norovirus?

A

viruses that cause gastraoenteritis

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51
Q

what is the H antigen?

A

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

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52
Q

norovirus is aka

A

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

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53
Q

why is it so difficult to stop the transmission of norovirus

A
  1. little host immunity
  2. efficient transmission (food borne)
  3. very stable virus, not inactivated by soap, EtOH, ammonia based products– you need bleach
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54
Q

rotavirus is primarily found in people of what age

A

young children (6 mo-2 yo)

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55
Q

how is the rotavirus spread?

A

fecal-oral

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56
Q

pathogenesis of the rotavirus?

A
  1. fecal-oral spread
  2. vomiting/diarrhea
  3. dehydration, recovery with hydration
  4. subsequent infections are subclinical (asymp)– but still shedding virus
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57
Q

if not treated, rotavirus can lead to

A

significant morbidity and death due to severe dehydration

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58
Q

the significance and epidemiology of rotavirus

A
  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
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59
Q

how is polio spread?

A

fecal-oral

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60
Q

pathogenesis of polio?

A
  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
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61
Q

4 different manifestations of polio

A
  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
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62
Q

two types of polio vaccines?

A
  1. Inactivated Polio Vaccine (Salk Virus)

2. Oral Polio Vaccine (Sabin)

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63
Q

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

A
  1. formalin inactivation

2. attenuated– passed in cell culture repeatedly until it’s no longer infectious

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64
Q

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

A
  1. no vaccine assoc. poliomyelitis
  2. humoral immunity
  3. can be combined with other vaccines that are injected
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65
Q

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

A
  1. injection– painful and inconvenient
  2. no mucosal immunity
  3. expense
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66
Q

advantages of OPV (oral polio vaccine) (4)

A
  1. humoral and mucosal immunity
  2. duration of immunity
  3. ease of administration
  4. cheap
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67
Q

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

A
  1. can mutate to virulent form through point mutations in the genome
  2. cold chain transport
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68
Q

what is the most infectious virus that we know about?

A

measles

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69
Q

the pathogenesis of measles (5)

A
  1. infects the respiratory epithelium
  2. primary viremia
  3. replication in the reticulo-endothelial system (RES)
  4. secondary viremia
  5. widespread replication
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70
Q

what is primary viremia

A

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

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71
Q

what is secondary viremia?

A

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

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72
Q

3 “c’s” of classic measles

A

cough, coryza, conjunctivitis

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73
Q

classic measles presentation

A

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

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74
Q

complications of measles (5 in 3 different body parts)

A
  1. respiratory: pneumonia
  2. CNS: encephalitis, SSPE (subacute pan encephalitis)
  3. GI: gastroenteritis, hepatitis
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75
Q

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

A

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

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76
Q

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

A
  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
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77
Q

Hepatitis A is very similar to…

A

hepatitis E

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78
Q 
Hep A
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:
A 
Hep A
spread: fecal-oral
incubation wks: 2-7
acute hepatitis: decreased in children
chronic hepatitis: no
hepatic cancer: no
vaccine: yes
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79
Q 
Hep E
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:
A

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

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80
Q 
Hep B
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:
A 
Hep B
spread: percutaneous, sex, vertical
incubation wks: 4-25 wks
acute hepatitis: yes
chronic hepatitis: approx 5%
hepatic cancer: yes
vaccine: yes
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81
Q 
Hep D
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:
A 
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
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82
Q 
Hep C
spread:
incubation wks:
acute hepatitis:
chronic hepatitis:
hepatic cancer:
vaccine:
A 
Hep C
spread: percutaneous, sex, vertical
incubation wks: 2-23 wks
acute hepatitis: yes
chronic hepatitis: approx 80%
hepatic cancer: yes
vaccine: no
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83
Q

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

A

fecal oral: A and E

percutaneous, sex, vertical: B, D, C

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84
Q

we have vaccines for which viral hepatitis?

A

hep A, E (outside of the US), and B

- you don’t need a vaccine for D, you can just get rid fo B

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85
Q

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

A

hep D is dependent on the existence of Hep B

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86
Q

which forms of hepatitis are associated with hepatic cancer?

A

Hep B, D and C

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87
Q

which form of Hep is primarily associated with chronic hepatitis?

A

C

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88
Q

liver injury in viral hepatitis is caused by

A

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

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89
Q

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

A
  1. serum aspartate and alanine aminotransferases (AST and ALT) are elevated with hepatic injury
  2. bilirubin levels are elevated slightly after
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90
Q

lab tests for viral hep A:
acute:
chronic:

A

lab tests for viral hep A:

acute: IgM anti-HAV
chronic: NA

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91
Q

lab tests for viral hep D:
acute:
chronic:

A

lab tests for viral hep D:

acute: IgM anti-HDV
chronic: IgG and IgM anti-HDV

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92
Q

lab tests for viral hep c:
acute:
chronic:

A

lab tests for viral hep c:

acute: anti-HCV Ab
chronic: anti-HCV +, HCV RNA and liver enzymes rise and fall

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93
Q

manifestations of acute viral hepatitis (5)

A
  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
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94
Q 
adolescents and adults and Hep B-
route of transmission:
immune response:
chronic risk:
risk of cancer:
A 
adolescents and adults and Hep B-
route of transmission: percutaneous, sex
immune response: good
chronic risk: 1%
risk of cancer: low
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95
Q 
infants and Hep B-
route of transmission:
immune response:
chronic risk:
risk of cancer:
A 
infants and Hep B-
route of transmission: perinatal/vertical
immune response: poor
chronic risk: 90%
risk of cancer: high
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96
Q

who gets chronic hepatitis B?

A

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

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97
Q

two paths for chronic hep B infection

A

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

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98
Q 
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:
A

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

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99
Q 
Chronic HBV
replicative phase:
nonreplicative phase:
HBeAg:
Anti-HBeAg:
HBsAg:
IgM anti-HBc:
IgG anti-HBc:
A

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

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100
Q 
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
A

none!

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101
Q 
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
A

HBsAg, HBeAG, IgM a-HBc

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102
Q 
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
A

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

103
Q 
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
A

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

104
Q 
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

a-HBs

105
Q

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

A

HBsAg

106
Q

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

A

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

107
Q

Hepatitis D is dependent on what for survival? Why?

A

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

108
Q

coinfection of HDV and HBV usually leads to

A

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

109
Q

superinfection of HBV with HDV usually leads to

A

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

110
Q

manifestations of chronic hepatitis C

A

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
Q

how are arboviruses defined?

A

by transmission via arthropods

112
Q

the two groups of arboviruses based on manifestations

A
  1. encephalitis viruses

2. hemorrhagic fever viruses

113
Q

Encephalitic Arbovirus manifestations

A

asymptomatic to severe encephalitis- fever and fusion

114
Q

transmission of encephalitic arboviruses is between _____ by _____?

A

between vertebrates, by mosquito vectors

115
Q

4 major encephalitic arboviruses

A
  1. WNV
  2. EEE
  3. WEE
  4. SLE
116
Q

how do humans fit into the arbovirus lifecycle?

A

they’re usually incidental hosts

117
Q

what type of mosquito transmits WNV?

A

culex mosquito

118
Q

pathogenesis of WNV

A
  1. gets in blood from the bite
  2. replicates in the lymphatic system
  3. viremia
  4. affects the brain
119
Q

3 manifestations of WNV

A
  1. asymptomatic- 75%
  2. West Nile Fever (25%)- fever, HA, myalgias, fatigue
  3. neuroinvasive disease (1%)- meningitis, encephalitis, WNV poliomyelitis
120
Q

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

A

ever, HA, myalgias, fatigue

121
Q

manifestations of neuroinvasive disease from WNV (1%)

A

meningitis, encephalitis, WNV poliomyelitis

122
Q

dengue virus is spread by what type of mosquito

A

aedes

123
Q

Dengue fever is also known as

A

breakbone fever

124
Q

Dengue virus enters your system through the…

A

blood (transmitted via mosquitos)

125
Q

pathogenesis of Dengue (4 steps)

A
  1. Enters blood (via Aedes mosquito)
  2. infection of macrophages
  3. ???
  4. suppression of hematopoiesis in infected individual and widespread replication
126
Q

symptoms of Dengue Fever (aka Breakbone fever)

A

fever, muskuloskeletal pain

127
Q

symptoms of dengue Hemorrhagic fever (3)

A

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

128
Q

symptoms of Dengue shock syndrome (4)

A

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
Q

3 different manifestations of Dengue Virus

A
  1. Dengue Fever (breakbone fever)
  2. Dengue Hemorrhagic Fever (DHF)
  3. Dengue Shock Syndrome
130
Q

How many serotypes are there of Dengue virus?

A

4

131
Q

the initial infection with Dengue virus causes ?

A

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

132
Q

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

A

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

133
Q

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

A

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

134
Q

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

A

hosted in primates and transmitted by the Aedes mosquito

135
Q

Pathogenesis of the yellow fever virus

A
  1. eners blood stream via the Aedes mosquito
  2. Infection of macrophages
  3. enters the bloodstream
  4. suppression of hematopoiesis and widespread replication
136
Q

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

A
  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
Q

is there a vaccine for yellow fever?

A

yes, vaccine with the attenuated virus

138
Q

when is it recommended to get the yellow vaccine

A

if you’re traveling in south america and africa

139
Q

Human Herpes Virus genome:

A

dsDNA that replicates in the host cell nucleus

140
Q

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

A
  1. primary infection
  2. latency
  3. reactivation
141
Q

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

A

nope, they’re different!

142
Q

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

A

HSV-1 is transmitted from person to person orally

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

143
Q

pathogenesis of HSV

A
  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
Q

how does HSV move within the host?

A

axonal transport

145
Q

where does HSV lay dormant?

A

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

146
Q

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

A

Latent associated transcript

147
Q

Oral and Genital HSV symptoms

A

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

148
Q

oral herpes is associated with

A

cold sore, fever blisters

149
Q

genital herpes in males is associated with

A

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

150
Q

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

A 
respiratory spread (chicken pox)
contact spread (uncommon-- shingles)
151
Q

chicken pox (VZV) is spread by…

A

respiratory route

152
Q

shingles (VZV) is spread via

A

contact

153
Q

pathogenesis of VZV

A
  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
Q

what two viruses are latent in neurons?

A

HSV 1/2

VZV

155
Q

primary VZV IFXN symptoms

A

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

156
Q

where do chickenpox start?

A

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

157
Q

VZV reactivation presents as

A

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

158
Q

who is given the vaccination for VZV?

A
  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
Q

How is Epstein Barr virus (EBV) transmitted?

A

in saliva– Kissing/sharing water bottles

160
Q

pathogenesis of epstein barr virus (EBV)

A
  1. primary infection in oropharynx
  2. viremia
  3. infection of B cells
  4. latency in B cells
  5. Reactivation in B cells
161
Q

what is the site of latency for EBV?

A

B cells

162
Q

what is aka the kissing disease?

A

EBV- Epstein Barr virus

163
Q

sx of primary ifxn of EBV in children

A

mild or asymptomatic

164
Q

sy of primary ifxn of EBV in adolescents and adults

A

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

165
Q

subsequent manifestations of reactivation of EBV

A
  1. lymphoproliferative disease
  2. Burkitt’s lymphoma
  3. nasopharyngeal carcinoma
166
Q

what are heterophile abs and who makes them?

A

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

167
Q

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

A

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

168
Q

how do you test for EBV ifxn?

A

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

169
Q

The Herpes Viruses and their primary manifestation (6)

A
  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
170
Q

manifestations of CMV (cytomegaly virus) primary infxn

A

heterophile negative monomucleosis

171
Q

manifestations of CMV- cytomegalyvirus- reactivation in transplant pt

A

GI inflammation, pneumonia, disseminated dz

172
Q

manifestations of CMV- cytomegalyvirus- reactivation in HIV pt

A

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

173
Q

CMV is generally reactivated in what two types of pt

A

transplant pt and HIV pt

174
Q

manifestations of HHV-6 primary infection

A

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

175
Q

HHV-8 reactivation causes

A

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

176
Q

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

A

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

177
Q

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

A

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

178
Q

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

A

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

179
Q

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

A

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

180
Q

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?

A

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

181
Q

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

A

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

182
Q

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

A

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

183
Q

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

A

because they cause renal toxicity

184
Q

How is HIV primarily acquired?

A

mainly by sexual transmission

185
Q

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

A

the higher the viral load, the more risk of transmission

186
Q

How do genital herpes affect transmission of HIV?

A

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

187
Q

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

A

anal sex > vaginal > oral

188
Q

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

A

without ARVs: 1/3

with ARVs: 1/100

189
Q

4 modes of transmission of HIV

A

sexual contact
perinatal transmission
IDU
medical use of blood/tissue

190
Q

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

A

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

191
Q

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

A

GP120

192
Q

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

A

gp41

193
Q

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

A

early: CD4 and CCR5
late: CXCR5

194
Q

life cycle of HIV (7 steps)

A
  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
195
Q

symptoms of acute HIV ifxn

A

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

196
Q

Pathogenesis of HIV

A
  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
197
Q

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

A
  1. The CCR5 delta32 knockout will make the host immune to HIV
  2. Various HLA types can lead to fast or slow progression
198
Q

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

A
  1. normal CD4’s
  2. smoldering viral load
  3. no anti-HIV antibodies
  4. little CTL activity
199
Q

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

A
  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
200
Q

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

A
  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
201
Q

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

A

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

202
Q

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

A

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

203
Q

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

A

pneumocystis carinii pneumonia

204
Q

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

A

pneumocystis carinii pneumonia
esophageal candidiasis
mucocutaneous herpes

205
Q

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

A
  1. toxoplasmosis
  2. cryptococcus
  3. coccidioidomycosis
  4. mycobacterium avium complex
  5. CMV
206
Q

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

A
  1. cryptosporidius

2. PML

207
Q 
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)
A

maybe the p24 Ag, definitely the HIV viral load

208
Q 
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)
A

all of them will be positive

209
Q

what is the p24 Ag?

A

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

210
Q

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

A

both

211
Q

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

A

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

212
Q

why is the measure of HIV RNA important?

A

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

213
Q

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

A

the amount of immunosuppression

214
Q

how is resistance testing done in HIV pts?

A

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

215
Q

what are the 5 targets of HIV drug therapy?

A
  1. gp41 viral fusion protein
  2. host CCR5 protein
  3. reverse transcriptase
  4. integrase
  5. protease
216
Q

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

A

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

217
Q

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

A

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

218
Q

how do protease inhibitors work?

A

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

219
Q

how do HIV fusion inhibitors work?

A

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

220
Q

how do CCR5 antagonists work?

A

they bind CCR5, preventing interaction with gp120

221
Q

what are the 5 different types of HIV meds

A
  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
222
Q

how do Integrase Strand-Transfer Inhibitors work?

A

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

223
Q

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

A

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
Q

two reasons ART is recommended

A
  1. to reduce the risk of disease progression in an individual
  2. to reduce transmission
225
Q

Initial therapy for HIV is:

A

2 NRTI plus one of the following:

  • NNRTI
  • Boosted protease inhibitor
  • Integrase strand transfer inhibitor
226
Q

what is a “boosted” protease inhibitor

A

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
Q

what is ritonivir?

A

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
Q

what are enteroviruses?

A

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
Q

which enterovirusal subgenera are responsible for polio?

A

polioviruses 1-3

230
Q

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?

A

coxsackieviruses A

231
Q

which enterovirusal subgenera are responsible for myocarditis and pericarditis?

A

coxsackieviruses B

232
Q

what is the most common cause of aseptic meningitis?

A

enteroviruses (polio, coxsackieviruses A and B)

233
Q

are there any vaccines or antivirals for enteroviruses?

A

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

234
Q

how is mumps spread?

A

respiratory route (droplets)

235
Q

manifestation of the mumps?

A

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
Q

common complications of mumps include (2):

A

orchitis (swelling of the testes) and aseptic meningitis

237
Q

rare complications with mumps

A
  1. hearing loss (children)
  2. encephalitis
  3. fetal loss in first trimester
  4. oophritis (swelling of ovaries)
  5. pancreatitis
238
Q

is there a vaccine for mumps?

A

yes and it’s effective and safe

239
Q

how are adenoviruses transmitted?

A

fecal-oral and fomite (ocular fluid) transmission

240
Q

manifestations of adenoviruses

A
  1. self-limited respiratory manifestations
  2. ocular ifxns: pharyngoconjunctival fever, epidemic keratoconjunctivits
  3. self-limited, acute, watery diarrhea
241
Q

what happens when immunocomp people get adenovirus

A

persistent virus can reactivate or new ifxn can occur

242
Q

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

A

hemorrhagic cystitis, enteritis, pneumonitis, hepatitis with viremia

243
Q

what two groups of people are particularly susceptible to adenoviruses?

A

HSCT- hematopioitic stem cell transplant pt

Solid organ transplant pt

244
Q

Parvovirus B19 is transmitted via

A

respiratory and verticle transmission

245
Q

Parvovirus B19 commonly manifests in childhood as…

A

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

246
Q

parvovirus B19 in adults commonly manifests as

A

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
Q

which disease is associated with slapped cheek rash?

A

parvovirus B19

248
Q

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

A

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
Q

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

A

in erythroblasts– which leads to anemia.

  • transient aplastic crisis with underlying hemolytic disease
  • pure red cell aplasia in immunocompromised
250
Q

why does teh parvovirus B19 virus persist in the host?

A

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

251
Q

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

A

Parvovirus B19– 5th dz and anemia

252
Q

which virus has linear ds DNA with an icosahedral complex

A

adenovirus

253
Q

which ds DNA viruses are enveloped? (3)

A

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

MICRO II (8 decks)

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