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Spring Semester 2014 > Virology > Flashcards

Virology Flashcards

1
Q

True or False: Positive RNA can be translated directed to protein.

A

True - generally translated to negative strands and then made into many positive strand

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2
Q

What is the best way to view viruses?

A

Electron microscope - 20nM

-300nM

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3
Q

True or false: Viruses do not need an extracellular phase to be considered a virus.

A

False - particles must pass from cell to cell, throughout body, or between individuals

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4
Q

What are 5 characteristics for classifying viruses

A
  1. Particle type - icosahedral, filamentous, enveloped, naked
  2. Tissue tropism
  3. Disease etiology
  4. Serology - cross reaction
  5. Genome type
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5
Q

Capsid

A

Protein shell of a virus - can be either naked or enveloped

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6
Q

Plaque Assey

A

Tissue culture for quantitating infectious virus - apply serial dilutions of virus and drug or neutralizing antibody

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7
Q

Focus Assay

A

Viruses promoting cell growth rather than death

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8
Q

Virus replication is characterized by an initial _______ and then rapid growth and _____.

A
  1. Gully

2. Burst

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9
Q

What are the properties of Picornavirus?

A 
Icosahedral
\+ssRNA
no lipid envelope 
no tegument 
Mostly pH stable
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10
Q

Enterovirus, rhinovirus, hepatovirus, parechovirus and kobuvirus are all types of what virus?

A

Picornavirus - most common agent of common cold

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11
Q

Enterovirus has what type of transmission?

A

Fecal/oral - via water supply - capsid is resistant to mild sewage treatment

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12
Q

What is characteristic of paralytic poliomyelitis

A

Asymmetric flaccid paralysis

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13
Q

What does polio virus isolated in the oropharynx look like?

A

Asympotomatic - viremia is what looks like slight flu

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14
Q

Where can picornavirus (polio) be isolated from?

A

Throat, stool, or CSF

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15
Q

What is the attributed as the cause of the polio epidemic?

A

Indoor plumbing: children no longer encounter the virus at a young age when they have maternal antibodies - worse disease

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16
Q

How does picornavirus/polio virus ensure its ssRNA gets translated quickly?

A
  1. Its + sense

2. It has a 5’ end that grabs ribosomes

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17
Q

How many proteins does picorna/polio virus encode?

A

One - it uses proteases to cleave different products

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18
Q

What are three targets for therapy for picornavirus

A
  1. Protease inhibitors
  2. RNA-dependent RNA Polymerase
  3. Block entry
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19
Q

Where does picornavirus replicate?

A

Cytoplasm

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20
Q

What is a major challenge for -RNA viruses?

A

Encode enzymes to translate it to +sense

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21
Q

What are characteristics of adenovirus?

A
  1. dsDNA
  2. Icosahedral capsid w/ penton spikes
  3. fecal/oral transmission
  4. Frequent unapparent
    respiratory infection
  5. Many serotypes
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22
Q

What is something that picornavirus and adenovirus have in common?

A

They both use the coxsackie/adenovirus receptor to mediate entry

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23
Q

Where does adenovirus replicate?

A

Nucleus

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24
Q

What are characteristics of an acute infection?

A
  1. Rapid onset
  2. Active virus + immune response ￫ pathogen cleared, memory
  3. Immunopathology from overactive immune response
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25
Q

What are characteristics of an acute/chronic infection?

A
  1. Acute onset + immune response ￫ Virus not cleared
  2. Initial response is subdued to prevent immunopathology
  3. Immune response of host is set to higher activation state overall - higher cytokines
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26
Q

Latent

A

A viral life cycle characterized by minimal–if any–expression of a subset of viral genes and absence or lytic replication and infectious virion production

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27
Q

What are two advantages of latent virus infection?

A
  1. Stealth

2. Cell maintains viral genome - difficult to target

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28
Q

What are two disadvantages of latency?

A
  1. Spread is limited

2. Death of latently infected cell is dead end for virus

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29
Q

How do viruses overcome the challenges of latency?

A
  1. Reactivation

2. Establish latency in long-lived cells - memory T and B, hematopoietic stem cells

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30
Q

What is a prototype virus for chronic persistant infection?

A

Hepatitis C

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31
Q

T cell exhaustion

A

Persistant infection leads to downregulation of T cells ￫ Loss of antiviral functions and death of T cells

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32
Q

Latent infections are quiescent, but result in a higher level of __________. Is this good or bad?

A

Circulating cytokines - this can be good since you clear infection quicker, but can also serve as a promotor for those predisposed to autoimmune infections

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33
Q

How is disease generated with latent infection?

A

Reactivation - the switch to the lytic life cycle

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34
Q

Tissue damage from persistant infections is associated with what?

A
  1. Mostly from inflammation and excessive immune response
  2. Very low levels from damage associated with replication
  3. ROS and cytokines can cause DNA damage ￫ cancer, diabetes
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35
Q

How do you target chronic persistant infection?

A
  1. Anti-viral therapy

2. Immunosuppression - careful balance

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36
Q

What functions do IFNs serve in the immune response?

A
  1. Activate macrophages
  2. Activate Th1
  3. Activate B cells ￫ IgG
  4. Activate memory and killer T cells
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37
Q

What limits interferons as therapeutics?

A

They induce inflammation, cause the symptoms associated with being sick

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38
Q

What is the “Type 1 interferon response”

A

Virus sensed by PRRs/TLRs triggers synthesis and secretion of IFN α/β which induce the “antiviral state” in nearby cells

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39
Q

How do nearby cells sense/implement the antiviral state?

A

IFN α/β bind receptors which lead to translation of PKR and OAS via Jak/Stat

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40
Q

PKR

A

Protein Kinase R - Shutdowns mRNA translation

  1. Binds dsRNA (becomes autophos’d/active)
  2. Phos eIF-2 - normally initiates peptide synthesis
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41
Q

OAS

A

2’-5’ Oligoadenylate Synthetase

  1. Binds/activated by dsRNA
  2. Catalyzes synthesis of oligoadenylate from ATP
  3. AAA then activates RNAse L (endoribonuclease) - dedgrades mRNA
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42
Q

What are characteristics of the antiviral state?

A

Overall a decrease in protein synthesis, mRNA degradation, and inc. in NK cell

  1. Increased MHC I expression
  2. Inc. PKR expression
  3. Inc. 2’-5’ OAS
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43
Q

What are the pro-inflammatory cytokines?

A

TNFα: Pyrogen, induces cell death - produced by activated Mφ, CD4, and NK cells
IL-1β: Pyrogen, produced by activated Mφ
IL-6

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44
Q

When a cell first senses a virus, what 2 classes of molecules are upregulated?

A
  1. Type 1 IFNs

2. NK activating ligands

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45
Q

What are 3 components of the innate immune response?

A
  1. Cytokines
  2. NK Response
  3. Complement
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46
Q

What are 3 components of the adaptive immune response?

A
  1. Cytokines: IFN-γ + IL-12 ￫ Th1 and IL-2 ￫ T cell proliferation
  2. T cell via Class 1 and CD8
  3. B cell response (antibodies)
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47
Q

Apoptotic Response

A
  1. From within - selfless

2. From outside - Fas or by TNFα on CD8 or NK cells

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48
Q

What genes regulate apoptosis?

A
  1. p53

2. caspase 9 and 3 mediate cascade ￫ activated by leaky mito losing cytochrome c

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49
Q

What are 5 mechanisms to circumvent the Type 1 IFN Response/Induction of the Antiviral State?

A
  1. Encode proteins to prevent IFN binding
  2. Direct cellular phosphatase to dephos eIF-2α
  3. Decoy mRNA to sequester PKR and prevent activation
  4. Sequester dsRNA to prevent PKR activation
  5. eIF-2α decoys to bind activated PKR
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50
Q

What are 3 mechanism to circumvent innate immune defenses?

A
  1. Sequester IL-1β w/ viral binding protein
  2. Encode homologs of complement control proteins → prevent MAC formation
  3. Encapsidate viral/host complement control proteins in their membranes to evade lysis
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51
Q

What are 6 mechanisms to avoid Class 1 MHC Presentation?

A
  1. Degrade TAP transporter
  2. Block TAP transporter - no peptide in ER
  3. Degrade MHC1 molecules
  4. Divert MHC 1 to lysosomes
  5. Retain MHC 1 in ER/Golgi
  6. Downreg transcription of MHC components
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52
Q

What are 3 mechanisms to evade NK cell killing?

A
  1. Encode decoy MHC 1 like molecules - more inhibition
  2. Prevent NK cell receptor ligands from getting to cell surface
  3. Remove HLA-A and HLA-B from cell surface- only HLA C - not as effective
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53
Q

Viruses can also induce the downregulation of ______ and ____.

A
  1. Adhesion molecule ICAM-1

2. Costim B7 (CD80/CD86)

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54
Q

Viruses also encode which inhibitors of apoptosis?

A
  1. p53 inhbitors
  2. Bcl-2 homologs
  3. Inhibitors of caspases
  4. Soluble TNF receptors - prevent TNF triggered apop
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55
Q

What other characteristics can make viruses difficult to kill?

A
  1. Latency
  2. Epitope mutation
  3. Infection of “privileged sites”
  4. Intracellular sequestration
  5. Infection via immune receptors
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56
Q

How does Merkel cell polyoma virus cause cancer?

A

A common deletion renders virus unable to complete replication cycle; persistant infection
More common in immunosuppressed

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57
Q

How does papillomavirus cause cancer?

A

E5: stimulates constitutive GFR signaling
E6 & E7: neutralize “brakes” p53 and Rb - target them for degradation
Uncouples cell division from regulatory control

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58
Q

What are the characteristics of papillomavirus?

A

dsDNA circular genome
1/3 infect GI, sexual transm.
Infects epithelium - causes cells in sratum spinosum to replicate

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59
Q

Rb protein

A

Blocks cells from going to G1 ￫ S

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60
Q

E6 (HPV)

A

Blocks p53 and activates telomerase

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61
Q

Development of carcinoma is associated with ___________ of the DNA into the host chromosome. ___ and ___ are always retained in cancer cells.

A
  1. Integration
  2. E6
  3. E7
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62
Q

What are some of the problems with the HPV vaccine?

A
  1. Need good mucosal immunity
  2. Must recognize multiple strains
  3. Can’t include oncogenes
  4. Political
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63
Q

Hybrid capture assay (HPV)

A
  1. Isolate DNA
  2. Introduce target RNA strands
  3. Use antibodies to amplify and ID
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64
Q

Gardasil

A

Tetravalent vaccine with recombinant L1 VPLs

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65
Q

What etiologies can be caused by retroviruses?

A
  1. No ill effects
  2. Tumors - capture host gene
  3. Wasting disease/neurological disorders
  4. Immune deficiencies
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66
Q

What is the general structure and composition of retroviruses?

A
  1. Enveloped (env) embedded in membrane, matrix under lipid bilayer
  2. Capsid (groups specific antigens - gag genes)
  3. 2 copies of +ssRNA genome - only “diploid” virus
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67
Q

Gag gene includes which proteins?

A
  1. Matrix MA
  2. Capsid CA
  3. Nucleocapsid NC
  4. Protease PR
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68
Q

What does the Pol gene encode?

A

Reverse transcriptase and integrase (IN)

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69
Q

What does the Env gene encode?

A
  1. Surface SU (gp120)

2. Transmembrane TM (gp41)

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70
Q

What generates tissue tropism in retroviruses?

A

Whether the TF expressed in a given cell type are capable of binding the U3 region on the LTR

71
Q

What generates tissue tropism in retroviruses?

A

The TF expressed capable of binding the U3 region on the LTR

72
Q

How do non-transforming retroviruses cause cancer?

A
  1. Downstream LTR is activated upon integration - up-regulates cell signals to cause growth
  2. Enhancer insertion - recruit RNA Pol to wrong spot
73
Q

When do retroviruses cleave their gag, and gag-pol proteins? What happens if this doesn’t occur?

A
  1. After budding

2. Non-infectious viral particles

74
Q

The decline in deaths due to AIDS coincided with the development of what?

A

Protease inhibitors and the development of HAART

-2 RT and 1 PI

75
Q

How is HIV transmitted?

A
  1. Inoculation in blood - transfusion, needle sticks
  2. Sexual
  3. Perinatal - Elective C section, don’t breast feed if HIV+
76
Q

How is HIV not transmitted?

A

Close personal contact - household members and healthcare workers NOT exposed to blood

77
Q

What are the accessory proteins of HIV?

A

Vif, Vpr, Vpu, Nef, Tat, and Rev

78
Q

Tat

A

Transactivator of transpiration - absolutely required for transcription

79
Q

Rev

A

Regulator of virion expression - promotes transport of unspliced RNA from nucleus to cytoplasm

80
Q

Vpu

A

Promotes virion release from cell by inhibiting host protein tetherin - blocks release of enveloped viruses from cell

81
Q

What is the receptor on immune cells that HIV binds? Is this sufficient for entry?

A

CD4 - conveys immune cell tropism

No. Need a co-receptor - confers further tropism

82
Q

M-tropic HIV use what co-receptor?

A

CCR5 - natural ligands are RANTES, MIP-1α, MIP-1β

83
Q

What type of HIV is the source of person to person transmission?

A

M tropic

84
Q

Resistance to M-tropic HIV is caused by what?

A

32bp-deletion in CCR5 gene - non-functional co-receptor
Heterozygotes: get infected, progress disease more slowly
Homozygous: highly resistant to infection - don’t express co-receptor

85
Q

What is the mechanism of HIV fusion?

A
  1. Binds CD4 - exposed co-receptor binding site
  2. gp41 fusion domains exposed and bind to PM
  3. Co-receptor binds - “snapback” ￫ membranes fuse
86
Q

How do HIV infect T cells?

A

Infection at mucosal surfaces - DC cells carry HIV to lymph nodes where T cells reside and are infected

87
Q

In early infection with HIV is replication high or low?

A

High in lymph nodes - immune system is keeping viremia low

88
Q

What are 3 main disease mechanisms of HIV?

A
  1. Directly killing CD4
  2. Immune system kills infected cells
  3. Immunosuppression due to loss of CD4 T cell help
  4. Dysfunctional Mφ
89
Q

What are characteristics of the acute infection phase of HIV?

A
  1. High viremia

2. Initial drop in CD4

90
Q

What are characteristics of the symptomatic phase of HIV?

A
  1. CD4 depleted <200/μL
  2. High viral load
  3. Opportunistic infections
91
Q

What are 5 classes of anti-HIV drugs?

A
  1. RT inhibitor (NRTI/NNRTI)
  2. Protease inhibitor
  3. Fusion inhibitor
  4. Entry Inhibitor
  5. Integrase inhibitor
92
Q

In what locations is HIV found in order of increasing half life?

A
  1. Circulation: 6 hrs
  2. CD4: 1 day
  3. Mφ: 1-2 years
  4. Memory T cells: 5 years
93
Q

What are symptoms of acute retroviral syndrome?

A

Fever, myalgia, weight loss, rash, malaise, oral ulcers - seen 2-6 weeks after infection

94
Q

What are the pros and cons of the antigen (RNA) tests for HIV?

A

Detects infection after 10-14 days - HIV viral load/RNA

Expensive - pooled RNA testing

95
Q

Combination test HIV antibody/antigen

A

Cheaper, quicker than ELISA, slower than HIV RNA test

96
Q

What is the chance of an untreated mother transmitting HIV to her baby? Treated?

A

25%

0-1% (HAART, AZT during labor, formula feeding)

97
Q

What determines the likelihood of HIV transmission?

A

Viral load

98
Q

What is the definition of a healthcare exposure to HIV?

A
  1. Percutaneous injury - needle stick
  2. Contact of mucous membrane or non-intact skin with
    Blood, tissue, CSF, amniotic fluids, etc
99
Q

Post exposure prophylaxis

A

2-3 drugs ASAP following exposure (<72 hours)

-expensive for

100
Q

Pre-exposure prophylaxis (PrEP)

A

2 anti-HIV drugs, prophylaxis for at risk individuals - adherence correlates to prevention

101
Q

Influenza virus is part of which family?

A

Orhtomyxovirus

102
Q

What are the influenza genus differences based on?

A

Matrix and nucleoprotein antigens - subtypes base on HA and NA

103
Q

What is the difference between antigenic drift and antigenic shift?

A

Drift: minor changes in HA or NA or both
Shift: occurs in HA or NA a result of gene reassortment between human and animal strains

104
Q

What is the pathogenesis of Influenza A virus?

A

Acute Respiratory Disease

  • Viral replication and CD8 response destroy epithelium
  • Interferon response ➝ Flu Symptoms
105
Q

What are complications with Influenza?

A
  1. Primary viral pneumonia
  2. Secondary bacterial pneumonia
  3. Myositis/cardiac involvement
  4. Neurologic syndromes: GBS, Reye’s, encephalopathy
106
Q

How is influenza diagnosed?

A

Clinical signs/epidemiology
Lab: Rapid antigen capture - detect NP in 15 min
RT-PCR

107
Q

What family does Rhinovirus belong to?

A

Picornavirus

108
Q

What are characteristics of Rhinovirus?

A
  1. +ssRNA
  2. IgA most important in limiting re-infection
  3. > 150 serotypes
  4. Common cold
  5. Like growing at 33 degrees
  6. Transmission via resp. secretions
109
Q

Are they any effective methods of controlling/preventing rhinovirus?

A

No. Protease inhibitors are experimental

110
Q

What are characteristics of Coronavirus?

A
  1. +ssRNA
  2. Cause common cold - URT
  3. No vaccine (SARS/MERS)
111
Q

What are characteristics of the Paramyxoviridae family?

A
  1. -ssRNA
  2. Proteins:
    F: Fusion protein
    HN: Hemagglutinin - attachment & Neuraminidase - release (Not in RSV)
    NS1 and NS2: nonstructural proteins that modulate immune response?
112
Q

Where do paramyxoviruses replicate?

A

Cytoplasm

113
Q

What steps are targets for treatment of paramyxoviruses?

A

Attachment/fusion
RNA replication
Transcription

114
Q

What are the 5 Paramyxoviruses for this class?

A
  1. Human Parainfluenza Virus
  2. Respiratory Syncytial Virus
  3. Human Metapneumovirus
  4. Hendra and Nipah Virus
  5. Measles
115
Q

What are the symptoms of human parainfluenzavirus (HPIV)?

A
  1. Acute upper and lower respiratory illness-often infants, elderly, IC
  2. Croup, bronchiolitis and pneumonia
116
Q

Is there a vaccine for HPIV?

A

No, currently in pediatric phase I trials

117
Q

What are the symptoms of Respiratory Syncytial Virus?

A

Localized infection of respiratory tract- no viremia
Pneumonia - syncytia
Bronchiolitis - host immune response Th2 (Hist/PGD2) in infants - wheezing

118
Q

What is the #1 cause of fatal acute respiratory tract infection in infants and young children?

A

RSV - narrow airways are obstructed via syncytia forming giant cells
Maternal Ig doesn’t protect
Natural infection doesn’t protect

119
Q

Is there a vaccine for RSV?

A

No

120
Q

How do you treat a premature/IC infant with RSV?

A
  1. Aerosolized ribavirin

2. Passive immunization w/ anti-RSV Ig and Ig against fusion protein

121
Q

How do you treat a premature/IC infant with RSV?

A
  1. Aerosolized ribavirin

2. Passive immunization w/ anti-RSV Ig and Ig against fusion protein

122
Q

How do you treat hMPV?

A

Supportive mostly

Immunoglobulins (IVIG) and humanized monoclonals for fusion protein

123
Q

Hendra and Nipah viruses

A

Emerging resp. viruses w/ high mortality rate in SE Asia and Africa (from bats)

124
Q

What are symptoms of Adenovirus infection?

A
  1. Pharyngitis, conjunctivitis, GI, Hemorrhagic cystitis

2. Viremia (Resp infection)

125
Q

In the respiratory tract, Adenovirus can cause destructive productive infection, _____________________, and latent infection in tonsils or adenoid tissue.

A

Persistant infection with virus shedding

126
Q

What populations is adenovirus common in?

A

Infants, young children, military recruits

127
Q

Is there a vaccine for adenovirus?

A

Yes - for military recruits

128
Q

Why is the MMR vaccine (live-attenuated) so effective?

A
  1. Natural infection protects against re-infection - single antigenic type
  2. Virus has systemic replication phase prior to establishing infection in target organ
  3. Humans are only known host
129
Q

What are the symptoms of measles?

A

Maculopapular rash w/ cough, conjunctivitis, photophobia, Koplik spots

130
Q

What are complications associated with measles?

A

Otitis media, croup, pheumonia, blindness, enchephalitis (immune systems been exposed worse rxn)

131
Q

What does atypical measles look like?

A

More intense rash distally, possible vesicles, petechiae, purpura

132
Q

Measles is _____ infectious among susceptible populations.

A

Extremely

133
Q

What are the symptoms of Mumps?

A
  1. Asymptomatic (~75%)
  2. Parotitis - b/l w/ fever
  3. Swelling of other glands
  4. CNS involvement (mild meningitis, rare encephalitis)
134
Q

What is the initial life cycle for Measles and Mumps?

A
  1. Inoculation of respiratory tract
  2. Local replication
  3. Viremia
  4. Systemic infection
  5. Targets tissue
135
Q

What are mumps outbreaks associated with currently?

A

College campuses - are boosters needed?

136
Q

What are the symptoms associated with Rubella?

A
  1. Mild rash - children
  2. Severe rash, arthritis, arthralgia - adults
  3. Congenital defects in neonates < 20 wks
    - can be asymptomatic
137
Q

What family does Rubella belong to?

A

Togavirus

138
Q

Congenital Rubella Syndrome

A

Heart defects, deafness, IU growth retardation, failure to thrive, mortality w/i first year, mental retardation

139
Q

What are the characteristics of Parvovirus?

A
  1. ssDNA
  2. Icosahedral, non-enveloped
  3. Replicates in nucleus
  4. Dependent on host DNA rep fx
140
Q

What cells does Parvovirus B19 infect?

A

Actively replicating (S-phase) RBC progenitors in bone marrow (viremia) via blood group P antigen

141
Q

What symptoms are associated with Parvovirus?

A
  1. Rash, bright red cheeks, arthralgia (circulating immune complexes)- Erythema infectiosum/Fifth Disease
  2. Slight drop in hemoglobin (normal host)
  3. Life-threatening aplastic crisis (chronic hemolytic anemia host)
142
Q

How long is the incubation period for Parvovirus B19? When do characteristic symptoms appear?

A
  1. 7 days

2. Day 20

143
Q

What happens if parvovirus gets transmitted to fetus?

A

Still birth, generalized edema, anemia, congestive heart failure – Associated with death, not abnormalities

144
Q

What is the most common cause of severe diarrheal illness requiring hospitalization in infants and young children?

A

Rotavirus

145
Q

What are characteristics of Rotavirus?

A

11 dsRNA segments - 12 genes
No envelope, 3 layer capsid
Multiple antigenic groups (Group A causes human disease)

146
Q

What are the antigens of Rotavirus?

A

VP4 neutralization antigen (P serotype-28)
VP7 neutralization antigen (G serotype-19)
VP6 subgroup antigen (A-E)
NSP4: acts as enterotoxin

147
Q

NSP4 (Rotavirus)

A

Enterotoxin

  1. Raises intracellular Ca → disrupts tight junctions
  2. Secreted into lumen, bind receptor → inc. Intracellular Ca
  3. Stimulate enteric nerves/act on goblet cells inc. Ca → efflux of Cl
148
Q

Is there a vaccine for Rotavirus?

A

Yes. Two.
RotaTeq: Live attenuated 3x orally at 2, 4, and 6 months
Rotarix: Live attenuated 2x orally at 2 and 4 months

149
Q

What are considerations for Rotavirus?

A
  1. Intussusecption
  2. Reversion to virulent strain
  3. Viremia
  4. Shedding of virus by vaccine recipients
  5. Immunosuppressed children
150
Q

What family is Norovirus apart of?

A

Calici family

151
Q

What symptoms are associated with Norovirus?

A
  1. Acute gastroenteritis - winter dt new strain
  2. Short-lived ~ 3 days D/V/N, cramps, headache, malaise, fever
  3. Most serious infection in young children/elderly
152
Q

What are characteristics of Norovirus?

A
  1. +ssRNA - Picornalike
  2. Protease (Pro)
  3. Polymerase (Pol)
  4. Structural proteins
153
Q

What is the most common cause of foodborne illness in the US?

A

Norovirus

154
Q

Why is Norovirus so easily transmitted?

A
  1. Low infectious dose
  2. Prolonged asymptomatic shedding ~2 wks
  3. Stable in environment
155
Q

What viruses that are apart of the Enterovirus group do we need to know for this class?

A
  1. Poliovirus
  2. Enterovirus
  3. Coxsackie A Virus
  4. Echovirus
156
Q

What determines tissue tropism for enterovirus infection?

A

Receptor bound

157
Q

How are enteroviruses transmitted and what is their life cycle like?

A
  1. Fecal/oral or respiratory
  2. Replicate in GI/oropharynx
  3. Viremia
  4. Target tissues
158
Q

What viruses cause hand, food and mouth disease?

A

Coxsackie A and Enterovirus 71

159
Q

What viruses cause muscle infections i.e. myocarditis and pericarditis?

A

Echo, Coxsackie A, B

160
Q

What viruses cause encephalitis and paralytic disease?

A

Polio and Coxsackie

161
Q

What viruses cause meningitis?

A

Echo, Polio and Coxsacie

162
Q

Everyone of the enteroviruses can cause which disease?

A
  1. Respiratory tract infections
  2. Undifferentiated fever
  3. Paralytic disease
  4. Encephalitis, meningitis
163
Q

Most viral meningitis in the summer is caused by what virus?

A

Enterovirus
Children; fever, irritability, poor eating, hard to awaken
Adults: Headache, F/C, N/V, stiff neck, sensitivity to light

164
Q

What are symptoms of hand, foot and mouth disease?

A

Mild fever, sore throat, fatigue, loss of appetite, vesicular lesions on hand, feet, mouth

165
Q

What factors contribute to emergence of new virus disease?

A
  1. Inc. population density
  2. Increased travel
  3. Changes in social behavior
  4. Changes in environment
  5. Changes in industry/technology
  6. Changes in microorganisms
166
Q

What are characteristics of herpesvirus?

A

Evenloped, iscosahedral, linear dsDNA

Not labile in environment

167
Q

What viruses are α herpesviruses?

A

HSV1 and 2

Varicella zoster virus

168
Q

What are some characteristics of α herpesviruses?

A

Short replication cycle
Broad host range
Latency in sensory ganglia

169
Q

What viruses are β herpesviruses?

A

Cytomegalovirus (CMV)

Roseolovirus (HHV-6)

170
Q

What are some characteristics of β herpesviruses?

A

Longer replication cycle
Latency in glands
Host range limited

171
Q

What viruses are γ herpesviruses?

A

EBV and Kaposi’s Sarcoma

172
Q

What are some characteristics of γ herpesviruses?

A

Slow replication
Limited host range
Latency

173
Q

What makes a virus a herpes virus?

A
  1. Encode TK, PK, DNA Pol
  2. Synthesis of DNA and capsid - nucleus
  3. Lytic replication & latency
174
Q

What is the general life cycle of a herpesvirus?

A
  1. Binding/fusion
  2. DNA → Nucleus
  3. vhs degrades host mRNA
  4. VP16 goes to nucleus to start transcription
  5. Viral DNA circularizes
  6. α→ β →γ gene transcription via host
  7. Packaging/budding

Spring Semester 2014 (6 decks)

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