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Block7 > IAH > Flashcards

IAH Flashcards

1
Q

What is the plaque forming assay?

A

tissue culture assay for quantifying infectious virus

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2
Q

What is a focus assay?

A

Counting the areas where cells overgrow

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3
Q

What are the components of virion particle?

A

genome, enzmes, auxialry protein, structural proteins, attachment proteins, fusion proteins, membrane

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4
Q

What is the physiology of picornavirus?

A

icosahedral, ssRNA+, no lipid envelope, no tegmentum, pH stability: enterovirus ph3-9
rhino virus only ph6+

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5
Q

Polio infection vs. disease?

A

most were innapparent (asymptomatic)
mild illness-minor febrile illness
only 0.1-2% resulted in paralytic poliomyeltitis:
complication paralysis

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6
Q

How was picornavirus diagnosed?

A

serologic, PCR, virus isolation from CSF, stool specimens and throat washing

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7
Q

Polio had three major epidemiological phases?

A

endemic
virus encountered at early age, high rate of sublinical infections, encounter at maternal antibodies
epidemic
late 1800s, encounter virus at later age, bc of hygeine, increased paralytic incidence
post-vaccine
few cases, all cases related to virus

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8
Q

Piolovirus produces how many proteins?

A

one protein, causes self limited proteases

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9
Q

How does poliovirus inject its +RNA genome into it?

A

injected after endocytosis, by utilizing hte capsid as an injection system

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10
Q

What is the physiology of adenovirus?

A

latent virus in adenoides and tonsils, 51 serotypes, causes gastrointestinal or respiratory disease,

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11
Q

What is adenovirus more dangerous in?

A

children and immunocompromised

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12
Q

How does adenovirus attach and entry?

A

viral surfing by attaching to myosin, enters through clathrin mediated endocytosis, viral fusion pore control

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13
Q

How is adenovirus shed from epithelial cells?

A

Enters throug apical end, shed on the basal side, and hte virus penton spike fiber disrupts adhesion gap junction to allow it back into the lumen

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14
Q

How do you quantify infectious virus?

A

plaque assay
focus forming assay
single-step growth curve

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15
Q

What are the basic steps in a viral life cycle?

A

attachment, penetration, uncoating, synthesis of components (synthesis of mRNA, translation of viral proteins, genomre replication),
assembly of viral components
exit maturation

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16
Q

What is virion attachment?

A

for both naked and envelopoed virus, a viral surface protein recognizes a receptor on the target cell

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17
Q

What is the receptor fro HIV?

A

Human CD4 on t cells

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18
Q

What is the receptor on cell for EBV?

A

Human complement receptor CD21

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19
Q

What is the receptor on cell for Rhinovirus?

A

Human ICAM1

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20
Q

What is the receptor on the cell for Influenza virus?

A

sialic acid

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21
Q

How do viruses cause disease?

A

Virus destruction of infected cells
viral modification of infected cell function
immune and inflammatory responses to virus infection
-fever,rash, myalgia
-immune-mediated damage or destruction
combination of several factors

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22
Q

What innate response from host defense is responsible for viral combat?

A 
soluble mediators (IFNs, cyokines, chemokines; antiviral response within infected cell; make surrounding cells resistant to infection, recruit effector cells)
apoptosis
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23
Q

What is the humoral adaptive response is sued to combat viral infection?

A

neutralizing antibody: block attachment or entry

complement fixing antibody: lyse virions or infected cells

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24
Q

What is the cell-mediated adaptive response to combat viral infection?

A

MHC presentation of viral peptides killing of virus-infected cells by cytotoxic T cells

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25
Q

What are the characteristics of chronic virus infection?

A

Initial steps of infection similar to accute; however virus is not cleared. Initial robust immune response is subdued to prevent immunopathology; immune response of host set to a higher activation state overall

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26
Q

What is hte definition of a latent virus infection?

A

a viral cycle chaaracterized by minimal if any expression of a subset of viral genes and absence of lytic replication and infectious virion production

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27
Q

What is the prototype of latent virus infection?

A

herpesvirus

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28
Q

What are the innate immunity to viral infection?

A 
Patterns by PRRs
Type 1 IFN secretion
cytokines -- IL1, TNFalpha
IFNgamma, chemokines
NK cells- direct killing of virus-infected cells by NK cells and NK cell are a huge source of IFNgamma
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29
Q

What are the order of immune responses for innate reaction to innate immune response?

A

Production of IFNalpha, IFNbeta, TNFalpha, IL12 early 2 day peak
NK cell mediated killing 3 day peak
T cell medaited peak 6 to 10 days

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30
Q

What is exogenous IFNalpha used to treat?

A

chronic Hep C

tx melanoma, hairy cell leukemia, chronic myelogenous leukemia, Kaposi’s sarcoma

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31
Q

What is exogenous IFN Beta used to treat?

A

used in treaatment of MS

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32
Q

Why is exogenous IFNgamma not used to treat disease?

A

limited clinical usefulness but side effects limit it’s ability

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33
Q

What is PKR?

A

induced by IFN, protein kinase R
binds to ds RNA and becomes autophosphorylates; phosphorylates eIF-2alpha
inhibits translation

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34
Q

What is OAS?

A

2’-5’ Oligoadenylate synthetase it is also induced by IFN
binds dsRNA
catalyzes synthesis of oligo adenlyate and activates RNAse L- endoribonuclease

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35
Q

IFNalpha and IFNbeta induce the anti-viral state which leads to waht?

A

increase surface class 1MHC
increased NK cells
decrease viral protein synthesis

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36
Q

What is the role of TNF?

A

tumor necrosis factor; a pyrogen which can induce fever
produced by activated macrophages, cD4 T cells and NK cells
induces death signaling

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37
Q

What is the role of IL1beta?

A

a pyrogen-can induce fever

major pro inflammatory; produced and secreted by activated macrophages

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38
Q

What is IL6?

A

major pro-inflammatory cytokine

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39
Q

What is the role of NK cells?

A 
kill targets after assessing the balance between inhibitory signals from class I molecules
activating signals from NK activating ligands
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40
Q

How are infected cells induced to undergo apoptosis?

A

from within; by internal factors and frm outside by Fas or TNFalpha, NK cells

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41
Q

What is the role of viral IFN-GammaR or viral IFNalpha/betaR?

A

blocks binding of IFN’s and is encoded by poxviruses

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42
Q

How does Adenovirus inhibit PKR?

A

encodes its own structured RNA and inhbitis activation by dsRNA

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43
Q

How does poxvirus counter PKR activation?

A

encodes dsRNA binding proteins that sequester the dsRNA and prevent PKR activation

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44
Q

What cancer does hepatitis B and Hepatitis C cause?

A

hepatocellular carcinoma

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45
Q

What cancers do EBV cause?

A

lymphoma and nasopharyngeal carcinoma

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46
Q

What cancer does HHV8 cause?

A

kaposi’s sarcoma KSHV

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47
Q

What cancer does HTLV1 cause?

A

adult T cell leukemia

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48
Q

What cancer does HPV cause?

A

cervical cancer; head and neck cancer

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49
Q

What patient population are virally caused cancers occurng

A

immunosuppressive

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50
Q

What does merkel cell polyoma virus cause?

A

merkel cell carcinoma a aggressive skin cancer in elder and immunosuppressed patients

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51
Q

What is the structure of papillomavirus?

A

member of paovavirus
infect cutaneous and mucosal epithelia
small circular double-stranded DNA genome

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52
Q

What proteins does the HPV genome encode?

A

virus encodes early and late genes?
E1 adn E2 mediate the replication and transcription of viral DNA
E4 disrupts cytokeratins to facilitate virus egress
L1 and L2 compose the capside

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53
Q

What are E5, 6, and 7 doing that is associated with onocogenesis?

A

E5-stim constitutive growth factor receptor signaling

E6 and E7 neutralizes the major brakes that regulate the cell cycle p53 and Rb

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54
Q

What HPV protein neutralizes p53 and Rb to uncouple cell division?

A

E6 and E7

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55
Q

What HPV proteins stimulate growth factor receptor signaling?

A

E5

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56
Q

How does replication of HPV work?

A

early gene expression in basal layers
late gene expression in spinous and graunlar layer
virion assembled and released in cornified layer

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57
Q

Where is HPV virion assembled and released?

A

the cornified and granular layer

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58
Q

Where is late gene expression and viral genome amplifaction occuring in HPV?

A

granular and spinosis layer

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59
Q

Where is the early gene expression E1, E2, E6 and E7 occuring?

A

basal and spinous level of HPV

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60
Q

At what level does HPV initially infect,

A

the dermis

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61
Q

How does HPV E7 regulate Rb?

A

binds Rb and targets it for degradation so prevents it blocking the progression to S phase

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62
Q

What inappropiate entry into the cell cycle can activate p53 protein?

A

Induces production of Cdk/cyclin inhibitors and stops the cell cycle

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63
Q

What is the role of E6 protein of papillomavirus?

A

recruits a ubiquitin ligase that targets p53 for degradation and prevents it from blocking progression to S phase or inducing apoptosis
also induces the expression of telomerase

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64
Q

What is the role of a pap smear?

A

cytological evidence of diplasia or neoplasia; detection of koliocytotic cells which are rounded and appear in clumps

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65
Q

What is the role of hybrid capture assay?

A

used for detection, strain analysis, and quantification of HPV DNA

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66
Q

What is the virion structure and composition of retroviruses?

A

env protein is hte envelope
group specific antigens (gag)
Capid core is made of Matrix, Capsid, Nucleocapsid, protease

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67
Q

What are the 3 groups of proteins in a retroviral genomic RNA?

A

gag, pol and env

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68
Q

What does R stand for in retrovirus?

A

repeat on both ends of genome

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69
Q

What is the gag gene?

A

encodes the Matrix, capsid, nucleocapsid, and protease

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70
Q

What is the polymerase gene (pol)?

A

encodes reverse transcriptaseand integrase which are made as an extended polyprotein

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71
Q

What is the envelope gene?

A

encodes the env protein, which is made as a precursor and gets cleaved into different domains

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72
Q

Complex retrovirus HIV organized how?

A

similar to simple retrovirus except numerous adtional genes

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73
Q

How are the accessory proteins mRNA’s generated in complex retrovirus?

A

complex alternative splicing

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74
Q

Replication cycle?

A

consists of a number steps seperated into two phases by the integration step

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75
Q

How does adsorption of HIV work?

A

HIV receptor is CD4/CCR5;

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76
Q

How does HIV penetrate and uncoat in human cells?

A

viral envelope fuses with cell membrane either at the cell surface or in endosomes after endocytosis

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77
Q

How does HIV uncoat in human cells?

A

genomic RNA is only partially uncoated, remains in a protein ‘particle’ particle in the cytoplasm
some of the gag proteins remian associated with incoming genomic RNA

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78
Q

How does reverse transcription work with HIV?

A

process of converting ssRNA to dsDNA; integrated DNA called provirus

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79
Q

How does integration work with HIV?

A

carried out by the integrase protein which enters cell with the virus and remains associated with the dsDNA

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80
Q

How does proviral transcription work in HIV?

A

major role of the LTR is to direct synthesis of viral RNA
organization of the LTR- U3 contains binding sites for cellular transcription factors acquired for high level RNA synthesis

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81
Q

How does RNA processing work in HIV?

A

as pol II transcripts all viral RNAs are polyadenylated, some must be spliced to generate teh env mRNA but a large portion must remain full length

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82
Q

How does translation occur in HIV?

A

most abundant protein is gag and gag-pol, made as a polyproteins from full length mRNA

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83
Q

What is the most abundant protein in HIV?

A

gag and gag-pol; initiates at an AUG start codon and ends at a stop codon

84
Q

What does env protein is made from what?

A

spiced mRNA on ER-bound robosomes, moves through ER-golgi is inserted into plasma membrane

85
Q

How does virion assembly and budding wokr in HIV?

A

how is the viral unspliced RNA selected for packaging instead of env spliced RNA or any other RNA

packaging: requires a psi signal; spicing removes psi signal
budding: viral gag and gag-pol polyproteins recruit RNA
maturation: as mentioned above proteolysis of gag and gag-pol by PR occurs after budding

86
Q

How does retroviral mediated oncogenesis?

A

non-transforming retrovirus- non-acute or slow tumor viruses; tumors are caused by activation of inactivation of host genes

87
Q

How does transforming retroviruses “acute” occur?

A

infections cause tumors within week; viruses harbor a mutated copy of a cellular gene involved in growth control

88
Q

What six accessory proteins of HIV are required for replication?

A

Vif, Vpr, Vpu, Nef, Tat, Rev

89
Q

What are the two regulatory HIV protein?

A

Tat and Rev

90
Q

What is the HIV protein absolutely required for transcription?

A

Tat- transactivator of transcription

91
Q

What does Rev do?

A

regulator of virion expression allows structural gene expression by promoting transport of unspliced RNA from nucleus to cytoplasm

92
Q

What are restriction factors fo HIV?

A

viral proteins that overcome cellular defenses

93
Q

What are teh two restriction factors of HIV?

A

Vif and Vpu

94
Q

What does Vif of HIV do?

A

virion infectivity factor- causes a cellular antiviral protein to be degraded: otherwise is incorporated into new virion where block RT in the next cell by inducing massive viral dsDNA

95
Q

What does vpu do in HIV?

A

promotes virion release from cell by inhibitin a host protien tetherin

96
Q

What are the two co-receptors, which HIV bind one or the other of?

A

CCR5 and CXCR4

97
Q

What are the presentl available drugs for HIV?

A 
RT inhibitor
protease inhibitors
fusion inhibitor
entry inhibitors
integrase inhibitor
98
Q

What is HAART?

A

highly active anti-retroviral therapy
considerablesuccess of cocktails triple terapies
long-term pts experience toxicity

99
Q

Can dendritic cells become infected?

A

no can bind HIV but not productively infected; can assist in dissemination

100
Q

What are the HIV tropisms?

A

M and T tropic
M infect macrophages in lab
T infect T lines in lab

101
Q

What is the basis for starin tropisms?

A

env sequence of different HIV types

102
Q

Which strain of HIV is most concerning?

A

M tropic bc source of person to person transmission

103
Q

What is the mutation that protects against HIV infection?

A

32 bp deletion in CCR5; double mutation leads to no HIV binding

104
Q

Co-receptor engagements triggers what?

A

a snapback of N and C terminal helices regions of gp41 which brings membranes together and fuses them

105
Q

What are the indirect effects of HIV?

A

immune resposne kills infected cells, soluble gp 120 may bind uninfected cells and now susceptble to ADCC

106
Q

What are the ways to diagnose HIV?

A

RNA RT-PCR
serology
Real time RT-PCR

107
Q

What is the half life of infected memtory T cells?

A

greater than 5 years meaning you would require over 75 years to clear this department

108
Q

what are some complications of influenza virus infection?

A

primary viral pneumonia
secondary bacterial pneuomnia
myositis and cardiac involvement
neurologic syndromes

109
Q

How is influenza diagnosed?

A

rapid antigen capture, detects nucleoprotein

RT-PCR

110
Q

Adenoviruses cause what type of disease?

A

A very wide variety, GI, UTI, conjunctivitis, respiratory, lymphoid infection

111
Q

What usually kills people when infected by measels?

A

pneumonia

112
Q

What does mumps infect?

A

pancreas, parotid gland, ovaries, testes other glands can cause neurological issues

113
Q

What is the host for mumps?

A

only humans

114
Q

Rubella virus is what type of virus?

A

togavirus

115
Q

What is the major concern from Rubella?

A

neonates younger than 20 weeks who are inected can result in congenital defects

116
Q

What are the prominent clinical finding in congenital Rubella syndrome?

A

cataracts and other ocular defects, heart defects, death in first year
retardation

117
Q

What is parvovirus B19?

A

single stranded DNA virus, icosahedral non-enveloped virus; dependent on host DNA replication functions

118
Q

What is bocavirus?

A

newly discovered parvovirus responsible for GI and respiratory infections

119
Q

Parvovirus infects what?

A

infects actively replicating red blood cell progenitors in bone marrow (viremia)

120
Q

What are the clinical features of Parvovirus B19?

A

erytha infectiosum, bright red cheeks, maculopapular rash, circulating immune complexes

121
Q

What are complications of B19 infection?

A

in chronic hemolytic anemia pts virus can cause aplastic crisus
when transmitted to fetus can cause still births and generalized edema

122
Q

What viruses are transmitted by fecal/oral transmission in childhood?

A

rotavirus and norovirus

123
Q

Rotavirus is what structure?

A

11 double stranded RNA segments with no envelope but a 3 layer capsid
group A most common cause of human disease
can have reassortment
Reovirus

124
Q

What is the most imoprtant non-structural protein of hte rotavirus?

A

NSP4, an extotoxin that increases intracellular calcium leading to diarrhea due to disruption of tight junctions

125
Q

What virus causes the largest number of sever diarrhea in children?/hospitalizations

A

rotavirus

126
Q

What is teh concern with rotavirus vaccines?

A 
protection
intussusception of intestines
viremia
immunosuppressed children
reversion
127
Q

What is norovirus causing?

A

major cause of acute gastroenteritis in school-aged children and adults

128
Q

What is the most common cause of foodeborne gastroentertiis in teh untied states?

A

norovirus

129
Q

What are the symptoms of hand and foot disease?

A

mild fever, sore throat, fatigue, vesicular lesions on hand feet and inside mouth

130
Q

What is the host of the hantavirus?

A

deer mouse

131
Q

What is the disease associated with hantavirus?

A

hantavirus-induced pulmonary syndrome

132
Q

What are two arthopod-borne viruses that are emerging?

A

West Nile and Dengue
three general type of disease fever
encephalitis
hemorrhagic fever

133
Q

What is Dengue spread by?

A

mosquito, climate expaneded host range of vector

134
Q

What allowed west nile to spread?

A

introduction of infected vector to new range

135
Q

When was the first case of West Nile in the United states discovered?

A

1999

136
Q

What is the natural resevoir of West Nile virus?

A

birds; only crows and Jays are affected negatively

137
Q

Horse or humans are what for west nile virus?

A

usually dead end host, viremia is hard for it to achieve

138
Q

What are the clinical features of west nile fever?

A

fever, fatigue, swollen lymph glands, headache, skin rash, eye pain
Severe disease in immunocompromised:
fever, ataxia, myelitis, GI sympoms, seizures, AMS

139
Q

How is WNV diagnosed?

A

relies on hihg index of clinical suspicion; usually fall greatest number of human cases`

140
Q

What is the first infection of dengeu fever described as?

A

breakbone fever, fever, muslce bone pain, joint pain

not fatal have protection against reinfection with same serotype

141
Q

What is the problem with getting a second infection of Dengue fever with different serotype?

A

antibodies that don’t properly neutralize increase infections of Monocytes and macrophages, release inflammatory and can cause hemorrhagic fever

142
Q

What is the diagnosis of Dengue done?

A

ELISA to detect antibodies

using touriquette will result in broken vessels

143
Q

What is the role of monkeypox?

A

relatively rare disease occuing mostly in Africa; virus a member of Poxvirus
first human case identified in 1970 not generally fatal

144
Q

What are the symptoms of monkeypox?

A

incubation of 12 days
fever, headache, muscle aches, and backache
raised bumps
emergence is due to change in behavior and movemnt of virus

145
Q

What are the symptoms of hantavirus?

A

fever, hemorrhage, 5-10%, headache, acute renal failure

146
Q

When did hantavirus become aproblem?

A

during the korean war

147
Q

Dengue virus is what type of virus?

A

a flavivirus

148
Q

What are causes of Dengue shock syndrome?

A

300000 cases/yr

occurs when individual with antibodies agianst one serotype is infected with another serotype

149
Q

How is Dengue hemorrhagic fever diagnosed?

A

ELISA to detect antibodies to determine antibodies along witha positive tourniquet test

150
Q

What is the cause of monkeypox?

A

relatively rare disease occuring in africa; small pox simlar but milder than smallpox

151
Q

Monkeypox has what symptoms?

A

fever, headache, muscle ache, lymph nodes swollen, scab

152
Q

what leads to developing and emergind diseases?

A 
Change in demographics increased urban centers often with poor sanitation
increasd interntaional trade
increased international travel
Change in behaveior
-antibiotic, IV drug use, Promiscuous sex
Changes in environmen
change in tech
change in virust
153
Q

What are the two emergin arborviruses?

A

west nile and dengue virus

154
Q

When was west nile released into north america?

A

1999

155
Q

What ar ethe features of severe west nile virus?

A

menigitis, encephalitis fever atazia myelitis GI symptoms seizures change in mental status

156
Q

How is WNV diagnosed?

A

relies on high index of clinical suspicion
consider WNV in adults greater than 50 years of age or older
local WNV activity
vaccine availbe for horses

157
Q

What are the gamma herpes viruses?

A

EBV

Kaposi’s Sarcoma

158
Q

What are the Beta herpes viruses?

A

cytomegalovirus
roseolovirus
HHV-7

159
Q

What are the alpha herpes viruses?

A

varicella zoster virus

Herpes simplex virus

160
Q

What occurs during the latent infection of the herpes virus?

A

Same strain of herpesvirus persists within the same host; Maintains itself as an episome

161
Q

HSV-1 and 2 are latent at what points?

A

HSV-1 – trigeminal ganglia

HSV-2 – sacral ganglia

162
Q

Latency associated transcripts do what?

A

these are NEVER translated into protein and function to repress HSV gene expression by an unknown mechanism

163
Q

Unknown stimuli trigger viral reactivation ccurs how?

A

few viral capsids are subjected to anterograde transport with mature virions produced around the site of innoculation– reinfection of epithelial cells–lesion–spread: reccurent infection

164
Q

Reinfection of a seropositive individual with a different strain of HSV is possible but uncommon, this is what?

A

an exogenous reinfection

165
Q

What is the mechanism of action of acyclovir?

A

a suicide inhibitor: competes with dGTP for viral DNA polymerase

166
Q

What is neonatal herpes?

A

inoculation during birth
inoculation during pregnancy results in multiple birth defects
dissemination replication
CNS is commonly affected
Disease usually manifests within days of life
mortality is high
survivors experience a very high rate of neurological abnormalities

167
Q

What CMV in healthy adults presented?

A

mild mononucleosis or cold-like symptoms

Asymptomatic in healthy adults

168
Q

What are the leading causes of congenital birth defects?

A

TORCH
TOxoplasmosis, Rubella, Cytomegalovirus, Herpes simplex
mild to severe mental retardation, deafness, death

169
Q

What becomes symptomatic upon immunosuppression?

A

chemotherapy, organ transplant, and HIV

170
Q

What long term persisten infection is associated with CMV?

A

atherosclerosis
immunosenescence
neuroblastoma

171
Q

What are basic characteristics of CMV?

A

230 kbp double stranded DNA genome
-stages of gene expression; immediate early, early and late
expresses 750different proteins
enocdes its own DNA replication machinery
icosahedral

172
Q

Cytomegalovirus transmission occurs how?

A

Direct contact with virus-containing secretions
inoculation onto a mucosal site
other routes
shedding with or without symptoms

173
Q

What is the immune response to CMV?

A

Macrophage, interferon and NK cells control but insufficient to control
humoral doesn’t play a role in clearance but limit reinfection or reactivation
cell mediated immune response is important up to 10%

174
Q

What are the symptoms of CMV in healthy adults and children?

A 
mild disease, often unapparent
fever, fatigue, sore throat headache
mononucleosis
liver function abnormalities
lymphocytosis
175
Q

How is CMV diagnosed?

A

IgM or IgG although can be difficult to tell
owl’s eye cells in urine or other tissues
culture virus from clinical material
PCR

176
Q

How is CMV treated?

A 
gangiclovir or valganciclovir
activated with phosphorylation by viral kinase inhibits viral DNA pol
Foscarnet
Cidofovir
Anti-CMV IgG
acyclovir is NOT effective
177
Q

congenital CMV does what?

A 
cause birth defects
first semester trimester infections have worse outcomes
poor outcomes if symptoms at birth
-petechial lesion
-small size at birth
-hepatoplenomegaly
Jaundice
permanent symptoms
hearing and vision loss
mental retardation
seizures
178
Q

Who is CMV infection a problem in?

A 
pregnant women
lifethreatening in
transplant patients
HIV patients
Immunosuppressive drug
pts undergoing chemo
179
Q

What is the rate of seropositivity of EBV?

A

95% or greater by early 20s world wide

a lot of asymptomatic infections

180
Q

What are cahracteristics of EBV?

A

immediate early, early and late gene expression
replication in B cells or epithelial cells
latent infection in memory B cells
stimulate and immortalize B cells

181
Q

What are the stages of EBV disseminationa nd latency?

A

transmission by blood and saliva
latency 3 occurs in proliferating B cells results in mononucleosis, post transplant lymphoproliferative disorder
latency type 1/2-viral antigens; can lead to Burkitt’s, Hodgkin lymphomas, nasopharyngeal carcinoma

182
Q

What are the EBV associated lymphomas?

A

Burkitt’s lymphoma- b cell lymphoma of jaw and face
Nasopharyngeal epithalial carcinoma-EBV DNA in epithelial tumor cells
B cell lymphomas-Hodgkin and non-hodgkin
Immunosuppressed pts and transplant pts

183
Q

What are the symptoms of EBV-mediated infectious mononucleosis?

A 
5-20% of B cells infected
fever, malaise, lymphadenopathy, exudative pharyngitis, splenomegaly
symptoms due to T cell response
self-limiting
asymptomatic in young chilren
184
Q

What is the disease post-transplant lymphoproliferative disorder?

A

EBV-mediate B cell proliferative disease
-immunosuppressive tx activates infection
-incidence 1-33% transplants depending on organ
within first year after transplant
donor B cells or reactivation in recipient
low risk if graft contains donor t cells
POOR PROGNOSIS 40-70% mortality
reduce immunosuppression
anti-CD20 antibodies eliminate B cells

185
Q

How is EBV diagnsed?

A

serology
EBV mononucleosis
-test for heterophile antibodies by agglutination of animal red blood cells
PTLD-fluorescent in situ hybridization to EBER RNA in neoplastic cells

186
Q

What is the is HHV-8?

A

Kaposis sarcoma herpes virus; causes Kaposi sarcoma, primary effusion lymphoma and multicentric Castlleman disease
replication occurs in CD19 peripheral B cells

187
Q

What is the hepatitis A virus?

A

single serotype worldwide
fecal oral transmission
acute disease and asymptomatic infection
no chronic infecction

188
Q

How often is jaundice causeed by Hepatitis A?

A

under 6 less than 10 percent

over 14 yrs 70-80%

189
Q

What are the complications associatedd with Hepatitis A?

A

fulminant hepatitis
chloestatic hepatitis
relapsing hepatitis

190
Q

Who is the hepatitis A vaccine recommended for?

A

those traveling to areas with high incidence
ppl with chronic liver disease
infants
ppl working with HAV

191
Q

Where are the hepatitis E outbreaks occuring?

A

US cases have travelt o HEV endemic areas and most outbreaks are associated with fecally contaminated drinking water

192
Q

How does the outcome of hepatitis B infection change by age at infection?

A

chronic infections are the greatest in those infected at birth
symptomatic fnfections occur more regulary after about 4 years of age

193
Q

What is the mechanism of hepadnavirus?

A

enveloped virus is bidning to sodium/bile acid contransporter
circular DNA genome partially double-sranded genome with DNA syntehsis occuring to form fully ds DNA and that goes to nucleus
mRNA “reverse-transcribedd” to ssDNA, DNA made partially ds
DNA can integrate into chromosome and remain in cell

194
Q

HBV infected cell produce what two things?

A

infectious virus as well as non infectious HbsAg particles; antigen without DNA

195
Q

What are the normal causes for initial infection by HBV?

A 
mothers milk
vaginal secretion
blood
semen
saliva
so IDU, sex, neonatal, breast feeding
196
Q

What are the symptoms of hepB?

A 
fever,rash arthritis
Jaundice
Dark urine
malaise
anorexia
nausea
RUQ pain
itching
197
Q

What are the normal clinical outcomes for HBV infection of adults?

A

90% have full resolution
9% have HbsAg+ for greater than 6 motnhs ; 50% of those resolve the rest have some osrt of chronic state which can result in carcinoma or cirrhosis
1% fulminant hepatitis

198
Q

What is hepatitis delta?

A

viroid that can only grow in hepatits B infected cells
small RNA copied by host RNA pol II, catalytically active ribozyme that processes itself
encodes 1 antigen becomes packaged in Hep B sAg

199
Q

What are the clinical features of Hepatitis D?

A

coinfection; sever acute disease and low risk of chronic infection
superinfections(subsequent to HBV) usualy develop chronic HDV and high risk of sever chronic liver disease

200
Q

What is the treatment of HBV?

A

vaccination is key to prevent infection of high-risk individuals and infants
polymerase inhibitors, nucleoside analogs, IFN-alpha; aka antivirals
new approaches silence HBV expression during chronic infection

201
Q

Hepatitis C is what structure?

A

flavivirus; pos strand, RNA virus. Enveloped virions
9 kB genome; 10 proteins, involves proteolytic processing
many quasi-species
encodes multiple immunomodulators
liver damage primarily due to immunopathology
hihg incidence of chronic and asymptomatic infections
assoicated with hepatic carcinoma

202
Q

What is the viral life cycle of hepatitis C?

A

hepatocyte specific- basis for developing therapies
intimate relationship with intracellular lipids and membranes
RNA replication; IRES-mediated translation
proteolytic processing
membrane associated RNA replication
assembly
maturation and release

203
Q

What are the most common sources of Hep C infection?

A

60% IVDU

15% Sexual

204
Q

What are teh clinical outcomes of HCV infection of Adults?

A 
15% resolution
85% persistent infection
--6% liver failure
--20% cirrhosis
--4% hepatocellualr carcinoma
205
Q

Why does HCV lead to a high incidence of carcinoma?

A

HCV core proteins interact and regulate many tumor suppressors; induce steatosiss
envelope protein E2 inhbiits NK cells
non-structural proein NS3 can enhance cell growth
NS5A enhances cell growth and prevents apoptosis

206
Q

How does the IL28B gene playa keyaoutcome in HCV infectin?

A

it encodes IFN-gamma and a polymorphism has a strong impact on teh response to IFN therapy as well as natural clearance; the primary genotye in the US has more trouble clearing

207
Q

What makes a virus an inmportant feasible target for vaccine development?

A

infection is serious enough
limited number of serotypes
virus doesn’t mutate rapidly
natural infection is acute and self-limiting and immunity is long-lasting

Block7 (10 decks)

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