Micro Test 3

Front 1

structure of a virus as compared to a bacteria

Back 1

small genome with protective covering
OBLIGATE INTRACELLULAR PARASITES

Front 2

what is the only thing viruses know how to do

Back 2

get inside susceptible cell and reproduce

Front 3

viruses associated with one genus of animals tend to be able to infect that one genus and sometimes only one species only

Back 3

HOST RANGE

Front 4

even within a single genus and species, a single kind of virus can infect a limited number of cell types

Back 4

CELL RANGE

Front 5

Viral genomes are made of

Back 5

DNA or RNA (never both)

can be ss or ds

Front 6

a single haploid virus particle

Back 6

virion

BUT

retroviruses are not haploid

Front 7

ds (MOST) or ss (Parvovirus)

genome is either closed circle or a single linear piece

Back 7

DNA viruses

Front 8

ds (Reovirus) or ss (MOST)

genome is either single linear piece or segmented into several linear pieces (influenza)

Back 8

RNA viruses

Front 9

surrounds the viral genome

protects genome from environment

****determines the infectivity of the virus***

Back 9

Viral Capsid

(ALL VIRUSES HAVE)

Front 10

made of protein molecules that are specified by the viral genome
can be several different proteins that aggregate to form building blocks (CAPSOMERES) which in turn coalesce to form a hollow sphere around the viral genome

Back 10

Viral Capsid

Front 11

component of the viral capsid that is a single, folded polypeptide chain

Back 11

subunit/protein subunit

Front 12

component of the viral capsid that is a collection of one or more nonidentical (or identical) subunits which form a building block for a larger unit

Back 12

Structure unit/protomer

Front 13

component of the viral capsid that is a set of structure units forming a sub-assembley of the capsid (ie pentamer, hexamer)

Back 13

Assembly unit

Front 14

component of the viral capsid that are "lumps or clusters" on the capsid surface which are visible in the electron mircoscope (CAPSOMERE)

Back 14

Morphological Unit

Front 15

type of capsid symmetry that is a spherical hollow shell made of 2 kinds of assembly units of different shapes

MINIMUM: 12, five-sided, Pentamers (NECCESSARY TO FORM A SPHERE

CAN HAVE: variable number of six-sided, hexamers (DETERMINES THE SIZE OF THE COMPLETED CAPSID

Back 15

Icosahedral

Front 16

in icosahedral symmetry, the spaces betwen the pentamers which expand the size are

Back 16

Hexamers

Front 17

triangles used as subunits to make the hexamers and pentamers in icosahedral symmetry

Back 17

quasi-equilvalence

Front 18

larger than assembly units and seen morphologically

Back 18

CAPSOMERES

Front 19

proteins that raidate out from the pentamers

**determines the infectivity (esp the knob on the end)

Back 19

Spike proteins

Front 20

type of capsid symmetery in which identical capsomeres aggregate to form a helical ribbon-like structure surrounding the viral genome

Back 20

HELICAL


ALL RNA VIRUSES HAVE!

Front 21

which virus has a combo of helical and icosahedral symmetry

Back 21

RABIES

Front 22

in some viruses, located exterior to the capsid,

derived from a lipid-bilayer membrane of the host cell (ie nuclear mem, cytoplasmic mem)

Unique, virally speicified glycoproteins (PEPLOMERS) inserted into them

Back 22

ENVELOPE

Front 23

lipid bilayer is derived from

Back 23

HOST

Front 24

glycoproteins are derived from

Back 24

virus

Front 25

what are essential to viral infecitivity

Back 25

Envelope and Peplomers

Front 26

glycoproteins inserted into the membranes comprising the viral envelope

determines and is essential for viral infectivity

Back 26

PEPLOMERS

Front 27

what determines a virus' ability to survive in an hostile environment BUT does not determine its pathogencity

Back 27

Envelope vs non-envelope

Env.--> easier to inactivate outside of the body with disinfectants

Front 28

if remove a viral envelope what is left

Back 28

nucleo-capsid

Front 29

intermediate proteins that are positioned between the viral envelope and the capsid

some are transmem proteins

some are held to the inner leaflet of the envelope by hydrophobic bonds

Back 29

MATRIX PROTEINS

Front 30

connect the nucleocapsid to the mem envelope

perform a crucial function during the assemble of progeny virions during replication

Back 30

MATRIX Proteins

Front 31

what can induce an immune response (cell mediated) (esp when glycoproteins adhere to the cell membrane)

Back 31

spike proteins

Front 32

what is best viral example of complex symmetery

Back 32

vaccinia virus

Front 33

used to immunize against small pox

large dumbbell-shpaed genome

genome is surounded by several layers of protein with no discernible capsid symmetry

protein is surrounded by sveral layers of lipid

Back 33

vaccinia virus

POX IN A BOX

Front 34

what is the largest animal virus

Back 34

pox viruses

Front 35

DNA virus that replicates in the cytoplasm of the host

(DNA viruses usually replicate in the nucleus)

Back 35

Pox viruses

Front 36

steps of viral replication

Back 36

1. attachment or adsorbtion
2. viral penetration
3. uncoating
4. eclipse (synthesis of genome and viral proteins)
5. assembly of progeny virions
6. release of non-enveloped / enveloped progeny virions

Front 37

cell attachment sites distributed over the viral surface



(ATTACHMENT CAN BE BLOCKED BY SPECIFIC ABS)

Back 37

capsid (non-envel viruses)
envelope peplomers (envel viruses)

Front 38

suceptible cells have what on their surfaces

Back 38

viral receptors

Front 39

process by which the virus enters the cytoplasm of a susceptible cell

Back 39

penetration

Front 40

penentration can occur by what 3 mechanisms

Back 40

Translocation (non-envel.)
Fusion (enveloped)
Viropexis (receptor-mediated endocytosis)--->MOST COMMON (both non-envel and envel)

Front 41

pushing the NON-ENVELOPED virus through the cell membrane (the whole virus (rare) or just the genome)

virus makes a self-sealing pore on the host membrane

Back 41

translocation

Front 42

ENVELOPED VIRUS fuses with the host cell membrane and is relased into the cell

Back 42

Fusion

Front 43

ENV or NON-ENV virus sends cascading signal to the host after a speific interaction between the spike proteins and the cell's viral receptor...these signals tell the cell to endocytose thevirus

Unusual process b/c most cells only do pinocytosis

Back 43

Viropexis

Front 44

step that relases the viral genome from the capsid

Back 44

uncoating

Front 45

uncoating occurs during

Back 45

viropexis - endocytotic vesicle is ACIDIFIED which disrupts the viral env and cpasid and allows the genome to enter the cytoplasm

fusion - uncoating happens during penetration

translocation - ?

Front 46

there is no physical evidence of viral infection at what stage of replication

Back 46

Eclipse

Front 47

DS DNA genomes of viruses are replicated how?

Back 47

by semi-conservative replication similiar to cellular DNA synthesis

Front 48

ss RNA viral genome replication strategies

Back 48

Positive strand genomic RNA --> needs replicative intermediate (IR)

Negative strand genomic RNA --> must carry RNA polymerase and also needs IR

Front 49

which RNA genomes have messenger function and can be immediately translated

Back 49

ss RNA positive

Front 50

which RAN genomes are anti-sense and have NO messenger function

Back 50

ss RNA negative

Front 51

which RNA genome is transcribed within the paritially opened capsid by a polymerase within the capsid (a + RNA strand)

Back 51

ds segmented reovirus genome

Front 52

+ RNA strands have 2 functions

Back 52

1. messenger function --> translated
2. assembles within a prescurser particle in which it serves as a template for the complimentary strand to yeild ds genomic segments

Front 53

in which viruses can protein synthesis be sequential (synthetic proteins are transcribed befroe the structural proteins)

mRNA is not transcribed all at the same time

Back 53

DNA virueses

Front 54

which viruses does the transcription and processing of all proteins occur at eh same time because translating the entire strand as a polyprotein

Back 54

RNA Viruses

Front 55

where does synthesis of retroviral RNA occur

Back 55

in the cytoplasm of the infected cell

Front 56

RDDP comes from

Back 56

the infecting virus

Front 57

RDDP does what

Back 57

reverse transcribes the +strand RNA into a single strand of complimentary DNA --> forming a heteroduplex within the genomic RNA.....the DNA is then used as a template to make a complimentary DNA resulting in ds DNA.....ds DNA is transported to the nucleus where it is incorporated into the host genome (PROVIRAL DNA).....proviral DNA is reanscribed to RNA to form progeny

Front 58

how do non-enveloped progeny virions assemble

Back 58

the structural proteins first self-assemble (NO ENERGY) and then capsomeres self-assemble into capsids....the genome (DNA or RNA) then can penetrate into the hollow capsid

Front 59

ways for the non-enveloped progeny virions to be relased

Back 59

Lysis (MOST COMMON)
Reverse endocytosis



in both host cell is killed

Front 60

how does enveloped progeny virions get realsed

Back 60

the assembly and realse occur at the same time (slow and continous event)

Front 61

there is no physical evidence of viral infection at what stage of replication

Back 61

Eclipse

Front 62

DS DNA genomes of viruses are replicated how?

Back 62

by semi-conservative replication similiar to cellular DNA synthesis

Front 63

ss RNA viral genome replication strategies

Back 63

Positive strand genomic RNA --> needs replicative intermediate (IR)

Negative strand genomic RNA --> must carry RNA polymerase and also needs IR

Front 64

which RNA genomes have messenger function and can be immediately translated

Back 64

ss RNA positive

Front 65

which RAN genomes are anti-sense and have NO messenger function

Back 65

ss RNA negative

Front 66

which RNA genome is transcribed within the paritially opened capsid by a polymerase within the capsid (a + RNA strand)

Back 66

ds segmented reovirus genome

Front 67

+ RNA strands have 2 functions

Back 67

1. messenger function --> translated
2. assembles within a prescurser particle in which it serves as a template for the complimentary strand to yeild ds genomic segments

Front 68

in which viruses can protein synthesis be sequential (synthetic proteins are transcribed befroe the structural proteins)

mRNA is not transcribed all at the same time

Back 68

DNA virueses

Front 69

which viruses does the transcription and processing of all proteins occur at eh same time because translating the entire strand as a polyprotein

Back 69

RNA Viruses

Front 70

where does synthesis of retroviral RNA occur

Back 70

in the cytoplasm of the infected cell

Front 71

RDDP comes from

Back 71

the infecting virus

Front 72

RDDP does what

Back 72

reverse transcribes the +strand RNA into a single strand of complimentary DNA --> forming a heteroduplex within the genomic RNA.....the DNA is then used as a template to make a complimentary DNA resulting in ds DNA.....ds DNA is transported to the nucleus where it is incorporated into the host genome (PROVIRAL DNA).....proviral DNA is reanscribed to RNA to form progeny

Front 73

how do non-enveloped progeny virions assemble

Back 73

the structural proteins first self-assemble (NO ENERGY) and then capsomeres self-assemble into capsids....the genome (DNA or RNA) then can penetrate into the hollow capsid

Front 74

ways for the non-enveloped progeny virions to be relased

Back 74

Lysis (MOST COMMON)
Reverse endocytosis



in both host cell is killed

Front 75

how does enveloped progeny virions get realsed

Back 75

the assembly and realse occur at the same time (slow and continous event)

Front 76

what are the 4 different ways that a cell can respond to viral infection

Back 76

1. no apparent effect --> very low level of viral rep in a secondary target cell (at portal of entry cells)

2. cytopathic effect with eventual cell death --> usual response to primary taregt infection (VERY SPECIFIC)

3. loss of growth control and transformation into a cancer cell --> both RNA and DNA tumor viruses

4. Latent infection --> viral genome remains in cell but an absence of total viral gene expression

Front 77

viruses are dependent on what to make their protein

Back 77

HOST

Front 78

the capacity of a cell to become infected

Means that the cell has receptors to which a particular virus can attach

Back 78

susceptibility

Front 79

what type of cell can not be infected because it expresses no receptors for a particular virus

Back 79

resistant cell

Front 80

what type of viral infection occurs when the susceptible cell is PERMISSIVE

the cell will make and express all the virally coded proteins

Back 80

Productive viral infection

Front 81

what type of viral infection occurs when the complete viral genome is available and the interaction will result in infeabus progeny viruses begin produced and realeased

PRODUCTIVE infection from virus's persceptive

Back 81

Productive viral infection

Front 82

what type of viral infection occurs when the cell may be susecptible and allow viral entry or the cell may be NOn-permissive and allow only a few viral genes to be expressed

Back 82

Abortive Viral infections

Front 83

what type of viral infection occurs when the infection could be in a permissive or non-permissive cell and the infecting virus lacks a full complement of genes (DEFECTIVE VIRUS), NO progeny produced

Back 83

Abortive Viral Infection

Front 84

what type of viral infection occurs when the cells may be only transiently permissive and the consequences are the virus persists in the cell until the cell becomes permissive and only a few cells in a population produce viral progeny at any time

Back 84

Restrictive/restringent viral infection

Front 85

what type of viral infection has a very low level of productive infection over an extended period of time

Back 85

Restrictive/restringent viral infection

Front 86

what type of viral infection is the latently infected cell nonpermissive and the cell retains the entire viral genome, the cell is also able to express and make some viral proteins and genomes and the cell is not killed

Back 86

Latent viral infection

Front 87

what type of viral infection does the latently infected cell allow abortive infection b/c not allowing virulent progeny to be formedbut the genome of the virus can often enter a permissive cell

Back 87

latent viral infection

Front 88

what type of viral infection occurs when the infected cell becomes transformed to the malignant state. this cell may or may not be permissive for th eproduction of progeny (RNA tumor viruses are replicated and DNA tumor viruses transform nonpermissive cells)

Back 88

Oncogeniv transforming viral infection

Front 89

what type of viral infection occurs when the RNA tumor virus experiences productive infection but the DNA tumor virus experiences abortive infection

Back 89

oncogenic transforming viral infectrion

Front 90

what type of viral infection occurs when the cells are never infected by the virus ...most resistance is due to lack of cell surface recptors for a particular virus

Back 90

cells resistant to viral infection

Front 91

what type of viral infection occurs when there is no infection, no replication, no progeny virus and a dead end for the virus

Back 91

cell resistant to viral infection

Front 92

what are cellular pathways that the viruses can use to mature their mRNA from the nucleus to the cytoplasm

Back 92

RNA splicing and transport to the cytoplasm

Front 93

what cleaves host cell nascent transcripts in the cytoplasm

Back 93

virus encoded endonuclease

Front 94

does viral or cellular mRNA have a higher affinity for ribosomes

Back 94

***viral mRNA****

some viruses can change the specificity of the host cell translational appartus in favor of the virus

Front 95

what is the ususal portal of entry for a virus

Back 95

external coverings of the body

have a low level of viral replication here (restrictive infection)

Front 96

how and where does the virus migrate to after entering

Back 96

goes to lymph nodes where there is a low level of replication and then the virus migrates via the thoracic duct to the circulation (VIREMIC PHASE), the virus then goes in search of target tissue

Front 97

what type of virus is most likely to induce a B cell response because will eventually o to the spleen

Back 97

virus in the blood (VIREMIC PHASE)

Front 98

where does the greatest cytopathic result occur....when have clinical diesease

Back 98

in the target tissue

Front 99

the reflection of the time required for the virus to reach its target tissue

measured formt he time of intial infection until signs and symptoms of clinical disease develop

Back 99

incubation period

Front 100

if the portal of entry is also the target tissue then the incubation period is

Back 100

short (2-4 days)
no viremic phase
ie influenza

Front 101

if the virus must go thru a viremic phase to reach its target tissue then the incubation period is

Back 101

LONG (14-21 days)
is chicken pox

Front 102

derived from bone marrow

appear as lymphocytes with numerous cytoplasmic granules

neither T nor B cells-->b/c lacks all of the surface markers associated with either T or B cells (no Igs, CD4/CD8, no T cell receptor complex)

make up 5-20% of the mononuclear cells in the blood and spleen and are rarely found in other lymphoid tissues or organs

Back 102

NK cells

Front 103

what do NK cells secrete to give rise to Apoptosis

Back 103

perforins and granzymes

Front 104

how do NK cells discriminate between self and nonself

Back 104

presence or absence of Class I MHC

NK cells target cells that lack self, class I MHC

Front 105

what are the primary effector functions of NK cells

Back 105

1. production of pro-inflammatory cytokines--INF gamma and TNF alpha

2. cyttotoxicity of NK cells mediated thru the production of cytotoxic granules that contain perforin and granzymes similer to T cytotoxic cells

Front 106

what is produced by CD4 cells and NK cells to activate macrophages

Back 106

INF gamma

Front 107

what activates NK cells to express INF gamma and also tells the NK cells to proliferate

Back 107

IL 12 and IL 15

Front 108

when does induction of NK cell effector functions generally occur

Back 108

within a day or two after primary viral infection-----long before the adaptive immune response develops

Front 109

what do NK cells do in the early stages of infection

Back 109

restrain viral replication before an effective immune response develops

Front 110

if the number of NK cells decreases then the susceptibility to infection

Back 110

increases


esp with the herpes viruses: HSV-1, EBV, HCMV

Front 111

for anti-viral activity are Type 1 or Type 2 INF's more potent

Back 111

Type 1 INFs are 10 to 100 more potent

Front 112

what are the 2 Type 1 INFs

Back 112

1. INF alpha -- produced by mononuclear phagocytes; family of polypeptides

2. INF beta -- produced by many cells best represented by fibroblasts; a single protein

both types share the same cell surface receptor

Front 113

what are the Type II INFs

Back 113

INF gamma -- signature cytokine of Th CD4 effector cells

Front 114

which INFs are not consitutively made....their syntethsis must be induced

Back 114

Type I Infs

Front 115

what is the potent inducer of type I INFs

Back 115

ds RNA

Front 116

when Type I INFs bind to the cell-surface rector of infected and noninfected cells the transcription of what is promoted

Back 116

anit-viral protein

Front 117

what are the 3 anti-viral proteins

Back 117

1. 2'-5' Oligoadenylate synthetase

2. PKR Kinase

3. Mx Protein

Front 118

which anti-viral protein polymerizes ATP into a series of 2'-5' linked oligomers---this activates an endonuclease which degrades viral RNA

Back 118

2'-5' olgioadenylate synthetase

Front 119

which anti-viral protein phophorylates the eukaryotic protein synthesis initiation factor dF-2 and therefore inhibits the translation of viral proteins

Back 119

PKR kinase

Front 120

which anti-viral protein produces cellular resistance specifically to influenza virus replication

Back 120

Mx Protein

Front 121

which 2 anti-vrial proteins are activated by engaging ds RNA

Back 121

2-5 oligoadenylate synthetase
PKR kinase

Front 122

the more class I MHC molecules that are expressed on a virally infected cell, the ?????? likely it is that an anitgen-sensitive T cell will recognize the virally infected cell and respond to it

Back 122

MORE ****

Front 123

which INFs induce the increased expression of class I MHC molecules on virally infected cells and surrounding cells that may become infected

Back 123

Type I INFs

Front 124

what are 2 excellent immunogens that can induce a B cell mediated Ig response

Back 124

viral peplomers and capsid proteins

ONLY IF EXTRACELLULAR

Front 125

what type of Igs can prevent viral infection of susceptible cells

Back 125

neutralizing Igs

Front 126

what type of Igs are specific for structural viral proteins and can facilitate phagocytosis of virus particles

Back 126

non-neutralizing Igs

Front 127

how can T cells recognize virally infected cells

Back 127

peptide fragments from viral proteins are displayed by class I and II MHC molecules on the surface of the infected cell

Front 128

what type of effector T cell consititutes the primary defense against virally infected cells

Back 128

CD8 effector T Cells because almost all nucleated cells express Class I MHC

Front 129

how can CD8 T cells elminate virus-infected cells

Back 129

1. release of perforins

2. induction of apoptosis by at least 2 different mechanisms

Front 130

what type of immune response is essential for the elimination of virally infected cells and recovery from viral disease

Back 130

cell-mediated response because once the cell is infected Igs are of little defense

Front 131

what are 4 properties that are present in cells but not in viruses

Back 131

no ribosomes
no mitochondria
no/few enzymes
no binary fission or mitosis

Front 132

what type of viruses HAVE to replicate in the nucleus

Back 132

DNA viruses (except pox viruses)

Front 133

name the family of viruses:

used to be papovaviridae family

nonenvel, icosahedral

ds DNA, supercoiled circle

rep in nucleus (early and late transcription)

long incubation

proliferative

Back 133

papillomavaviridae

Front 134

proliferative squamous lesions (cutaneous or mucosal)

usually BENIGN some undergo malignant transformation

Back 134

Paillomas (warts)

Front 135

cutaneous papillomas are described as being

Back 135

plantar, common, flat

Front 136

mucosal papillomas are described as being in the

Back 136

oral cavity, larynx, and anogenital area

Front 137

how are papillomas transmitted

Back 137

person-person and indirect

Front 138

HPV are classified into different types based on ?

Back 138

DNA sequence homology and serology

Oral HPV = HPV6,11
Cervical dysplasia = HPV16, 18, 6, 11

Front 139

HPV may play a major role in development of a variety of ?????, esp ?????

Back 139

carcinomas, cervical neoplasia

Front 140

at least 85% of cervical carcinomas contain ??? DNA rather than circular, extrachromosomal DNA

Back 140

intergrated HPV DNA

Front 141

what 2 HPV 16 and HPV 18 proteins are oncogenes? What can they bind to and inactivate and what does this do to the cell?

Back 141

E6 and E7 (expressed from early genes)

Binds to and inactivates the cellular growth suppressor proteins p53 and p105RB. the cell then becomes more susceptible to mutation, chromosomal aberrations, or action of a cofactor leading to cancer


p53 and p105RB are normal cell proteins that allow for routine cell replication ---> cellular growth cycle policemen

Front 142

****WARTS FREQUENTLY UNDERGO???****

Back 142

SPONTANOEOUS REGRESSION

Front 143

what are some ways to treat warts

Back 143

topical (salicyclic acid, formalin)
surgical
cryotherapy (freezing off)
laser therapy
interferon injections

Front 144

what does the current HPV vaccine consist of? When should it be given?

Back 144

non-infectious virus like particles (VLPs)

3-dose series given to girls 11-12 or as a catch up ages 13-26


***DOES NOT TREAT EXSISTING HPV INFECTIONS, GENITAL WARTS, PRECANCERS, CANCERS****

Front 145

what family of viruses was originally isolated in respiratory secretions and adenoid tissues

capable of eliciting tumore in animal hosts only

being currently studied as potential vectors for gene replacement therapy (cystic fibrosis)

nonenveloped, icosahedral

linear ds DNA

rep in nucleus (early and late transc)

ubiquitous

can establish a latent infection in tonsils and adenoids

Back 145

adenoviridae

Front 146

how is adenoviridae transmitted

Back 146

direct....respiratory droplets and fecal matter

Front 147

what are the main clinical manifestations of adenovirus

Back 147

1. endemic respiratory disease
2. phayngoconjunctival fever
3. acute follicular conjunctivitis
4. epidemic keratoconjunctivitis
5. acute respiratory disease
6. gastroenteritis
7. acute hemorrhagic cystitis
8. systemic infection in immunocomp pts
9. obesity?

Front 148

what is the most common adenoviral eye infection and how is it transmitted? unilateral or bilateral?

Back 148

acute follicular conjuncitivitis

direct contact

unilateral

Front 149

ship-yard worker's disease

unilateral or bilateral

adenovirus

ocular trauma causes, then direct inoculation will predispose to disease

Back 149

epidemic keratoconjuncitivitis

Front 150

what type of adenovirus manifestation is common in military recruits

Back 150

acute respiratory diesease

Front 151

what types of vaccine is available for adenovirus

Back 151

oral vaccine

lyophylized live viruses in enteric capsule

d/c in 1999

Front 152

what family of viruses is the simplest animal DNA virus

non-envel, icosahedral

ss DNA linear with 2 coat proteins

rep in nucleus

Back 152

Parvoviridae

Front 153

what are the 2 members of the parvoviridae family

Back 153

parvovirus genus
dependovirus genus

Front 154

which parvoviridae virus replicates autonomously in rapidly dividing cells

Back 154

parvovirus (human parvo virus B19)

Front 155

which parvoviridae virus replicates only in the prescence of a helper viruse (usually adenovirus)

Back 155

dependovirus

Front 156

how is human parvovirus B19transmitted?

Back 156

respiratory, blood transfusions, vertically from mother to fetus

Front 157

what cells does Human parvovirus B19 target? and why?

Back 157

*****immature cells in the erythroid lineage (pre-RBCs)*****

b/c rapidly dividing

Front 158

what are the clinical mainfestations of human parvovirus B19

Back 158

1. erythema infectiosum (fifth disease)
2. transient aplastic crisis
3. infection in immunodeficient pts
4. infection during pregnancy

Front 159

what is the most common human parvo b19 manifestation

in early school age children (rare in adults)

mild constitutional symptoms PLUS RASH**

joint involvement in adults

Back 159

erythema infectiosum (fifth disease)

Front 160

which human parvo b19 manifestation lowers the production of RBCs and may produce crisis in chronic hemolytic anemia pts (SICKLE CELL PTS)

Back 160

transient aplastic crisis

Front 161

immunocompromised pts with human parvo b19 can develop

Back 161

chronic supression of bone marrow and chronic anemia

Front 162

infection of human parvo b19 during pregnancy can lead to

Back 162

hydrops fetalis and fetal death

Front 163

what family of viruses have a **** double envelope not derived from any host cell membrane (entirely de novo synthesis)****

ds linear DNA

rep in cytoplasm ** in areas called "virus factories"

***does not need any of the cell's nuclear enzymes for transc, rep of DNA***...still need ribosome from host

Back 163

Poxviridae

Front 164

what are the 3 stages of poxviridae Transcription

Back 164

1. immediate early
2. early
3. late

Front 165

contagious, febrile disease characterized by vesicular and pustular lesions

Back 165

smallpox (variola)

Front 166

smallpox is considered by the CDC to be a

Back 166

Catergory A biological agent

Front 167

how is smallpox transmitted

Back 167

directly (resp.)

humans are the only natural host

Front 168

what is the smallpox vaccine

Back 168

live vaccinia virus

causes a limited infection that creates a cross-reaction with smallpox

Front 169

which type of virus family has 3 subfamilies

ubiquitous

enveloped, icosahedral

rep in nucleus

envelope from nuclear (not cytoplasmic) membrane

ds linear DNA

CAN CAUSE LATENT INFECTIONS ****

Back 169

Herpesviridae

Front 170

3 subfamilies of herpesviridae

Back 170

alpha
beta
gamma

Front 171

alpha Herpes viruses

Back 171

HSV 1 and 2
Varicella zoster virus (ZVZ, HSV 3)

Front 172

what is the primary target of alphs herpes viruese

Back 172

mucoepithelial cells

Front 173

what is the site of latency for alpha herpes viruses

Back 173

neuron

Front 174

how is HSV 1 and 2 transmitted

Back 174

direct contact , sex

Front 175

how is HSV3 and ZVZ transmitted

Back 175

close contact, respiratory

Front 176

what is the primary infection of HSV 1 and 2

Back 176

herpetic gingivostomatitis, labialis, and gentialia

Front 177

what is the primary infection of VZV and HSV3

Back 177

chicken pox and if reactivated shingles

Front 178

what are the beta herpesviruses

Back 178

Cytomegalovirus (CMV, HHV5)
Human herpesvirus 6 (HHV6)
Human herpesvirus 7 (HHV7)

Front 179

what is the primary target cell of cytomegalovirus

Back 179

monocyte, lymphocyte, epithelial cells

Front 180

what is the primart target cell of HHV 6 and 7

Back 180

T cells and ???

Front 181

what is the site of latency of CMV

Back 181

monocyte, lymphocyte and ???

Front 182

what is the site of latency for HHV6 and HHV7

Back 182

t cells and???

Front 183

how is CMV transmitted

Back 183

close contact, transfusions, tissue transplant, congenital

Front 184

how is HHV6 and HHV 7 transmitted

Back 184

respitatory and close contact?

Front 185

What is the main clinical manifestations of CMV

Back 185

cytomegalic inclusion disease, mononucleosis

Front 186

what is the main clinical manifestations of HHV6

Back 186

exanthem subitum (roseola, sixth disease)

Front 187

what are the gamma herpes viruses

Back 187

Epstein Barr virus (EBV)
Human Herpervirus 8 (Kaposi's sarcoma-associated viruse, KSVH, HHV8)

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what is the primary target cell of EBV

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B cells and epithlial cells

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What is the primary target cell of HHV8

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lymphocytes

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what is the site of latentcy of EBV

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B Cell

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What is main clinical manifestations of EBV

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infectious mononucleosis, Burkitt's lymphoma, oral hairy leukoplakia, poat-transplantation lymphoproliferative disorder

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What is the main clinical manifestations of HHV8

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AIDS assoicated Kaposi's syndromwe

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how is EBV transmitted

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saliva

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how is HHV8 transmitted

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close contact (sex), saliva?

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what holds the space between the capsid and the envelope

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tegument proteins

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how does herpesvirus get into the cell

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FUSION

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how does herpesvirus get realsed from the cell

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BUDDING

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how are HSV viral genes transcribed

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cell RNA polymerase II

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primar infection with this usually occurs in childhood via contact with infected adults....primary infection is asymp but some are life threatening

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HSV-1

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usually acquired later in life, slightly more common in women

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HSV2

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infection occuring in absence of detectable abs against HSV, symptomatic cases last 2-3 weeks

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primary infection

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generally milder than symp primary infections,

may be either reactivation of latent HSV from primary infection or reinfection by a different strain of HSV

1 week duration

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recurrent infection

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in what order do the Igs respond to HSV

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IgM-->IgG-->neutralizing abs (B and D)

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What are the primary clinical manifestations of HSV1

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orofacial lesions
-acute primary herpetic gingivostomatitis
- recurrent herpes labialis

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what are the primary clinical manifestations of HSV2

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genital lesions but can occur as orofacial lesions

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what is the most common herpetic infection of early childhood

soreness of mouth, fever, malaise, irritability

cervical lymph node enlargement

eruption of multiple vesicular lesions

localized or throughout the oral cavity

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acute primary herpetic gingivpstomatitis

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what occurs with every case of acute primary herpetic gingivostomatitis

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gingivitis (may bleed spontaneously)

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"fever blisters"

"cold Sores"

usually mild, NO fever

few lesions in isolated areas

often a PRODROME - itching, burning at site

No systemic signs usually

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Recurrent herpes labialis

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what are all the clincial manifestations of HSV

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1. orofacial infections
2. ocular infections (keratoconjunctivitis)
3. gential infections
4. traumatic infections
5. encephalitis
6. neonatal herpes
7. eczema herpeticum
8. disseminated, systemic disease in immunocom pts

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how does the HSV manifestationof keratoconjunctivitis usually come about

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usually result of auotinoculation during gingivostomatitis....BUT can be acquired at birth from mother with genital infection

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corneal involvement-->dendritic ulcer fomration followed by keratitis

recurrent episodes lead to dense scarring, loss of sight

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Kerotoconjunctivitis

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What do you NEVER treat Kerotoconjunctivitis with

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corticosteriods

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pathology and pathogenesis of ????? is essentially the same as HSV orofacial infections

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gential infections (herpes genitalis)

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early symptoms: itching, burning in anogenital area, pain in legs, butt, genital area, vaginal fluid discharge, abdominal pressure

development of vesicular lesions

fever, headache, swollen lymph nodes in groin area

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primary infection of herpes genitalis

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milder infection

sometimes no visible lesions

virus shedding from cervix may be asymp

potential problem at term in pregnant women

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recurrent infection of herpes genitalis

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introduction of HSv into microabrasion or wounds on hands, fingers

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herpetic whitlow

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what type of viruses are HSV1 and HSV2

----they remain latent in regional sensory ganglia

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neurotropic

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how do you distinguish between HSV 1 and HSV2 in the lab

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genotyping

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how is VZV transmitted

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via contact with infected secretions or air droplets (dried scabs are NOT infective--unlike smallpox)

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how does VZV enter and how does it spread

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thru URT, oropharynx then disseminates through lymph and blood (viremia) then spreads centrifugally beginning on trunk and neck, the vesicles may occur in the mouth, nose, of throat