Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Virology 2 > virology 2 > Flashcards

virology 2 Flashcards

1
Q

describe the measles and mumps in terms of the structure of the virus and their nucleic acid content

A

paramyxovirusesRNAsingle strandednegative senseenvelopedhelical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

do paramyxoviruses have to carry RNA polymerase?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

are measles and mumps capable of radical antigenic shifts?

A

no- paramyxoviruses only contain one strand of RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does the type of infection dictate the incubation period and subsequent immunity for measles and mumps?

A

they travel through the blood as viremia and cause systemic infections. thus:1 incubation time is longer2 IgG provides life long immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how many serotypes of mumps are there?

A

1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how many other animals act as resevoirs for mumps?

A

just humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the normal incubation period for mumps?

A

3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the symptoms of mumps?

A

after 3 weeks, prodromal symptoms will developfever, malaise, anorexiafollowed shortly by asymmetrical parotiditis and potentially orchitis post puberty. parotiditis is the presenting symptom.aspetic meningitis is also common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe transmission of mumps

A

occurs usually via respiratory exposure to saliva droplets containing virionviremia spread from the parotids to the salivary glands, where virions produced there enter the mouth and spread via coughs and sneezes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe antiviral therapy for mumps

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the vaccine used for mumps

A

live-attenuatedparted of the MMR vaccine given twice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

explain the occurrence of 3 year cycles of epidemics for measles

A

measles is the most contagious disease known. an outbreak would result in herd immunity, but as years go by and new people are born, the proportion of immune people decreases to a critical point where herd immunity is no longer effective, causing a new epidemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe measles transmissoin

A

transmitted through respiratory droplets (coughs/sneezes) and infects respiratory tract.it multiplies in the lymph and respiratory epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe measles symptoms

A

prodromal symptoms occur first:fever, cold-like symptoms, runny nose, red eyes, coughing, sneezing, photophobiafollowed by Koplik spots (bright red lesions w white central spot inside mouth)- predicts measles rashrash begins after 14 days. maculopapular erythematous rash generated at least partially by immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe measles virus excretion

A

excreted from respiratory tract and in tears and urine in the days before and after rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

measles incubation period

A

14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

measles complications

A
  1. pneumonia2. otitis media3. acute encephalitisdeath in 1/1000complications more common in kids under 5, people over 20, and immunocompromisedgiant cell pneumonia- sometimes pneumonia results w/o measles rash d/t suppression of cell mediated immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

measles treatment

A

nonetreatment with vitamin A in developing countries has helped reduce mortality- death often occurs w/ measles and malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

does mumps or measles cause syncitia

A

measles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe what measles does to cell mediated immunity

A

suppresses it, causes anergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how many serotypes of measles are there?

A

1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how many animals act as a resevoir for measles?

A

just humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe measles immunization

A

live attenuatedgiven twice in MMRlife long protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

“slow viruses”

A
  1. long incubation period (years)2. relentless course leading to death3. genetic predisposition4. re-emerge from latency b/c of immune suppressionexamples: HIV, JC, BK neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

JC virus

A

papovaviruscauses progressive multifocal leukoencephalopathy (PML)PML is a progressive demyelinating disease of the brain (affects oligodendroglia) w/o inflammationoccurs w/ immunosuppressionprogression includes blindness, dementia, and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

SSPE

A

subacute sclerosing panencephalitisonset of intellectual deterioration, psychological disturbance, blindness and terminal paralysisassociated w/ measles- - high Ab to measles- CNS contains measle antigendistinct inclusion bodies. relation to measles unclear. does occur after vaccination (one in a million)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

prion characteristics

A

1 long incubation period2. slow relentless course to death3 confined to CNS4 produce spongiform encephalopathy5. genetic predisposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are prions?

A

theorized to be infectious proteins w/o nucleic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the 5 spongiform encephalopathies caused by prions?

A

KURUCDJ Cretzfeld-Jacob diseasevariant CDJ mad cowGSS- gerstmann straussler scheinker syndromefatal familial insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

scarpie

A

chronic progressive CNS disorder in adult sheepgenetic predisposition indicatedincubation period of less than a yearprion disease- no nucleic acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

KURU

A

progressive degenerative disorder of the CNS, especially the cerebellumlimited to small tribe in new gunieano environmental factors- partially geneticcould be transmitted to apes by eating the human brains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

CDJ

A

most common human prionmost are the result of a mutation, w/ obvious cause. risk increases w/ agesome reported cases were iatrogenic- caused by physicians using contaminated surgical equipmentsome variants are linked to families fCDJsome are sporadic sCDJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

mad cow

A

variant CDJcaused an epidemic in great britain as a result of using brains/bone marrow of cows to feed other cows, which became infected, and when consumed, infected other people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

describe the structure of a herpes virus

A

DNA, double strand, enveloped, icos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

describe the herpes life cycle

A

adsorption and fusion w/ hostnucleocapsid releases viral DNA into nucleusDNA becomes circularmRNA, viral protein synthesis inside nucleusprogeny nucleocapsids assemble in nucleus causing inclusion bodiesviral glycoproteins are inserted into membrane (can cause syncitia)progeny bud out from membrane**needs nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

describe how herpes is eliminated from the body

A

herpes is not eliminated from the body, even upon asymptomatic recovery. instead, herpes becomes latent. even in asymptomatic latency, pts may sporadically create infectious virions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

describe the subclassifications of herpes virus and some examples

A

alphaherpesvirus- HSV1- wide host range, latency in neuronsbetaherpesvirus- CMV- narrow host range, latency in monocytesgammaherpesvirus- EBV- narrow host range, latency in B lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

latency

A

all herpes viruses can become latent:non destructivelifelongpersistence of viral genome in non infectious statepotential to be reactivated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

is latency active or static?

A

active-creating gene products that prevent apoptosis, but opens the virus to immune recognitionalso have asymptomatic shedding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

why could herpes be good for you?

A

chronic stimulation of immunity by non-lethal pathogens could be beneficial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

HSV1- primary and recurrent infection mechanisms

A

“cold sores”primary infection often subclinical and most commonly causes stomatitis virions produced at the site of initial infection travel up sensory neurons to nearest ganglion (often trigeminal ganglia) and establish latent infectionrecurrent infection occurs when viral multiplication resumes and virions are tranported down axons to cutaneous site of primary infection- results in cold sores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what % of the population has HSV1?

A

> 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the incubation period for HSV 1

A

1-2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what factors can aggravate latency, causing a recurrent infection?

A

UV lightfeveremotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

HSV1 vaccine

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

HSV2

A

“genital herpes”primary infection of genital mucosa, virus follows sensory neurons back to ganglia and establishes latency (sacral ganglia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

HSV2 incubation period

A

1-2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what % of the population has HSV2?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

describe the complications of HSV2 and perinatal infection

A

virions released by vaginal secretions can cause systemic disease in newborns ~6 days after birthdisease is often fatal, with destruction of liver and adrenalmost dangerous scenario is when mother has just gotten primary infection and has no AbHSV2 shedding before deliver is indication for C-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

HSV1 and 2 also cause what in addition to skin lesions

A

encephalitisocular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

herpes simplex encephalitis

A

most common cause of sporadic encephalitis- usually HSV1causes high fever, confusion, lymphocytes in CSF, lesions on MRIoften death w/o early recognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

treatment for herpes simplex encephalitis

A

acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

herpes simplex keratitis

A

herpes simplex infection of eyeunilateral red eyecan cause blindness if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

does herpes simplex cross placenta

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

how do you diagnose herpes simplex?

A

isolation and cultureELISADNA PCR of CSFserology (IgM in primary infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

HSV2 vaccine

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are the treatments for herpes simplex

A

acyclovir- gold standardherpes thymidine kinase will phosphorylate ACV, which can then be subsequently be phosphorylated by host and incorporated into DNA, which halts synthesis and causes death in infected cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

varicella zoster virus

A

chickenpox/shinglesprimary infection causes chickenpox- infection through respiratory tract- causes viremia. then spreads to the skin andcauses small itchy vesicles (rash) and fever. then travels retrograde to sensory neuronsoften fatal to immunosuppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

varicella zoster virus transmission

A

aerosolspread from mucosa in skin lesions to the respiratory tract. vesicles in respiratory tract may also rupture and spread disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

treatment for varicella zoster virus

A

can get IgG- VZIG or acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

congenital varicella syndrome

A

fetal infection from a pregnant mothercauses limb atrophy and scarring of the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

zoster

A

shingles- more common w/ agereactivation in a sensory ganglia that results in pain distributed along a specific dermatome, followed by lesionscan be followed by post-herpetic neuralgia- residual painmore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

zoster treatment

A

acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

vaccinations to varicella zoster virus

A

vaccines to both varicella (live attenuated, requires boosting) and zoster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

CMV

A

causes enlarged cells w/ “owl eye” inclusion bodiescauses retinits, colitis, heterophile negative monoleading cause of congenital abnormalities- from infection in 1st trimester- can go through placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

CMV immune evasion

A

has 6 genes to evade T cell activation via disrupting antigen presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

CMV transmission

A

blood/ bodily secretions (urine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

CMV infects what

A

epithelia- moves to ganglia- infects monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

easiest way to test for CMV in neonates

A

CMV in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

CMV vaccine

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

CMV treatment

A

ganciclovir or foscarnet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

CMV findings in newborns

A

retinal inflammationjaundicelarge spleen and liverlow weightmineral deposits in brainrashseizuressmall headretardationdeafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

EBV

A

causes heterophile positive mono and cancersubclinical infections in kids, but more prevalent post puberty1st symptom is sore throatalso: fever, sore throat, lethargy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

EBV transmission

A

salvia or oral contactseen in college aged peopleinfects mucosal epithelia before spreading to B lymphocytes. can become latent w/ these b lymphocytesseen in people post puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

EBV vaccine

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

EBV incubation period

A

2-4 weeks

77
Q

% of population with EBV

A

90%

78
Q

describe the immune response to EBV

A

CTLs develop to clear infected B cells, causing abnormal cellular phenotype in blooddevelop Abs that cross react w/ sheep RBCs, creating a diagnostic test

79
Q

diagnostic tests for EBV

A

look for CTLs or test for agglutination with sheep RBCsIg to viral capsid

80
Q

EBV treatment

A

no treatment

81
Q

HHV6

A

most prevalent herpes virus > 90%genome can integrate w/ human genome and becomes heritablecauses: roseola infantum and exanthm subitum (rashes) w/ high fever

82
Q

HHV7

A

causes infections but w/o symptoms

83
Q

HHV8

A

Kaposis Herpesvirusnot seen in 1980s b/c of AIDS.common in sexually transmitted HIVforms spindle epidermal cellsalso in GI and lungsrarely seen in US b/c of antivirals tumor virus

84
Q

HHV8 treatments or vaccines

A

none

85
Q

B virus

A

infection of rhesus macaques (benign in monkeys, not in humans)very rare- seen in people who work in animal facilitiescaueses encephalitis, serious neurological squelae, and death

86
Q

B virus treatment

A

acyclovir

87
Q

triflurodine

A

useful in treating keratitis simplex infections causes nucleotide form of triflurodine to be incorporated into DNA and to halt DNA synthesis.cells in cornea replicate slowly enough that only infected cells will die off

88
Q

adenine arabinoside

A

analogue of deoxyadenosine that gets phosphorylated by host enzymes an incorporated into DNA, halting DNA synthesis

89
Q

foscarnet

A

inhibits DNA polymerase of herpes virus selectivelyalternative to ganciclovir in CMV

90
Q

what does transformation mean?

A

cell can grow indefinitely and growth cannot be arrested. it requires less serum, does not exhibit contact inhibition, and is anchorage independentis “tumorigenic”

91
Q

what is the mechanism by which viruses cause tumors

A

two ways:RNA viruses will introduce, upregulate, or mutate proto-oncogenesDNA viruses will degrade or sequester tumor suppressor genes

92
Q

how can you detect oncogenic viruses in tumors?

A
  1. take cell free extract and inject into animal model/cells to see if tumors form2 use fluorescent Abs, western blot, ELISA, etc. to look for viral proteins3 use PCR, northern blotting, southern blotting, etc. to look for nucleic acids
93
Q

describe how the morphology of cancer cells differs from regular cells in vitro

A

regular cells grow flat, in an ordered waycancer cells grow rounded, disordered

94
Q

describe the biochemical differences between cancer cells and regular cells in vitro

A

cancer cells have higher rates of glycolysis and glucose transport. they have lots of proteinases, but reduced fibronectin and actin

95
Q

papovirus characteristics

A

DNA, double stranded (circular), naked, icosahedralproduces 10 genes, all of which are essential for tumor growth

96
Q

what are some examples of papoviruses?

A

papilloma virus- infects humanspolyoma virus- rodentsSV40- monkeys

97
Q

describe papovirus replication. how is this related to its tumorgenic properties?

A

replication divided into early and late stagesearly replication involves host RNA polymerase transcribing the T-antigenT-antigen binds the origin of replication. host DNA poly recognizes and binds the T-antigen, beginning replication.following replication, late replication starts and transcribe the viral capsidsviral capsids self assemble and cause lytic burst of cellin addition to binding origin of replication, T antigen also binds and inactivates p53 and Rb tumor suppressors

98
Q

what cells does HPV infect?

A

epithelial cells- no viremia- grows locally,

99
Q

what does HPV cause

A

warts and condylomas (genital warts)6 and 1 1- most common cause of condylomas16 and 18- cause cervical cancer

100
Q

which strands of HPV cause cervical cancer? how?

A

16 and 18- they have oncogenes E6 and E7, which bind p53 and Rb respectively, targeting them for destruction and thus inactivating them

101
Q

what is another large cofactor for developing cervical cancer when infected w/ HPV

A

cigarette smoking

102
Q

describe the gardisil vaccine

A

protects against 6, 11, 16, and 18dead virusgiven in 3 doses over 6 months to people 9-26

103
Q

describe the cervarix vaccine

A

protects against 6 and 11 onlydead virus3 doses over 6 months

104
Q

do adenoviruses cause cancer in humans?

A

no- cause cancer in rats

105
Q

how do adenoviruses cause cancer?

A

two important proteins: E1A binds and inactivates Rb, p300, and CBPalso binds to transcription factors to initiate S phaseE1B upregulates E1A

106
Q

describe herpes virus characteristics?

A

DNA, double stranded, enveloped, icosahedral

107
Q

what herpes viruses cause cancer?

A

EBV and Kaposis sarcoma virus (HHV8)

108
Q

EBV cancer

A

causes burkitts lymphoma- a B cell lymphomacauses tumors in jaw, heart, abdomen, but does respond to chemo(can also cause nasopharyngeal carcinoma in Asia but mechanisms not understood)

109
Q

how does EBV cause cancer

A

extrachromosomal EBV genomes always found in b-cellsinfection is latent, and integration is not required for transformationtranslocation puts c-myc proto-oncogen under transcriptional control of an Ig- over expressionT-cell normally controls these B-cell except under immunosuppression or in immunocompromised individuals

110
Q

what are two important EBV genes that cause transformation

A

EBNA-2 transcriptional activatorLMP-1- CD40 analogoue

111
Q

where is Burkitts lymphoma found

A

equitorial africa- coincidence w/ AIDS and malaria

112
Q

Kapsois Sarcoma herpes virus cancer mechanisms

A

Kapsois sarcoma most common cancer w/ AIDS, but is uncommon w/o immunosuppresiontumors present w/ multiple, pigmented, high vascular skin nodules. tumor cells express VGEFviral genes: GPCR (VGEF) and LANA (cell growth)

113
Q

retrovirus characteristics

A

RNA, single stranded, positive sense, enveloped, helical

114
Q

essential retrovirus genes

A

gag- nucleocapsid proteinspol- reverse transcriptase and integraseenv- envelop glycolipids

115
Q

retrovirus classification

A

divided into oncoviruses and lentiviruses (no cancer)oncoviruses have 3 classifications:transducing- have captured an onco-gene and insert it directly. transformation is short. usually cannot replicatenon-transducing- don’t have an oncogene, instead cellular oncogene is activated by provirus. replication intact. intermediate transformation timenon-transducing, long latency- long transformation. viral protein influencing transcription

116
Q

provirus

A

retroviruses are positive sense single strande RNARNA transcriptase converts the RNA into double stranded DNA and integrates it into host genome. this serves to make mRNA for future progeny and is called a provirus

117
Q

long tandem repeats

A

Reverse transcriptase adds regulatory elements to the ends of the DNA it creates

118
Q

describe retrovirus replication

A

enters cytoplasm. reverse transcriptase begins at primer tRNA, creating a RNA-DNA hybrid. RNase H degrades the viral RNA, and reverse transcriptase finishes the DNA.DNA is longer because of LTRs. it moves into the nucleus and integrates, becoming a provirushost DNA polymerase and replication machinary create and translate mRNA and viral proteins, eventually creating entire viral genome copies that can then leave

119
Q

RSV

A

rous sarcoma virus- transducing virus- transforms w/in 24 hours of introduction to chickenencodes src oncogene (tyrosine kinase)

120
Q

what types of proteins make good protooncogenes

A

growth factorsgrowth factor receptorskinasesG proteinsproteins that regulate transcription and regulation

121
Q

how do acute transforming viruses replicate?

A

they cannot replicate themselves because one of their 3 essential genes has been replaced with an oncogene. if they are to grow, they need a helper retrovirus to coinfect the cell and provide the missing proteins

122
Q

what are the human carcinogenic retroviruses?

A

HTLV 1 and 2. they do not have oncogenes

123
Q

how is HTLV transmitted

A

blood, semen, perinatal (bodily fluid)

124
Q

where does HTLV infect?

A

mucous membranes- viremia- t-lymphocytes

125
Q

what does HTLV 1 cause?

A

adult t cell leukemia (.1% of infected, everyone else is usually asymptomatic. takes years)

126
Q

hepatitis B cancer

A

5% of hep b cases become chronic. 5% of those cases get liver cancer.cause unknown, but hep viral genome integrates w/ host.theories: inserts near proto-oncogenehas an oncogenedestruction and redevelopment of liver provides opportunities for errors

127
Q

what are the differences in how hepatitis b and retroviruses use reverse transcriptase

A

retrovirus is an RNA virus, and uses it to create DNA provirus that can integrate into the nucleushep B is a DNA virus. it creates mRNA copies of itself, which are then put into the capsid, and reverse transcriptase then generate the proper DNA format at the end of the lifecycle

128
Q

hep C cancer

A

20% of people with chronic hep C develop cancer. there is no oncogene and integration does not occur.

129
Q

arbovirus characteristics

A

RNA, single stranded, plus stranded, enveloped, icosahedral

130
Q

how are arboviruses transmitted?

A

via blood sucking arthropod hosts (mosquitos and ticks)

131
Q

difference between intrinsic incubation and extrinsic incubation

A

intrinsic- incubation in humans- usually 1 weekextrinsic- inside the arthropod, virus is not infectious until 14 days. arthropod is then infected for life

132
Q

in the USA, what is the only serious disease concern stemming from arboviruses?

A

encephalitis

133
Q

can you get human to human transmission?

A

not really- not unless blood transfusions

134
Q

describe the progression of arboviral encephalitis

A

incubation is 1 weekviremia occurs quickly. virus multiplies in vascular endothelium.causes febrile malaise followed by encephalitis, paralysiss, coma and death

135
Q

what is the treatment for arboviral encephalitis?

A

none

136
Q

describe eastern equine encephalitis (EEE) and western equine encephalitis

A

togavirus- RNA, ss, +, enveloped, icosassociated w/ focal outbreaks in summer months, usually near swamps or after rainy seasonshorses and humans are dead-end hosts- usually die before can infect mosquitosinstead, the virus is maintained in nature via transmissions between mosquitos and birds, neither of which develop symptoms

137
Q

west nile virus

A

flavivirusRNA, ss, +, enveloped, icosmost common cause of arbovirus in US. imported from egypt recently, now in every state.maintained by bird-mosquito cycles. humans are dead end hosts. most fatal cases are in elderly

138
Q

st louis encephalitis

A

flavivirusRNA, ss, +, enveloped, icosantigenically related to west nile, native to US. most fatal cases in elderly

139
Q

dengue fever

A

arbovirus- flavivirusRNA, ss, +, enveloped, icos4 typesincubation period 1 week- humans are not dead-end hostsfever, severe headache, muscle and joint pains, rash

140
Q

what are the symptoms of dengue fever

A

fever, severe headache, muscle and joint pains, rash

141
Q

dengue hemorrhagic fever

A

more severe form, notable for hemorrhage, vomiting blood, and shockcaused w/ sequential infections of cross reacting dengue fevers result in excessive inflammation and vascular permeability

142
Q

yellow fever

A

arbovirus- flavivirusRNA, ss, +, enveloped, icoscauses fever, nausea, jaundice, hemorrhageextensive multiplication in liver, spleen, and kidneys

143
Q

how are yellow fever and dengue transmitted?

A

human-mosquito-human-mosquitoin the jungle, monkeys can also become infected w/ yellow fever and serve as a resevoir from which we can get infected

144
Q

yellow fever vaccine

A

live attenuated

145
Q

zika

A

arbovirus, flavivirusRNA, ss, +, enveloped, icoscauses a mild form of dengue, may cause microcephaly

146
Q

what defenses does a fetus have against viral infection?

A

placentamaternal IgGfetal IgMinterferoncell mediated immunity?

147
Q

parvovirus B-19 characteristics

A

DNA, single stranded, unenveloped, icos

148
Q

how is parvovirus transmitted?

A

through respiratory tract or transplacental

149
Q

what is the parvovirus incubation period?

A

14 days

150
Q

what are the symptoms of parvovirus?

A

asymptomatic orfever, malaise, erythema infectiosum (slapped cheek), transient athritis

151
Q

where does parvovirus replicate?

A

RBC precursors- causes lack of new RBCs for a week, which is tolerated fine normallytransient aplasic crisis- person w/ anemia infected with parvovirus has severe deficit in O2 carrying ability

152
Q

hydrops fetalis

A

transplacental infection during first or second trimester can cause death w/ severe swelling

153
Q

rubella characteristics

A

togavirus- NOT ARBOVIRUSRNA, ss, +, enveloped, icos

154
Q

rubella incubation

A

18 days

155
Q

rubella transmission

A

respiratory aersols

156
Q

rubella multiplication

A

respiratory epithelium followed by viremia

157
Q

rubella symptoms

A

skin rash (3 days), fever, lymphadenopathy, transient arthritis

158
Q

rubella vaccine

A

live attenuatedpurpose is to prevent congenital rubella

159
Q

congenital rubella syndrome

A

virus crossing the placenta in the first trimester can have a variety of effects including:cataractsheart defectsdeafnessretardationspontaneous abortion

160
Q

describe poxvirus characteristics

A

DNA, double stranded, asymmetric capsid, both enveloped and uneveloped

161
Q

what characteristics of poxvirus distinguish it from other viruses?

A

it has an asymmetrical capsid and can be infectious enveloped or unenveloped

162
Q

does the virion require host RNA polymerases?

A

no, it carries its own.poxviruses are the only viruses that carry a DNA dependent RNA polymerase with them

163
Q

where do poxviruses form their inclusion bodies?

A

cytoplasm

164
Q

what do inclusion bodies indicate

A

they indicate sites of virion or nucleocapsid assembly.can be used to help distinguish viruses

165
Q

molluscum contagiosum

A

poxvirus transmitted by intimate cutaneous contactcauses white skin papules- bumps on the skinmuch worse in immunosuppressedresolves on its own w/ t-cell immunityharmless

166
Q

how is molluscum contagiosum transmitted?

A

intimate cutaneous contact

167
Q

how long is the incubation period for molluscum contagiosum?

A

2-8 weeks

168
Q

why can it be difficult to diagnose molluscum contagiosum

A

grows poorly in culture

169
Q

smallpox characteristics

A

DNA, double stranded, asymmetric, both enveloped and nonenveloped

170
Q

smallpox transmission

A

respiratory

171
Q

describe smallpox infection

A

infects respiratory mucosa and lymph, establishes viremia that attacks lungs, liver, spleensecond viremia infects skin

172
Q

what is the clinical presentation of smallpox

A

papules, vesicles, pustules.lesions in oral mucosa are the main source of new infection

173
Q

smallpox virus vaccine

A

live- vaccinia virus

174
Q

how many serotypes of smallpox are there?

A

1

175
Q

how many other animals act as resevoirs for smallpox?

A

0- just humans

176
Q

complications of smallpox vaccinations

A

encephalitisvaccinia necrosum- spreading necrosis at site of infection d/t t-cell immunityeczema vaccinatum- pread of lesion in pre-exisitng eczemageneralized vaccinia- spread of lesions in the absence of eczemaheart infection

177
Q

when is the smallpox vaccination useful?

A

prior to infection or w/in 4 days of infection

178
Q

what other treatments work for small pox

A

passive immunization w/ IgG

179
Q

rhabdovirus characteristics

A

RNA, single stranded, minus strand, enveloped, helicalrabies

180
Q

rabies transmission

A

bite from infected animal

181
Q

rabies infection

A

no viremia- tropism for nervous systemreplicates into salivary glands

182
Q

incubation period of rabies

A

week to months

183
Q

rabies prognosis untreated?

A

human and canines- fatal

184
Q

rabies symptoms

A

fever, anorexiaLater: hydrophobia (d/t swallowing pain), paralysis, coma, death

185
Q

rabies diagnosis

A

negri bodies- cytoplasmic inclusions in nerve cellsuses fluorescent Abs to confirm

186
Q

where are herpes inclusion bodies?

A

nucleus

187
Q

rabies vaccine

A

killed vaccinecan be given any time during the incubation period, but once CNS symptoms begin, will not stop death

188
Q

rabies treatment

A

combination of passive and activeIgG given to delay symptoms and then killed vaccine used to activate active immunityused in all cases of unknown bites or prophylactically w/ vets

189
Q

how does transmission usually occur in the US?

A

bites from wild animals’ (bats, foxes, racoons, etc.)dogs are not a big source (except near mexican border) b/c of vaccination requirements

Virology 2 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions