Final Exam Flashcards

1
Q

when was influenza first described

A

400 BC

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2
Q

t/f

virologists believe another influenza pandemic that could kill millions is inevitable

A

true

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3
Q

most diseases are caused by _____ viruses

A

rna

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4
Q

why did influenza epidemics become unmanageable at alarming speeds (3)

A

short incubation period (1-4 days)

one droplet can contain 100,000-1,000,000 virus particles

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5
Q

what is the approximate R0 of influenza

SARS-CoV2

A

1.4

2-3

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6
Q

who normally dies from influenza

why

A

babies and elderly

bc their immune systems are either not fully developed or no longer function at their prime

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7
Q

what is a hallmark clinical symptom of influenza

how long does it last

A

fever (100-103 degrees)

3-4 days

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8
Q

how long does it typically take for flu symptoms to clear themselves up

A

7 days

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9
Q

what two secondary infections lead to death after a flu infection

A

bronchitis

pneumonia

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10
Q

t/f

flu infections tend to have age-dependent side effects

A

true

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11
Q

what three secondary infections are common for young children with the flu?
elderly?

A

croup, secondary bacterial pneumonia, middle ear infections

life-threatening secondary pneumonia, worsening of preexisting conditions (like heart failure)

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12
Q

what is the family name for influenza

what are the three main genera

A

Orhtomyxoviridae

Alpha, Beta, Gamma

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13
Q

what type of virus is influenza (segemented vs nonsegmented; +/-)

A

neg ssRNA, segmented

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14
Q

t/f

only Influenza A can infect humans

A

false

A, B, and C can infect humans

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15
Q

which influenza is rare

A

C

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16
Q

t/f

being infected with one type of flu protects you from the others

A

false

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17
Q
Name that flu boo:
infects humans and animals
goes through antigenic shift and drift
can cause pandemic that mostly affect young people
8 gene segments
10 viral proteins with unique M2
A

influenza A

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18
Q
Name that flu boo:
humans only
antigenic drift only
leads to severe typically in at risk and elderly 
doesn't cause pandemics
8 gene segments
11 viral proteins, unique NB
A

influenza B

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19
Q
Name that flu boo:
humans and piggies 
antigenic drift only
mild disease, common in kids
7 gene segments
9 viral proteins, unique HEF
A

influenza C

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20
Q
Am I driftin' or shiftin'
slow gradual change
responsible for localized/ seasonal  epidemics by A, B, and C
mutation in H and N subtypes
---------------------------
sudden dramatic change
cause pandemic
influenza A only
viral re-assortments leading to novel flu virus
A

antigenic drift

antigenic shift

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21
Q

what is the animal reservoir for Influenza A

are they symptomatic or asymptomatic

A

wild water fowl

asymptomatic

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22
Q

what are the two tests for laboratory diagnosis of the flu

A

ELISA tests

RT-PCR

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23
Q

Name that testing method (flu):
some distinguish between A and B
results in 10-20 minutes
LOW SENSITIVITY HIGH SPECIFICITY

A

ELISA assay

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24
Q
Name that testing method (flu):
used to confirm 
conventional virus isolation detection in cell cultures
expensive 
results take 2-10 days
A

RT-PCR

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25
Q

Outline Flu Pathogenesis Here

A
  1. transmitted by droplets
  2. virus gets into respiratory tract
  3. virus attaches to the ciliated columnar epithelial cells lining the sinuses and airways
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26
Q

what is the primary site of infection in someone infected with the flu

A

tracheobronchial tree and nasopharynx

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27
Q

what happens to the cilia in the respiratory tract as the flu virus replicates
what does this lead to….

A

they are destroyed

  1. lungs aren’t cleaned well
  2. mucus stays in the airway and causes coughing
  3. lead to secondary infections
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28
Q

what two proteins can we develop immunity to on the surface of the flu virus

A

N: neuraminidase
H: hemagglutinin

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29
Q

Antibodies against _____ neutralize the flu virus and those against ______ do not neutralize, but can help with the reduction in the release of the virus from infected cells

A

H

N

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30
Q

immediately after isolation flu particles are _____ in shape, but after several passages they’re _____

A

filamentous

spherical or pleomorphic

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31
Q

who am i:
enveloped
80-120 nm
12-14 kb

A

influenza A

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32
Q

how many subtypes of H and N are found in influenza A

how many proteins particles on the surface of the virus

A

18; 11

400; 100

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33
Q

name the 6 proteins that make up Influenza A

what do they do

A
  1. M1 matrix- wraps around rna
  2. M2 ion channel-lets in hydrogen ions
  3. NP- nucleoprotein around RNA
  4. PA, PB-1, PB-2 -RdRp
  5. NS-1- blocks IFN and stops cellular mRNA from leaving nucleus preventing translation
  6. NS-2- helps viral RNA out of the nucleus
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34
Q

how is a flu virus is named (in order)

A
  1. influenza type
  2. species isolated from (unless human)
  3. place of isolation
  4. strain of designation
  5. year of isolation
  6. H and N subtype number
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35
Q

when naming a flu virus do you designate the H and N subtype if it’s B or C

A

no

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36
Q

what leads to antigenic drift

A

changes in H and/or N because viral RdRp does not have a proofreading mechanism

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37
Q

what causes antigenic shift

A

two versions of influenza A co-infect a cell and lead to a virion product with a combo of gene segments

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38
Q

t/f

mutations are common in influenza A viral infections

A

true

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39
Q

____ cleaves virus from sialic acid so that when the virus is released it does not reattach to the infected cell

A

neuraminidase

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40
Q

why doesn’t avian flu infect people

A

because the H proteins struggle to attach to the sialic receptor

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41
Q

which season is the flu more prevalent in?

why? (include humidity and temp in explanation)

A

winter
aerosol spread easier at 20% humidity and temperatures of 5 C or 41 F
people are closer together in contained spaces

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42
Q

what unique effects were seen with the 1918 Spanish Flu

A

killed 20-40 year olds
killed in 2-3 days
hemorrhagic symptoms

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43
Q

what spread faster than any plague in history

A

1918 spanish flu

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44
Q

what was the precursor to the spanish flu

A

an avian flu strain

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45
Q

what antivirals are used to treat the flu

what do they do

A

M2 inhibitors- prevent uncoating

N inhibitors- prevent neuraminidase from cleaving sialic acid during budding

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46
Q

what is the most effective way to prevent the flu

A

vaccine

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47
Q

what are the 2 flu vaccines

A

Trivalent: 2 strains A and 1 strain B
Quadrivalent: 2 strains A and 2 strains B

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48
Q
name the flu viral RNA:
shorter than template genome
has poly A tail
5' cap
synthesis is insensitive to protein synthesis inhibitors
A

+ viral mRNA

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49
Q
name the flu viral RNA:
exact copy of genome segment
no poly A
no 5' cap
synthesis requires continuous viral protein synthesis
A

+ antigenome/viral copy RNA

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50
Q

what family does the flu virus belong to

A

orthomyxoviridae

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51
Q

what family does rabies virus belong to

A

rhabdoviridae

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52
Q
name that virus family:
monopartite 
15-16 kb
helical 
enveloped
virion size: 150-200 nm
A

paramyxoviridae

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53
Q

what two viruses fall under the family paramyxoviridae

A

measles morbillivirus

mumps orthorubulavirus

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54
Q
  1. what is the common name for measles morbillivirus
  2. what is the R0 for this virus & how is it spread
  3. incubation period
  4. what appears about 2-3 days in
  5. when does a rash that appears on the face that eventually spreads downward
A
  1. rubeola
  2. 12-18; respiratory
  3. 7-14 days
  4. Koplik spots– white spots in the mouth
  5. 3-5 days
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55
Q

t/f

you can shed rubeola (measles) 2 days prior to and post symptom appearance

A

false

four

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56
Q

for what age group is measles most serious

A

5-20

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57
Q

______ leads to death or neurological complications after infected with measles

A

encephalitis

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58
Q

what effect does rubeola have on pregnant women

A

can lead to babies with low birth weight or premature birth

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59
Q

______ occurs _____ yearspost measles at a rate of about 1/10,000 and can lead to death in __-__ years.

A

SSPE Subacute Sclerosing Panencephalitis
7-10
1-2

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60
Q

what is a hallmark symptom of mumps orthorubulavirus
what is the incubation period
how is it spread

A

swollen salivary glands
16 days
respiratory

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61
Q

who tends to experience the most complications from mumps but is typically rare

A

adults

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62
Q
name that family:
monopartite
19 kb
helical 
enveloped
80 and 650-1400 nm
A

filoviridae

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63
Q

what two viruses (genera) fall under filoviridae

which genera was discovered first

A

ebolavirus
marburg marburgvirus
marburg

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64
Q

when and where was marburg marburg virus discovered

A

1967 in marburg, germany

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65
Q

what are the five species of ebolavirus
which infect humans
which infect primates

A

bundibugyo, reston, sudan, tai forest, zaire
b, s, z, tf
r

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66
Q

what is the mortality rate for ebolaviruses

which one has the highest mortality rate

A

40-80 %

zaire

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67
Q

which ebola virus was discovered by an outbreak at a facility in DC that was transmitted via respirator droplets that only caused disease in primates

A

reston

68
Q

how is ebola typically transmitted

what is the animal reservoir

A

direct contact with body fluid of infected peoples

fruit bats or primates

69
Q

all about ebolavirus:

  1. incubation period
  2. how long does it last
  3. when and where was the first outbreak
A

2-21 days
10 days- 2 wks
1976 in Democratic Republic of the Congo

70
Q

infectious proteins with no genetic material that cause a group of diseases of the brain and nervous system

A

prions

71
Q

what is the name of the brain and nervous system diseases that prions cause

A

Transmissible spongiform encephalopathies

72
Q

disease that causes a noninflammatory process that results in vacuolation or spongiosis of GREY matter in the brain

A

tse

transmissible spongiform encephalopathies

73
Q

small pathogenic RNA that has no proteins that cause virus like diseases in plants

A

viroids

74
Q

what is the first recognized TSE
what causes it
where was it seen
when was it seen

A

Kuru
cannibalism
New Guinea in South Fore people
1950s-60s

75
Q

Name that prion disease:
caused by consumption of contaminated beef
survival after symptoms = 13-14 months

A

variant Creutzfeldt-Jakob disease

vCJD

76
Q

Name that prion disease:
caused by inherited germline mutation in PrP gene, sporadic, or iatrogenic
survival after symptoms: 4-5 months

A

Creutzfeldt-Jakob disease

77
Q

Name that prion disease:
caused by inherited germline mutation in PrP gene
survival after symptoms: 2-6 years

A

Gerstmann-Straussier Scheinker disease

78
Q

Name that prion disease:
caused by inherited germline mutation in PrP gene
survival after symptoms: 12 months

A

Fatal familial insomnia

79
Q

what are the three stages of symptoms in kuru

A

ambulant
sedentary
terminal

80
Q

name that kuru symptom stage:
unsteady gait
tremors
loss of coordination

A

ambulant

81
Q

name that kuru symptom stage:

can’t sit without support, difficulty swallowing, incontinence

A

terminal

82
Q
name that kuru symptom stage:
can't walk without support
jerky movements
outbursts of laughter
depression
A

sedentary

83
Q

what does prion stand for

A

proteinaceous infectious particle

84
Q

what did stanley prusiner do in 1972

what did he discover in 1984

A

initiate research to help isolate agent that cause kuru

gene that encoded the prion was found in the brain of all animals

85
Q

what year did Wickner discover a yeast prion (Ure2p) that could change shape and cause other yeast proteins to change to a similar shape

A

1994

86
Q

t/f

prions are highly resistant to routine methods of decontamination

A

true!

87
Q

how are instruments used to process prions decontaminated

A

1 N of NaOH or undiluted fresh household bleach followed by autoclaving at 132 C for 4.5 hours

88
Q

where is PrP the most abundant
how does it contribute to infectious disease
how does it damage nerve cells

A

neurons
when it is post-translationally misfolded and resistant to protease digestion
by accumulating into clumps

89
Q

which chromosome is the PRNP gene located on

how long is the protein

A

chromosome 20

254 aa

90
Q

when does the conversion of normal PrP to PrP(res) occur

A

during the recycling process where PrP is taken into endocytic vesicles and sent back to the cell surface or degraded

91
Q

what three ways can prions invade the brain

A
  1. the vagus nerves from abdomen
  2. hypoglossal nerve of the tongue
  3. diet
92
Q

what is the average incubation period for TSEs

A

10-20 years or even 40

93
Q

what are some changes seen in the brain during TSE infection

A

neuronal loss due to apoptosis
vacuolization
amyloid plaques

94
Q

which prion dieases broke the species barriers and led to vCJD
how did this occur

A

BSE/bovine spongiform encephalopathies

there’s a high degree of homology between the 2 species

95
Q

what is the proposed origin of BSE

when was it first diagnosed

A

cows being scrapie infected sheep organ meat

1985

96
Q

when was the first US scrapie case

A

1947

97
Q

when was the first vCJD epidemic in the UK

A

1994-1996

98
Q

prion disease found in deer, elk, moose

transmission occurs directly or indirectly through food or water sources

A

chronic wasting disease

99
Q

what are some symptoms of cwd

A

emaciation
excessive thirst/drooling
frequent urination
aspiration pneumonia

100
Q

what % of deer in captivity get CWD

wild?

A

15

more than 90

101
Q

t/f

plants can act as carriers for CWD and play a role in horizontal transmission

A

true

102
Q

t/f

CWD can infect people

A

false

103
Q

Viroids are __ssRNA and covalently closed circular pathogenic molecules. The have ______ base-pairing and depend upon _____ enzymes for replication and other functions.

A

+
internal
host

104
Q

what are the two viroid families

A

avsunviroidae

pospiviroidae

105
Q

name that viroid family:
branched, quasi rodlike structure
accumulate and replicate in chloroplast

A

avsunviroidae

106
Q

name that viroid family:
true rodlike secondary structure
nuclear localization

A

pospiviroidae

107
Q

what are the FIVE structural domains of a viroid

A
Central 
Pathogenicity 
Variable 
Terminal domain 1
Terminal domain 2
108
Q

name the viroid structural domain:

  1. critical for replication and processing
  2. highest variability in the sequence
  3. role in viral movement
  4. symptoms of viroid infected plaints
A
  1. central
  2. variable
    3, terminal domains 1 and 2
  3. pathogenicity
109
Q

what enzyme synthesizes viroid RNA

A

cell’s DNA dependent RNA polymerase 2

110
Q

what was the FIRST viroid characterized
when
what does it infect

A

Potato spindle tuber viroid
1971
tomatoes and potatoes

111
Q

what creature are you most likely going to contract rabies from in the US
what is the primary reservoir of rabies in the eastern shore

A

bat!

raccoons

112
Q

how does rabies travel to the brain

A

bite—–>muscle—->PNS—->CNS—–>brain

113
Q

In ___/____ Pasteur and Roux developed an attenuated rabies vaccine using dried strips of spinal cord from infected rabbits. The first animal was tested on was a ___. In ____ they tested the vaccine on a 9 year old boy

A

1884-1885
dog
1886

114
Q

when were rabies vaccine animal baits for wildlife implemented in the US

A

1990s

115
Q
  1. what are the two forms of rabies
  2. incubation period
  3. how many days before coma
  4. when does death occur
A
  1. furious (encephalitic) and paralytic (dumb)
  2. 5 days-several years (furious); 2-3 months for paralytic
  3. 2-14 days
  4. 18 days after symptoms
116
Q

am i furious or paralytic rabies:

  1. reclusive behavior, drooling and salivation, startled by sudden noise
  2. excitation, aggressiveness, biting stuff
A
  1. paralytic

2. furious

117
Q

am i furious or paralytic rabies:

  1. hydrophobia, difficulty swallowing, hallucination, hypersalivation, jerky movements
  2. NO hydrophobia, NO seizures, NO hyperactivity, weakness
A
  1. furious

2. paralytic

118
Q

when are routine rabies tests performed

A

antemortem (before death)

119
Q

what are medical professionals looking for when they do skin punch biopsies at the nape of the neck

A

Ag in cutaneous nerves at the based of hair follicles

120
Q

what sort of immunization do individuals who do rabies testing have to receive?
what about those who are exposed to rabies

A

pre-exposure prophylaxis

post-exposure prophylaxis

121
Q

there are less than ___ known human survivors who received pre/post exposure rabies prophylaxis
when was the first recorded survivor

A

20

2004

122
Q

how was the first rabies survivor treated

A

without PEP

treated using Milwaukee protocol using drug induced coma and antivirals

123
Q

tell me about the pre exposure prophylaxis

  • dose (as well as days given)
  • how long to induce immunity
  • how long does it last
A

3 doses on days 0, 7, 21, or 28 intramuscularly
7-14 days
2 years

124
Q

immunization consists of antibodies from vaccinated blood donors

A

post exposure prophylaxis

125
Q

what type of immunity does post exposure prophylaxis confer

A

passive until the antibodies kick in to confer active immunity

126
Q

which form of the post-exposure prophylaxis vaccine is given if the person exposed to rabies has never been vaccinated?

what if the have been vaccinated before

A

4 dose on day 0, 3, 7, 14

2 dose on day 0 and 3

127
Q

what family does rabies belong to

genus

A

rhaboviridae

lyssavirus

128
Q
name that virus:
unique bullet shape
75 nm wide and 180 nm long
covered in glycoproteins
helical 
enveloped
A

rabies

129
Q

what is the purpose of the matrix protein in rabies

A

hold onto the genome

130
Q

what proteins make up RdRp in rabies virus

A

L and P

131
Q

tell me about rabies:
how long is the genome
+ or - ssRNA
how many genes

A

12 kb
-ssRNA
5

132
Q

when did HIV appear and what other symptoms popped up with it

when was the first HIV1 sample found in blood

A
1980s
Kaposi's sarcoma (skin cancer)
CMV
pneumonia cased by atypical bacteria
1959
133
Q

What did Gallo and Montagnier contribute to the discovery of HIV

A

described a retrovirus isolated from T helper lymphocytes from a AIDS patient with lymphadenopathy

134
Q

which strain of HIV is less infectious, rare in the US and progresses more slowly to AIDS

A

HIV2

135
Q

what is the HIV-1 Hunter Theory

A

HIV began as a zoonosis that from SIV which infected chimp that crosses the species barrier when hunters killed and ate chimp meat

136
Q

how is HIV spread

can it be spread by mosquitoes

A

via direct contact with body fluids ie blood, semen, vaginal fluids, and breast milk
nope

137
Q

___ and ___ easily disrupt HIV because it is enveloped. It is also ___ susceptible to drying out

A

soap
water
highly

138
Q

globally, ___% of people do not know they have HIV. In the US __% do not know

A

25

14

139
Q

what cells does HIV destroy

A

CD4+ Th lymphocytes

140
Q

what are the phases of an HIV infection

A

primary infection (acute)
chronic asymptomatic
AIDS

141
Q

name that stage of HIV infection:
starts 2-4 weeks after infection
happens between appearance of detectable HIV RNA and the first detection of antibodies
CAN BE ASYMPTOMATIC

A

acute infection

acute retroviral syndrome

142
Q

which primary antigen is found in high abundance during infection and is part of the nucleocapsid for HIV

A

p24

143
Q

name that stage of HIV infection:
neither signs or symptoms are present
fully developed positive IgG response
progress to AIDs in 10-12 yrs w/o treatment

A

clinical latency or chronic asymptomatic

144
Q

name that stage of HIV infection:

CD4+ Th lymphocyte count below 200 cells/uL and one or more opportunistic infections

A

AIDS

145
Q

how are AIDS patients treated

A

antimicrobial prophylactic treatments

146
Q

when was HIV first isolated
when were the first detection tastes made available
how does one test for HIV

A

1983
1985
using an ELISA test look for antibodies in the blood or testing for viral nucleic acid or p24 antigen

147
Q

what family does HIV belong to

genus

A

retroviridae

lentivirus

148
Q
2 +ssRNA (10 kb)
100 nm icosahedron-like
gp120 and gp41 surface proteins
reverse transcriptase(p64) and integrase(p32)
protease(p10)
A

HIV

149
Q

where is the protease in HIV bound?
reverse transcriptase?
integrase?

A

nucleocapsid
viral genome
viral genome

150
Q

HIV infects ____ early in disease and ____ later in disease

why

A

macrophages; CD4+ Th lymph
because they have a high affinity for CCR5 coreceptor on macrophages in the beginning and high affinity for CXCR4 coreceptor on T lymphocytes later

151
Q

what initiates DNA synthesis in HIV

A

tRNA lysine

152
Q

what are the three regions in a retrovirus

A

gag
pol
env

153
Q

what are the accessory proteins in HIV and what do they do

A

tat- enhances viral mRNA transcription
rev- controls mRNA exit from nulceus
nef and vpu- downregulate CD4 to prevent reattachment

154
Q

fusion of cells that lead to multiple nuclei and causes cellular death in HIV

A

syncytia

155
Q

what is the smallpox hypothesis in terms of human genetic resistance to HIV

A

some environmental stressor (ie smallpox) led to there being a higher incidence of people to be either homozygous or heterozygous for the CCR5 defect that contributes to resistance against HIV

156
Q

what is the defect that makes people HIV resistant

what does it do

A

CCR5 -32

it is a truncated protein that prevents the gp120 and gp41 proteins from binding the cell

157
Q

how many classes of gene therapy are there for HIV

what are they

A

6

  1. nucleoside analog reverse transcriptase inhibitor
  2. non nucleoside “”
  3. protease inhibitor
  4. fusion inhibitor
  5. CCR5 blocking entry inhibitor
  6. integrase inhibitor
158
Q

outline the steps for HIV replication

A
  1. gp12o binds CCR5 cell receptor
  2. gp120 and 41 go through conformational change where gp41 becomes coiled and hooks virus and cell membrane together leading to uncoating
  3. genetic material enters cytoplasm and is replicated via reverse transcriptase which uses trna lysine as primer
  4. viral dna gets transported to the nucleus and inserted into a chromosome hotspot using p32 (integrase)
  5. virus is transcribed in to 9 kb long mRNA strands using cell dependent machinery
  6. gag and gag-pol proteins are translated into long polyproteins and env proteins a glycosylated in the golgi and then cleaved into gp120 and gp41 before getting sent to the cell membrane surface
  7. virion is assembled at budding site and gag/gag-pol proteins are cleaved to make a mature virus particle
159
Q

outline flu replication

A
  1. H protein binds sialic acid receptor and enters via rme
  2. uncoating occurs to due low pH
  3. M2 proteins allows for the influx of H ions which disrupt the M1 matrix around the RNP releasing RNP into the cytoplasm
  4. viral gene segments (RNP) enter the nucleus
  5. PA and PB1&2 remove 5’ caps and 10-13 nucleotides from cellular mRNA and attach it to viral genome
  6. 10-13 nt are used for transcription primer by cell dependent RNA poly 2
  7. H, N, and M2 proteins are folded and glycosylated in the ER before being transferred to the Golgi for assembly
  8. virus leaves via budding
160
Q

outline rabies replication

A
  1. binds nicotinic acetylcholine receptor and enters via rme
  2. drop in pH leads to uncoating and nucleocapsid enters the cytoplasm
  3. virus travel to neuronal neuronal body to begin replication and transcription
  4. L and P protein transcribe viral genome and in +ssRNA transcripts for each gene and L gives each a poly A tail and cap
  5. N, P, M, L are translated by free ribosomes and G is translated by membrane bound ER ribosomes and posttranslationally modified at the Golgi
  6. virus is released via budding when enough -ssRNAs, L, N, and P proteins have accumulated
161
Q

what is the primer used in flu replication

A

the 10-13 nucleotides snatched by PA and PB1&2

162
Q

when does the synthesis of full length +ssRNA begin in rabies genome replication

A

when there is enough N protein available

163
Q

how many copies of genomic -ssRNAs produced per one +ssRNA copy in rabies

A

50

164
Q

what type of protease cleaves the env protein in HIV

gag and gag-pol

A

cell

HIV specific

165
Q

how many pieces is the 9kb mRNA polyprotein product spliced in to in HIV
how many promoters are used

A

30

1