Brainscape's Knowledge GenomeTM

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


See full index

pathophysiology > the last last test ever > Flashcards

the last last test ever Flashcards

1
Q

ebola

A

ebola hemorrhagic fever

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

ebola can actually be caused by

A

one of 5 closely related viruses called ebola viruses

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

ebola outbreaks happen frequently

A

in African countries are usually small

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

Ebola viruses’s genomes contain

A

just 7 genes

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

ebola virsues characterized as

A

zoonotic

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

how did ebola spread first through

A

bats, then to primates then to humans

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

human to human ebola is thru

A

body fluids»» blood, feces, vomit, tears, breastmilk

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

Ebolavirus spread to humans is thought to be linked to

A

eating bushmeat - meat from wild animals

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

primary virulence factor of ebolaviruses

A

GP

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

GP

A

glycoprotein

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

what are glycoproteins

A

membrane proteins that hold out long chains of sugars

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

what has glycoproteins

A

viruses, bacteria, human cells

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

recall: humans have a

A

glycocalyx that serves as a cellular ID tag

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

ebolaviruses show many normal disease symptoms like

A

malaise, sore throat, pain

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

three scariest symptoms of ebola

A
  • severe leukopenia
  • hemorrhage (extensive bleeding)
  • liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

leukopenia

A

reduced white blood cell count

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

ebola causes disease by targeting what 4 main cell types

A
  • dendritic cells
  • macrophages
  • endothelial cells in blood vessels
  • hepatocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

dendritic cells and macrophages

A

both are WBCs that hang neat mucosal surfaces

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

hepatocytes

A

liver cells

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

macrophages and dendritic cells have

A

protein on their membrane: DC-SIGN

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

DC-SIGN

A

dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin

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

what do DC-SIGNS look for

A

host glycoproteins… but recognize ebolavirus GPs as host GPs

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

As all good adhesion molecules do…. DC-SIGNS

A

adhere to ebola and host glycoproteins&raquo_space;> TRAP

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

after ebolaviruses bind to DC-SIGN

A

ebola viruses are engulfed and reproduce in about 8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

after ebolaviruses are engulfed by the host cell and reproduce

A

newly assembled viruses exit hosts through budding&raquo_space;» but eventually host lysis happens too

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

after ebolaviruses exit the host through budding (lysis eventually too)

A

infect other white blood cells

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

white blood cells like macrophages and dendritic cells

A

tend to hang out in the lymph system

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

interferons (ebola)

A

produced in response to viral infection»> kill adjacent cells

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

in the lymph nodes (ebola0

A

more WBCs&raquo_space;> ebola causes interferons to cause leukopenia

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

because the lymph system connects

A

with the circulatory system… it also does the transport of fluids itself

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

because the lymph system connects with the circulatory system (and does transport of fluids itself), (ebola)

A

ebola is able to easily spread to other sites around the body

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

in response to infection (ebola), white blood cells also secrete

A

many proinflammatory cytokines in response

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

secretion of proinflammatory cytokines causes

A

swelling of blood vessels

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

so since cytokines cause the inflammation of blood vessels (ebola)

A

inflammation of blood vessel increase their permeability to WBCs

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

when The inflammation of blood vessels increases their permeability to WBCs (ebola)

A

allows cells w/ ebolavirus to dig deep into blood vessels

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

so if cells with ebolavirus are able to get deep into blood vessels

A

free ebola then encounters usually-isolated endothelial cells

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

once ebolaviruses encounter endothelial cells

A

causes newly-exposed endothelial cells to stop sticking to one another

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

how do ebolaviruses causes newly-exposed endothelial cells to stop sticking to one another.

A

not completely understood, but it is proposed that Ebolavirus GP binds to endothelial adhesins

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

when Ebolavirus GP binds to endothelial adhesins

A

physically stops them from sticking to one another

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

so since Ebolaviruses cause newly-exposed endothelial cells to stop sticking to one another

A

blood vessels quickly disintegrate all across the body

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

when ebola viruses causes blood vessels to quickly disintegrate across the body

A

causes widespread bleeding (hemorrhage)

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

hemorrhage from blood vessel disintegration in ebola

A

leads to DIC

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

DIC

A

disseminated intravascular coagulation—- tiny blood clots

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

DIC leads to

A

organ failure, which leads to death

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

ebolaviruses also sometimes enter

A

hepatocytes (liver cells) , typically not until later in infection

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

infection of ebola in hepatocytes

A

(how or why not sure?) leads to hepatocyte apoptosis

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

enough dead liver cells

A

LIVER FAILURE

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

cure for ebola

A

no cure for ebola virus fevers, treatment by managing symptoms

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

no vaccine for ebola». now there IS ???!

A

VSV add ebola’s GP gene to genome `

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

VSV

A

Vesicular Stomatitis Virus,

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

VSV is what?

A

Baltimore group V virus, typically infects cattle

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

from VSV and ebola GP gene vaccine humans

A

build antibodies to target ebola GP and gain (full?) immunity to ebola.

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

viruses that use ____ defy

A

use reverse transcriptase defy the central dogma of biology

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

central dogma of biology

A

DNA is read and “turned into” RNA (transcription) RNA is read and “turned into” protein (translation)

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

reverse transcriptase

A

enzyme that reverses transcription: turns RNA into DNA

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

after reverse transcriptase turns RNA into DNA

A

viruses take the DNA produced and insert it inside the host’s DNA

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

how do viruses take the DNA produced and insert it inside the host’s DNA

A

protein integrase

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

reverse transcriptase is

A

notoriously unreliable: extremely high rate of mutation

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

rate of mutation reverse transcriptase

A

appox. 1 in 2000 bases!

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

viruses using reverse transcriptases fall into two groups

A
  • retroviruses

- hepadnaviruses

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

retroviruses

A
  • Baltimore Group VI

- Have (+) ssRNA

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

most important example retroviruses

A

HIV

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

hepdnaviruses

A
  • Baltimore Group VII

- Have dsDNA

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

most important example hepdnaviruses

A

hepatitis B

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

what Baltimore classification uses reverse transcriptases

A

group VI group VII

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

in the viral life cycle (RT), reverse transcription inserts

A

right after entry!

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

in the viral life cycle (RT), insertion into Host DNA

A

right after reverse transcription

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

reverse transcription the viral

A

viral RNA converted to VIRAL DNA

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

insertion into host DNA:

A

Viral DNA joins human chromosomes

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

HIV

A

Human Immunodeficiency Virus

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

HIV leading cause of death

A

from infectious disease (or 2nd to TB)

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

HIV enveloped

A

IS ENVELOPED

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

HIV falls into what

A

Baltimore group VI

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

how many genes HIV

A

9

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

how can HIV be transmitted

A
  • only blood contact
  • sexual contact
  • childbirth/breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

infection of HIV most associated with

A

AIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

AIDS

A

Acquired Immunodeficiency Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what is AIDS

A

condition defined by a severe deficiency of important immune cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

T cells

A

type of white blood cell produced by the thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

thymus is just

A

just superior to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

like B cells, T cells

A

T cells are also antigen-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

T cells has special receptors on their membrane are caused

A

T cell receptors(TCRs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

T cell receptors(TCRs).

A

look for digested pieces of stuff that macrophages anddendritic cells have broken apart in phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

if T cells find bad stuff

A

trigger events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

types of T cellls

A
  • cytotoxic T cells
  • helper T cells
  • regulatory T celld
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

cytotoxic T cells

A

they will hunt down and kill cells that contain a certain antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

helper T cells

A

producing cytokines that will attract B cells, cytotoxic T cells and macrophages and cause white blood cell hematopoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

regulatory T cells

A

they shut down other T cells at the end of an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

HIV virion has

A

glycoprotein made of two subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

glycoprotein of HOv subunits

A

p120 and gp41

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Gp120 binds to

A

CD4 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

CD4 receptors

A

glycoproteins located on the membrane of a variety of white blood cells including helper T cells, macrophages, and dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Gp120 binding to CD4 receptors goves HIV

A

its primary attachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

after HIV gets primary attachment`

A

a second host membrane protein is required (called a co-receptor) for viral entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

main co-receptor HIV

A

CCR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what does CCR5 do

A

looks for host chemokines but instead binds to gp120

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

when gp120 is bound to CR4 and CCR5

A

gp41 will imbed itself inside the host cell’s membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

once gp41 imbeds itself inside the host cell’s membrane (HIV entry)

A

fusion between virus envelope and host membrane begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

the man who couldn’t catch HIV

A

Stephen Crohn , homosexual, lots of his friens died ….. BUT he never got it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Genomic analysis Stephen Crohn

A

32 base pair deletion mutation in both genes coding for CCR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what was the name of Crohn’s mutation

A

CCR5 (draw triangle) 32

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

CCR5 (draw triangle) 32 altered to the point

A

CCR5 protein so that it did not function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

WITHOUT FUNCTIONING CCR5

A

HIV virus could not enter cells so people could not get infected!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

HOMOZYgOTES for CCR5 (draw triangle) 32 mutation

A

extreme resistance to HIV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

the the number of HIV viruses in the body multiply

A

as the number of viruses in the body multiplies exponentially, ONLYYY the number of CD4+ WBCs dramatically begins to drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

eventually in an HIV infection the immune system

A

catches up, begins defeating virus at faster rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

when the immune system catches up and begins defeating HIV virus at faster rates

A

he number of viruses in the body decreases sharply, but it is too late: t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

when the immune system starts defeating HIV viruses, why is it too late?

A

HIV genome has already been inserted into the DNA of millions of white blood cells across the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

when the immune system causes the number of viruses to decrease sharply, but HIV genome has already been inserted

A

latency period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

latency period HIV

A

no obvious symptoms are present, but there is a slightly decreased CD4+ WBC count and a person is still contagious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

graph

A

memorize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

recall reverse transcriptase

A

is very sloppy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

HIV does what at high rates

A

mutates at alarmingly high rtes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

HIV rate of mutation

A

as many as 10 billion unique HIV strains each day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

the rapid mutation of HIv causes

A

makes it harder for immune system to detect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

slowly, during (HIV) latency

A

viral levels slowly rise and CD4+WBC levels drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

A patient has aids when

A

levels of WBCs with CD4 drop below 200 cells/mm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

normal levels of CD4+WBC

A

500-1500 cells/mm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

immune systems of people with aids

A

so weak, they are vulreable to new infection most healthy wouldn’t get

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

infections of people with aids care caused by

A

opportunistic pathogens , sometimes FATAL :(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

various causes of death in AIDS patients

A

rare cancers or rare infectious diseases

122
Q

in many cases the infectious diseases of AIDS patients……

A

caused by pathogens that are present but latent in most people

123
Q

all blood cels come from one cell type

A

hematopoietic stem cells

124
Q

if more B lymphocytes are need

A

B lymphocytes do not divide

125
Q

to get more B lymphocytes

A

hematopoietic stem cells divide and one daughter becomes a B lymphocyte.

126
Q

HIV is what type of virus

A

retrovirus…causes mutation in host cell DNA

127
Q

even though HIV is a retrovirus

A

hasn’t been shown to cause increased rates of cancer in those cells

128
Q

why dosen’t HIV cause increased cancer in host cells

A

HIV infects mostly T cells and other white blood cells that have already finished their growth cycle»»

129
Q

since HIV infects mostly T cells and other white blood cells that have already finished their growth cycle»»

A

hese cells don’t divide and you won’t get cancer!….. except you will…..(but not in those cells)

130
Q

HIV kills

A

which strongly weakens the immune response

131
Q

since HIV strongly weakens the immune response

A

weakens the immune response to other viruses that can cause cancers

132
Q

examples of AIDS-defining cancers

A
  • Human herpesvirus 8

- Huuman herpesvirus 4

133
Q

Human Herpesvirus 8

A

usually lies latent in people,10 5 are infected

134
Q

HHV8

A

Human Herpesvirus 8

135
Q

if a person is immunocomprimised HHV8 can cause

A

cause Kaposi’s sarcoma to form in connective tissue.

136
Q

tell-tale sign of aids

A

Kaposi’s sarcoma

137
Q

HHV mechnaism

A

not a retrovirus - \\stealing host genes and turning them up or down to cause cance

138
Q

human herpesvirus 4 also called

A

Epstein-Barr virus, is present but latent in 45-70 of people

139
Q

human herpesvirus 4 can cause what lymphoma

A

Non-Hodgkin’s lymphoma if its levels get too high (from immunocompromisation)

140
Q

Epstein-Barr virus is also

A

no a retrovirus,

141
Q

Epstein-Barr binds to

A

mdm2 and stops it from unbinding p53, so p53 is inactive

142
Q

cure HIV

A

no cure no vaccine, but treatments

143
Q

one of main treatments HIV

A

ART

144
Q

ART

A

Antiretrovial therapy

145
Q

Antiretrovial therapy

A

is a series of many different medications that aim to stop HIV activity.

146
Q

some targets of ART to stop HIV are

A
  • CCR5 protein blockers
  • integrase inhibitors
  • reverse transcriptase inhibitors
  • protease inhibitors
147
Q

protease inhibitors

A

may stop budding

148
Q

ART treatments work to

A

extend the latent period of HIV, slow development of AIDS

149
Q

all viruses are

A

obligate intracellular parasites

150
Q

what does it mean to be an obligate intracellular parasite

A

cannot make ATP or proteins without using hosts’s parts

151
Q

a full virus unit

A

virion

152
Q

three parts of a virus

A

capsid
genome
accessories

153
Q

capsid

A

protein coat around the outside of a virion

154
Q

genome

A

the DNA or RNA a virus contains

155
Q

accessories

A

envolelope (?), matrix, spikes and other stuff

156
Q

viruses range in size from

A

10-400 nm

157
Q

bacteria range in size

A

500-5000 nm

158
Q

questions to ask to classify viruses by examining the genetic material they contain

A
  • is it DNA or RNA
  • single-stranded or double-stranded
  • (+) sense or (-) sense
159
Q

if genetic material is sense or positive sense

A

means that an mRNA sequence with the same sequence will code for a protein

160
Q

grouping system based on examining the genetic material

A

Baltimore Classification system

161
Q

2nd way to classify viruses

A

enveloped or naked

162
Q

what is the viral envelope

A

phospholipid bilayer that surrounds the capsid

163
Q

what does the viral capsid do when it exits the host

A

steal the membrane of the host cell to form the viral envelope

164
Q

before the viral capsid exists host cells

A

they force the host to produce their own viral membrane proteins and put them in that membrane (that they will steal for their envelope)

165
Q

the result of the viral envelope pathway

A

viral envelopes with host phospholipids but THE its VIRAL PROTEINS are made by the host’s ribosomes

166
Q

soooooo viral capsid to enveloped virion

A

viral capsid takes some of host cell membrane that produced viral glycoproteins

167
Q

pros for a virus containing a viral envelope

A
  • does not need to kill host cells to spread

- cannot be fought off only with antibodies (harder to vaccinate)

168
Q

cons for a virus containing a viral envelope

A
  • sensitive

- requires a more complex genome to make envelope proteins

169
Q

what are viral envelopes sensitive to

A

pH, temperature, drying out, heat

170
Q

since viral envelopes are sensitive to pH, temperature, drying out, heat

A

cannot survive in GI tract or outside of body, sensitive to detergents

171
Q

the life cycle of a virus

A
  • attachment
  • entry
  • replication and protein synthesis
  • assembly
  • release
172
Q

ATTACHMENT

A

virus recognizes and attaches to victim cell

173
Q

ENTRY

A

virus (or virus parts) enters victim cell

174
Q

REPLICATION AND PROTEIN SYNTHESIS

A

victim cell hijacked, makes viral DNA/RNA and proteins

175
Q

ASSEMBLY

A

viral parts come together and make new viruses

176
Q

RELEASE

A

new viruses exit the victim cell

177
Q

Step 1: attachment is mediated by

A

envelope or capsid proteins called VAPs

178
Q

VAPs

A

viral attachment proteins

179
Q

there is usually what that a virus specifically targets

A

one specific surface protein or pattern that a virus

180
Q

since there is usually one specific surface protein or pattern that a virus specifically targets

A

many viruses target just one specific tissue

181
Q

step 1: attachment can be blocked by

A

antibodies…… so the immune system often tries to inhibit attachment

182
Q

in step 2: entry, the

A

process is different depending on if the virus is enveloped or naked

183
Q

entry naked

A

virus is taken through endocytosis

184
Q

entry enveloped

A

viral phospholipid bilayer fuses with host cell or virus is taken through endocytosis

185
Q

in step 3: replication and protein synthesis

A

-DNA is “turned into” RNA in the nucleus (transcription)-RNA is “turned into” protein in a ribosome (translation

186
Q

translation occurs

A

outside the nuckeus

187
Q

depending on a viruses genetic materia, DNA/RNA replication can happen in many ways: if the virus has DNA

A
  • the DNA must enter the nucleus to be copied into RNA before making proteins outside the nucleus (usually)
188
Q

dna/Rna replication: if the virus has RNA

A

-If the virus has RNA, it may or may not need to be transcribed to a positive form, but does not need to enter the nucleus (usually)

189
Q

unlike bacteria an eukaryotic cells, virsues

A

don’t replicate through division, instead new viruses are asembled

190
Q

where are DNA viruses assembled

A

in the nucleus

191
Q

where are RNA viruses assembled

A

in the cytoplasm

192
Q

assembly enveloped viruses

A

produce some of their envelope proteins in the host’s membrane, which they plan to pull off with it later.

193
Q

how do the parts of virus assembly know where to go

A

slight magnetic forces

194
Q

step 5; release

A

virus levea host cell, different depending if its enveloped or naked

195
Q

naked release

A

lysis: virus is copied many, many times inside, then invokes host cell “popping”.

196
Q

enveloped virus release is…..

A

lysis or budding, generally the host remains intact but part of the membrane is stolen

197
Q

enveloped virus release

A

virus is copied inside, assembled, and released by “budding” off of the original host cell.

198
Q

viruses can cause harm by inhibiting

A

host cellular DNA, RNA, or protein synthesis

199
Q

viruses can cause harm by damaging

A

endosomes or lysosomes by releasing cutting enzymes

200
Q

viruses can cause harm by adding

A

viral proteins to host cell membranes (autoimmunity)

201
Q

viruses can cause harm because some

A

some viral proteins are toxic to host cells

202
Q

a large buildup of viruses

A

inclusion bodies

203
Q

viruses can cause harm because inclusion bodies

A

physically block cellular processes from haooenning

204
Q

which damage is unique to retrovirus

A

chromosome damage , cancer causing mutation such as proto-oncogenes areunique to retrovirus

205
Q

retrovirus

A

viruses that add their DNA to ours

206
Q

types of viral infection

A

acute, chronic, latent, viruses can show different diseases at different stages

207
Q

acute infection

A

you get the virus, you get sick a few days later, you die or beat the infection

208
Q

chronic infection

A

you get sick, you may or may not show symptoms, you have the virus for a long time or forever

209
Q

latent infection

A

you get the virus, you may or may not show symptoms, then there is a long delay before symptoms show again

210
Q

how do we fight off viral infections

A

antibodies, type 1 MHC, interferons

211
Q

to fight off viral infection, the antibodies we make

A

block most VAPs, and are most effective on naked viruses

212
Q

MHC

A

membrane protein on all human cells

213
Q

MHC is a form of

A

form of self-ID : Proteins destroyed by proteasome are dangled from the membrane and “sniffed” by WBCs

214
Q

if proteins dangled from MHC are non-self

A

the cell is killed by WBCs

215
Q

IFNs

A

interferons

216
Q

interferons

A

a type of cytokine that cause all adjacent cells to turn on many anti virus genes

217
Q

interferons signals uninfected

A

neighboring uninfected cells to destroy RNA and reduce protein synthesis

218
Q

interferons signals infected

A

neighboring infected cells to undergo apoptosis

219
Q

interferons activate

A

activate immune cells

220
Q

influenza and ebola are caused by

A

Baltimore group V viruses

221
Q

what type of RNA causes influenze and ebola

A

ssRNA

222
Q

what else are caused by group V viruses

A

Measles, mumps, rubella, rare and lesser-known disease

223
Q

influenza and ebola are env

A

ENVELOPED

224
Q

influenza and ebola survival

A

do not survive long outside of a host and are spread only through fluids

225
Q

genetic material of group V viruses

A

(-) ssRNA

226
Q

ssRNA must be

A

turned into an antigenome of (+) mRNA to make proteins , happens in cytoplasm of host

227
Q

after (-) ssRNA is turned into (+) mRNA

A

copied into more (-) RNA to make more viruses

228
Q

3 forms of influenza

A

influenza A
influenza B
influenza C

229
Q

influenza A

A

the scariest and most contagious form… since affects many species , mutates fastest

230
Q

what species do influenza infect

A

humans, birds, pigs, seals , horses

231
Q

influenza is further broken into

A

classes based on the presence of H and N antigens

232
Q

influenza B

A

only transmitted by humans (and seals?)

233
Q

influenza B mutations

A

2-3x slower than influenza A

234
Q

influenza C

A

rarely causes human disease and is not considered a threat

235
Q

influenza A strains have how many genes

A

just 11

236
Q

two of the influenza A genes code for

A

important envelope proteins

237
Q

one of the important influenza A genes

A

HA

238
Q

HA

A

codes for hemagglutinin

239
Q

how any HA pattenrs

A

18, (H1-H18)

240
Q

Hemagglutinin is responsible for

A

attaching influenza virus to sialic acids

241
Q

sialic acids

A

sugars found outside the membrane of many human cells

242
Q

hemagglutinin promotes

A

viral attachment

243
Q

almost all human flu strains have only the

A

H1, H2, or H3 antigen

244
Q

H1, H2, H3 antigens attach to

A

2,3-linked sialic acid

245
Q

2,3-linked sialic acid is

A

found outside the membrane of upper respiratory cells

246
Q

thus……… because of the H1, H2, H3 antigen

A

the flu attaches to, and invades and infect cells in the upper respiratory tract

247
Q

the H5 is

A

found in avian flu viruses

248
Q

H5 antigen attaches to

A

2,6-linked sialic acid

249
Q

2,6-linked sialic acid is found

A

outside the membrane of lower respiratory cells

250
Q

deep tract influenza from H5

A

BAD…… bird flu… 50 PERCENT MORTALITY

251
Q

what is the other influenza A gene that codes for an important envelope protein

A

NA

252
Q

NA codes for

A

neuraminidase

253
Q

how many known NA patterns

A

11 (N1-N11)

254
Q

neuraminidase is responsible for

A

cleaving sialic acids off cell membranes, allowing the flu virus to detach

255
Q

only which NA patterns are seen in the human flu

A

N1 and N2 , and rarely (N3, N7, N8)

256
Q

before the flu virus detaches

A

it attaches initially w/ hemagglutinins on sialic acid

257
Q

the flu exhibits both

A

genetic shift and genetic drift

258
Q

genetic shift

A

combination of different flu types in one cell

259
Q

in genetic shift the genetic material is

A

swapped around and a new superflu develops

260
Q

what was an example of genetic shifting 2009

A

H1N1 swine flu outbreak of 2009

261
Q

example of genetic shift

A

Avian H5N2 and swine H2N1 create dangerous H5N1

262
Q

influenza pandemic of the 20th century

A

spanish flu, asian, hong kong…. all A

263
Q

genetic drift

A

the slow mutation of one flu type….. usually just one amino acid at a time.

264
Q

antibodies are super

A

specific

265
Q

since human antibodies are extremely specific, so one small mutationn

A

can make antibodies ineffective

266
Q

because of genetic drift you can catch the flu

A

many different times

267
Q

how many total amino acids in HA

A

527

268
Q

example of genetic drift

A

H1N1 mutates to have slightly different H structure many antibodies no longer recognize

269
Q

because genetic drift you can get sick

A

You can get sick again - just maybe not as sick as last time.

270
Q

In genetic drift, some antibodies

A

still recognize the antigen, but others do not (you have a “partial” immunity but not a full one)

271
Q

why did the swine flu kill so many young adults

A

many older people had antibodies that recognized H1 or N1 components from much earlier infection…. young didn’t

272
Q

exciting news for H antigens

A

antibody shown to recognize all variations of all H antigens in influenza A!

273
Q

yearly flu vaccines

A

guess he most likely flu infection to happen each year

274
Q

to guess the flu

A

ook at data from previous years to choose the H and N subtypes most likely to be found the next year

275
Q

flu vaccines are the form of

A

attenuated or killed version of the vaccine

276
Q

flu vaccines predict the genetic -______

A

genetic drift of the flu virus

277
Q

flu vaccines are typically

A

trivalent: they include three separate guesses

278
Q

two guess for flu vaccine

A

influenza A (H1M1 and one for H3N2)

279
Q

one guess for flu vaccine

A

influenza B

280
Q

they are NOT guessing (flu)

A

whether the main strain is carrying H1, H3……. but which version of H1 or H3 will be carried

281
Q

what is often given to flu patients

A

antibiotics,,,, even though the kill bacteria

282
Q

most flu symptoms

A

caused by own immune system

283
Q

flu ymptoms caused by immune system

A

fever, cough, mucus, inflammation

284
Q

the flu also invades and kills

A

ciliated, mucus-secreting cells

285
Q

when the flu also invades and kills ciliated, mucus-secreting cells.

A

reduces the defense of the airway

286
Q

becuse the flu reduces the defense of the airway it is associated w/ a

A

secondary respiratory infection

287
Q

the ______ protein in influenza has been shown to stop______

A

NS1 protein……. shown to stop host cell mRNAs from being completed

288
Q

NS1 protein……. shown to stop host cell mRNAs from being completed …….. causes

A

slowing production of host porteins…… NOTEWORTHY»»> interferons

289
Q

the current version of the H5N1 bird flu has

A

single nucleotide mutation that makes NS1 protein far more virulent

290
Q

we’re lucky about H5N1 because

A

it’s hard to invade humans…. for now

291
Q

major cytokine in the body is

A

TNF-a

292
Q

TNF-a

A

tumor necrosis factor alpha

293
Q

tumor necrosis factor alpha has many functions is effective @

A

stopping influenza infection.

294
Q

release of TNF-α has been shown to be

A

“dose-dependent”…. more flu = more TNF-α.

295
Q

dose-dependant is normally fine…… but like most cytokines TNF-a causes

A

inflammation, swelling, and white blood cell migration.

296
Q

too much inflammation, swelling, and white blood cell migration @ site of infection

A

ARDS

297
Q

ARDS

A

acute respiratory distress syndrome

298
Q

acute respiratory distress syndrome

A

lungs swelling shut and filling with fluid

299
Q

ARDS is common in flu types that

A

target lower respiratory tracts

300
Q

ex of flu causing ARDS because it target lower respiratory tracts

A

like the 1918 H1N1 Spanish flu outbreak that killed 30-40 million people.

pathophysiology (24 decks)

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