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Exam 3 Flashcards

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1
Q

_______ was instrumental in developing the field of virology and expanding the field of biology

A

Bacteriophages

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2
Q

First animal viruses discovered

A

Foot and mouth disease

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3
Q

First human virus discovered

A

Yellow fever virus

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4
Q

Viruses replicate when

A

Provided a host

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5
Q

Viruses are _____ ______ parasites

A

Obligate intracellular

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6
Q

Viruses are not

A

Autopoietic

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7
Q

Viruses are ____in nature

A

Ubiquitous

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8
Q

Theories of Virus origin: Cellular Origin

A

Proposes that viruses were once cellular components but over time they evolved separately

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9
Q

Theories of virus origin: Autopoietic origin

A

Proposes that viruses once entities became dependent on cells for replication

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10
Q

Attributes for virus classification

A 
Virus particle structure
Genome
Replication features
Serology
Stability
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11
Q

Virus particle structure

A

Composition
Shape
Size

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12
Q

Nucleocapsid

A

RNA or DINA in a core that is protected by a protein coat

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13
Q

Virus is defined by the ______ structure

A

Nucleocapsid

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14
Q

3 Nucleocapsid structural symmetry

A

Helical
Pleomorphic
Icosahedral

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15
Q

Nucleocapsid is comprised repeating

A

Protein subunits=capsomerese

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16
Q

Capsomeres

A

Comprised of repeating protein subunits

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17
Q

Virus envelopes

A

Virus modified cellular membranes acquired upon ext from host

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18
Q

Exposure of virus envelope to lipid solvents

A

Renders enveloped viruses noninfectious

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19
Q

Enveloped viruses may

A

Have nucleocapsids with different structures

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20
Q

Smallest virus particle structure size

A

18 nm

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21
Q

Largest virus particle structure size

A

300 no

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22
Q

Viruses Genome : DNA

A

Double stranded

Single Stranded

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23
Q

Virus Genome: RNA

A 
Double stranded
Single Stranded
-Plus sense (+)ssRNA
-Minus sense (-)ssRNA
-Ambisense
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24
Q

Virus Genome: Structure

A

Linear
Circular
Segmented
Diploid

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25
Virus Replication
``` Attachment Entry Transcription Translation Replication Assembly Release ```
26
Virus cellular receptors
Signaling molecules-induced cellular response to binding Cell adhesion Transport
27
Viral receptors
Usually do not mimic cell receptors normal ligand Typically are spike like projections on particle surface May require a co-receptor
28
Genetic engineering can change
Receptor recognition
29
Integrin RGD sequence
Used by Ad, engineered into lambdaphage
30
Pseudotyping particles
Improve retroviral entry, VSV, Ebola, LCMV
31
Attachment is a major of virus ______
Tropism (host range)
32
Viruses infect
essentially all known life forms
33
Zoonosis
Specific host ranges, some can infect humans and animals
34
Virus infection not shared
Across divergent hosts ranges Plants Bacteria Fungi
35
Smallpox
Only humans
36
Yellow fever
Mosquitoes and humans
37
Host range is a major factor in
Eradication
38
Nonenveloped virus entry
Not well understood Pores:picornavirus Membrane disruption: adenovirus reovirus
39
Virus entry
Receptor mediated endocytosis Direct penetration of plasma membrane
40
Enveloped virus entry
Membrane fusion Best understood fo influenza Receptor conformational change -low pH -Receptor induced
41
Influenza entry
Enveloped HA protein -attachment and fusion
42
Virus Uncoating
Nuclear replication Cytoplasmic replication
43
Nuclear replication
Genome and remaining protein coat transported to the nuclear membrane Delivery of genome to nucleus
44
Cytoplasmic replication
Release of the genome in cytoplasm Transportation of the genome to intracellular site of replication—man RNA viruses replicate in membrane associated complexes dsRNA viruses never relates their genomic material from the entering particle
45
Transcription-Virus replication
Production of messenger RNA templates for protein synthesis DNA viruses usually rely upon cellular RNA polymerase There are a variety of strategies used to subvert the cells transcription
46
The genome of +ssRNA virus an serve as
mRNA Production of new transcripts can occur later using a (-)ssRNA template
47
(-)ssRNA, dsRNA viruses must bring their own
Polymerase into the cell
48
Translation-virus
Production of proteins
49
All viruses need the cells ribosome to produce
protein | -no exceptions
50
Viral protein production can be regulated at the
transcript (mRNA) level or translation level
51
Structural proteins are produced
in high quantities
52
Non-structural proteins are only seen
inside the infected cell
53
Genome replication objective
Make additional genome copies
54
Genome replication : (+)ssRNA
Genome serves as template for translation Polymerase makes (-)ssRNA copy as template for new genomes
55
Genome replication : (-)ssRNA
Virus made particle must include the viral polymerase Polymerase makes messenger RNA for translation Genome replication through full length (+)ssRNA intermediate
56
Genome Replication: dsRNA
Virus particle includes viral polymerase dsRNA induces innate immune response so genome stays inside particle mRNA synthesized in particle and exported to cytoplasm mRNA serves as (+) strand in virus genome, (-) strand synthesized during assembly
57
Genome Replication: ssDNA and dsDNA
Must gain access to the nucleus -poxviruses are an exception virion contains the necessary RNA polymerase and the genome encodes the DNA polymerase for replication Prepare the cell for DNA replication -growth phase dNTP production replication machinery Ensure genome ends are copied
58
Virus replication assembly
Package new genomes into functional particles Localize strucutral proteins to aid assembly -cellular viral factories
59
Genome contains
Packaging signals
60
Assembly mechanisms: Adenovirus
Empty protein coats imports genome
61
Assembly mechanisms: Reovirus
RNA packaged during capsid assembly
62
Assembly mechanisms: Retrovirus
Preassembly on a membrane
63
Lysis
Best known for bacteriophage Viral molecules that rupture cellular membrane
64
Weak lysis
Depends on membrane breakdown after cell death
65
Budding
Enveloped only Enveloped viruses use cell membranes as the out coat of the virus particle
66
One step growth cure
Infect every cell at same time Every cell dies at end of infection
67
Replication phases
Eciplise -attachment and uptake Exponential growth - replication and assembly Plateau-cell death
68
Useful to assess
Mutations Cell entry Process design
69
Time for one step growth
Start of infection to beginning of plateau Bacteriophage 30 min Vesicular stomatitis virus 6 hours Vaccinia 24 hours
70
Productivity
Measure application VSV 1: 1000 Vaccinia 1: 100
71
Principal of detection and quantification methods
Infectvity Physical Genome Serological
72
Infection assays: Cytopathic effect
Cell rounding Syncytia formation Inclusion bodies
73
Infection assays: Fluorescent focus assay
Infect cells Expose virus antigen Stain with labeled antibody Count areas that fluoresce
74
Infection assays: Plaque assay
Cell monolayer Inoculate with dilute virus infected cells die leaving a clear area-plaque
75
Infection assays: Infectious dose
Tissue cultures, eggs, animals Inoculate with different dilutions of virus Calculate concentration based on number infected
76
Particle assays: Electron microscopy
Direct image of virus particles | Calibrate with latex bead standard
77
Particle assays: hemagglutinin assay
Viruses that bind red blood cells Mix contestant number of RBCs with various virus dilutions If virus concentration is sufficient a matrix of RBCS and virus is formed Matrix does not allow RBCs to pellet
78
Genome Assays: PCR
DNA primary specific to virus Amplify the gene Very sensitive
79
Genome Assay: Southern DNA and Norther RNA blots
Isolate DNA or RNA Seperate by electrophoresis Used labeled DNA probe to detect
80
Serological Assays: Virus neutralization
Antibody binding to virus can block infection Virus concentration determined by amount of antibody needed
81
Serological Assays: Enzyme link immunosorbant assay
Antibody recognition of virus Amplification by enzyme linked to antibody
82
Serological Assays: Western blot
Separate proteins by electrophoresis | Probe proteins by using an antibody
83
Poxvirdae
Small pox Vaccinia dsDNA Enveloped-brick shaped Cytoplasm replication
84
Filovirdae
Marburg Ebola (-)ssRNA Enveloped-filamentous Cytoplasm replication
85
Arenaviridae
Kasa Junin Matchups LCMV Segmented ambisense ssRNA Enveloped pleomorphic Cytoplasm
86
Flaviviridae
``` Yellow fever Dengue fever West Nile JE St. Louis E ``` TBE (+)ssRNA Enveloped spherical Cytoplasm enveloped gained internally
87
Orthomyxovidrade
Influenza 8 segments (-)ssRNA Enveloped Nucleus replication
88
Togaviridae: alphavirus
``` EEE WEE VEE Is dubs Semliki Forest Chikungunya ``` (+)ssRNA Enveloped spherical Cytoplasm enveloped gained by budding
89
Reoviridae
rotavirus, blue tongue, reovirus segmented dsRNA Non-enveloped-spherical Cytoplasm replication
90
Coronaviridae
SARS (+)ssRNA enveloped – protein crown cytoplasm – subgenomic RNA
91
Retroviridae
murine leukemia virus, HIV (+)ssRNA – two copies per virion enveloped - spherical nucleus – reverse transcription
92
Picornaviridae
poliovirus, rhinovirus (+)ssRNA non-enveloped - spherical Cytoplasm replication
93
Adenoviridae
Adenoviridae 5 dsDNA Adenoviridae Nucleus replication
94
Bunyaviridae: Phlebovirus
Rift Valley Fever, Crimean Congo 3 segments ssRNA, ambisense enveloped - spherical Cytoplasm replication
95
Bunyaviridae: Hantavirus
Hantavirus 3 segments (-)ssRNA Enveloped spherical Cytoplasm replication
96
Measles Virus virion and genome
Paramyxovirus Genome (-)ssRNA Virion: enveloped
97
Measles proteins
``` L-polymerase P-phosphoprotein H-hemagglutinin F-Fusion M-Matrix N-Nucleocapsid ```
98
Measles virus replication
Replication in the cell Fusion protein causes syncytia formation
99
Measles transmission and incubation
Inhalation of aerosolized droplet 10-14 days incubation period—primary infection in respiratory epithelial tissues—>primary viremia
100
Measles symptom onset
Coincides with second round of virus replciation. Occurs in LN, tonsils, lungs, GI tract, and spleen—-> secondary viremia Recover 20 days after infection
101
Characteristic rash of Measeles
Virus and immune response damage to epithelial and endothelial cells Koop like spots
102
Measles Complications: Immune suppression
Interference with CD46 and signaling lymphocyte activation molecule (SLAM) receptors
103
Measles Complications: Opportunisitic infections
Strep. Pneumoniae Staph. Aureus Haemophilus influenzae
104
Measles Complications
Blindness in Vitamin A deficient children Acute disseminate encphalomyelitis Subacute sclersoing panencephalitis
105
Measles Diagnosis
``` Fever Cough Cortazzo Conjunctivitis Koplik spots ``` Lab: Virus isolation in culture Serology ELISA, RT-PCR
106
Measles Prevention
One of the most contagious diseases known People are infections 2-3 days prior to rash Humans are only host
107
Measles Prevention
Vaccination - Primary option - life long immunity - Live attenuated vaccine - Safe Provide vitamin A can reduce severity No antiviral
108
Respiratory Syncytial Virus Genome and Virion
Paramyxovirus Genome: (-)ssRNA Virion: enveloped
109
Respiratory Syncytial Virus Proteins
``` L-polymerase G-glycoproteins F-Fusion M-Matrix P-phosphoprotein N-Nucleocapsid NS1&NS2-replication and immune response ```
110
Respiratory Syncytial Virus: replication
Replication i n the cell -similar steps as for measles virus Infects ciliated cells in respiratory tract epithelium Fusion protein creates syncytia Virus buds from cellular surface
111
Respiratory Syncytial Virus: Infection
By inhalation of aerosol, fomites Virus replication limited to respiratory tract 4-5 incubation 1-3 lower respiratory tract after upper 7-12 days recovery after symptoms onset
112
Respiratory Syncytial Virus that infects humans....
Does not infect other animals—no animal reservoir
113
Respiratory Syncytial Virus infections does not
Yield life long immunity
114
Respiratory Syncytial Virus infection is limited to
Respiratory tract epithelial cells where IgA response is short lived. Low cytoxicity thought to result in slower immune response
115
Respiratory Syncytial Virus Risk factors for infection
Attending day care School age siblings
116
Respiratory Syncytial Virus risk for more sever disease
Premature birth Male Second hand exposure to tobacco Lack of breast feeding
117
Respiratory Syncytial Virus Prevention
Ribarvirin administered by inhalation No Vaccine
118
Respiratory syncytial virus: passive immunoprophylaxis
Palivizaumab-humanized monoclonal antibody - Targets F protein - Given IM once a month
119
Varicella Zoster genome and virion
Alphaherpesvirus Genome: dsDNA (large) Virion: enveloped Hundreds of proteins
120
Varicella Zoster: replication in the cell
Active cell for replication Resting cell (neuron)-latent infection (circular genome) Infects neighboring host cells first
121
Varicella Zoster: Chickenpox
INfection through inhalation of aerosolzied droplets 10-21 incubation period
122
Varicella Zoster: symptoms
Fever, malaise, headache Rash 1-2 days after onset Rash progresses 3-6 days Rash on scalp face trunk Recover by 2 weeks—cell mediated immunity most important
123
Varicella Zoster: Latent reactivation
Shingles
124
Chickenpox Prevention: vaccination
Primary option Life long immunity Live attenuated vaccine
125
Chickenpox Prevention: Antivirals
Acyclovir - interferes with genome replication - can not elimante latent virus - Does not prevent infection of cells - Drug resistance is being observed
126
Poliovirus Genome and virion
Genome: (+)ssRNA Virion: Non Enveloped
127
Poliorvirus proteins
Capsid-VP1, VP2, VP3, VP4 Non-structural-proteases, polymerase, others
128
Poliovirus replication
In cell after ingestion of material containing virus Virus particle creates pore in cell membrane Genome serves as mRNA
129
Poliovirus primary replication
In Peters patches of small intestine | -minor viremia
130
Poliovirus secondary replication
Major viremia Mild disease Fecal shedding of virus for 6 weeks
131
Poliovirus: CNS involvement
1:200 of infections Virus replications in gray matter of brain and spinal cord - limb paralysis from anterior horn cell damage - respiratory paralysis from damage to medulla oblongata
132
Poliovirus Prevention
Vaccination Salk-killed Sabin-live attenuated Humans , no animal reservoir targeted for eradication
133
Rotavirus Genome and Virion
Genome: dsRNA, 11 segments Virion: non-enveloped
134
Rotavirus Proteins
VP1-polymerase VP2-RNA binding VP3-Transferase VP4-attachment and fusion Other structural and non structural proteins
135
Rotavirus replication
In cell Membrane disruption Genome never exposed
136
Rotavirus the disease
Infection by ingestion of material contains the virus 2 days incubation -vomiting and fever 2-3 days- diarrhea —3-8 days in duration Virus shedding for weeks before symptom onset and days after recovery Severe disease most common in 6 to 24 month old children Diagnose by antigens in stool
137
Rotavirus Prevention
Infant vaccines available No antivirals Hygeine treatment -oral rehydration
138
Mumps virus
Paramyxovirus Mumps
139
Rubella virus
Togaviruses German measles
140
Parvovirus b19
Parvovirus Fifth disease
141
Human Herpesvirus-6
Betaherpesvirus Roseola
142
Virus infection of the liver
Hepatitis viruses Primarily infect and replicate in hepatocytes Liver damage from virus and host response Some cause acute infections some cause chronic infections
143
Hepatitis B Virus: Genome and virion
Genome: dsDNA (smallest genome of the human viruses) Virion: enveloped Hepadnaviridae
144
Hepatitis B Virus: Proteins
``` HBsAG-S-virion assembly HBsAG-M-? HBsAG-L-Cell attachment HBcAG- capsid POL-reverse transcriptase ```
145
Hepatitis B Virus cannot be
Grown in cell culture
146
Hepatitis B Virus genome has a ____ intermediate
RNA
147
Hepatitis B Virus cccDNA is
Template for transcription
148
Hepatitis B Virus requires
Liver specific transcription factors
149
Hepatitis B Virus produces many
Empty particles
150
Hepatitis B Virus: infection
Sexual and drug use 30-180 day incubation period
151
Hepatitis B Virus: symptom onset
``` General malaise Anorexia Vomiting Fatigue Cough Serum like sickness ``` Jaundice Elevated alanine transaminase levels 3-4 months recovery after jaundice
152
Hepatitis B Virus: chronic disease
Sporadic episodes of hepatitis Cirrhosis of the liver Increased risk for hepatocullar carcinoma
153
Hepatitis B Virus: Vaccination
First recombinant vaccine approved for use in humans requires multiple inoculations Not effective against chronic infection
154
Hepatitis B Virus: treatment for chronic cases
Interferon alpha therapy Nucleoside analogs: Adefovir, Iamivudine, tenofovir
155
Hepatitis D Virus
Subviral Agent Rare in human viruses Only other example is Adeno-associated virus which requires adenovirus infections Requires active HBV infection RNA genome encodes a single protein
156
Hepatitis C Virus: Genome and Virion
Genome : (+)ssRNA Virion: enveloped Flaviviridae
157
Hepatitis C Virus: Proteins
E1/E2 attachment and entry C: core Various non structural
158
Hepatitis C Virus: replication
Genome passed into cytoplasm Genome template for translation -missing cap, ribosomes, recognize internal ribosome entry sites
159
Hepatitis C Virus: symptoms
Typically milder signs and symptoms than observers for HBV Chronicle infection are much more common
160
Hepatitis C Virus: Extrahepatic disease
Mixed cryoglobulineima Antibody and virus complexes despot in other tissues eliciting an immune response and subsequent tissue damage
161
Hepatitis C Virus: treatment
No vaccine Zepatier can treat some genotypes
162
Hepatitis A Virus
Recalls contaminated water -absorbed through intestine and moves to liver via portal system 15-40 day incubation Symptoms: Consistent with hepatitis infection: malaise anorexia vomiting jaundice More severe in adults than children Resolves approximately 8 weeks post infection Prevention -Vaccine
163
Hepatitis E Virus
Causes Foodborne and waterborne hepatitis Disease is very similar to that caused by HAV distinguished by serology Infection can be life threatening for pregnant women No prevention available -vaccines are under development
164
HAV Summary
15-40 day incubation Asymptomatic No chronic infections No long term sequelae Fecal oral, Sexaul, parenteral (+)ssRNA Nonenveloped Picornavirdiae
165
Hep A Genome virion
(+)ssRNA Nonenveloped Picornavirdiae
166
Hep B Genome and Virion
Circular dsDNA Enveloped
167
Hep C Genome and Virion
(+)ssRNA Enveloped
168
Hep delta Genome and Virion
(-)ssRNA Enveloped
169
Hep E Genome and Virion
(+)ssRNA Nonenveloped
170
HAV route of transmission
Fecal Sexual Parenteral
171
HBV transmission
sexual Vertical Parenteral
172
HCV transmission
Sexual Vertical Parenteral
173
HDV transmission
Sexual Vertical Parenteral
174
HEV
Fecal oral Sexual Parenteral
175
HBV
Asymptomatic often Chronic yes Long term sequelae yes
176
HCV
60-120 days Asymptomatic often Chronic yes Long term sequelae yes
177
HDV
60-180 days Asymptomatic possible Chronic yes Long term sequelae exacerbation of HBV
178
HEV
21-42 Asymptomatic often Chronic no Long term sequelae no
179
Eastern equine encephalitis
Togaviridae (+)ssRNA Enveloped
180
Venezuelans equine encephalitis
Togaviridae (+)ssRNA Enveloped
181
West Nile
Flaviviridae (+)ssRNA Enveloped
182
Rabies
Rhabdoviridae (-)ssRNA Enveloped
183
Select togaviruses and flaviviruses are transmitted through
A vector Arthropod transmission
184
Arthropod transmission: common vectors
``` Mosquitoes Aides Culiseta Culex Ticks ```
185
Arthropod transmission: Reservoirs
Birds | Small mammals
186
Transmission requires _____ in vector
Replication
187
_______ determined by vector and reservoir habitat
Geographic location
188
EEE and VEE virus biology
Togaviridae Togaviridae (+)ssRNA Enveloped
189
EEE and VEE proteins
E1 and E2: cell attachment and entry Capsid protein Various non structural proteins
190
EEE and VEE virus is introduced
Through he bite of an infected arthropod Infects cells locally and carried by larger hands cell to LN Replication and release into blood stream Infection in other target organs such as CNS
191
Encephalitis Disease
Fever Headache Irritability vom Diarrhea convulsions coma 1/3 of encephalitis cases die from disease 2-10 days after onset Those who recover can have long term sequelae -seizures, personality disorders, paralysis
192
West Nile Virus Disease
Incubation 2-14 days Most asymptotic 20% fever headache fatigue Neuroinvaise less than 1% Aseptic meningitis, encephalitis, flaccid paralysis altered mental state tremors
193
West Nile Prevention and Control
No approved vaccine No treatment Mosquito control Repellant
194
Main transmitters of west Nile
Culex sp.
195
Zika Virus
Flavivirus Envelope;d RNA genome Hosts: Life long infections in mosquitos Transient infection in primates rodents
196
Zika Fever
Resemble dengue fever Lasts several days, fever, red eyes, joint pain, rash Transmitted by mosquitoes possible via sex, blood transfusion vertically
197
Zika complications
Gillian barre syndrome- autoimmune disease attacking autonomic nervous system New born microcephalic
198
Rabies Virus
Rahabdoviridae -ssRNA Enveloped
199
Rabies Proteins
``` N-nucleoprotein P-phosphprotein M-matrix G-gylcyoprotein -attachment and entry L-polymerase ```
200
Rabies has broad
Tropism
201
Rabies replicates
In cytoplasm only
202
Rabies genome order dictates
Abundance of transcripts and proteins
203
Rabies binding of N to
RNA triggers genome replications
204
Rabies frequently produces
Defective interfering particles
205
Rabies reservoir
Bats Skunks Raccoons
206
Rabies transmission
15% bite | 60% if on face or head
207
Rabies spread
Replicates locally until it finds neurons Moves passively in axoplasm of peripheral nerves to spinal ganglia spinal cord and brain Spreads back to periphery highly inner gated salivary glands and replicates
208
Rabies symptoms
Pricking or itching where bitten fever headache Hydrophobia-difficulty swallowing even saliva leads to foaming Cerebral dysfunction anxiety confusion delirium halucatnoiinms insomnia
209
Rabies outcome
Once symptoms appear disease is nearly always fatal
210
Rabies prevention and control
Vaccine available Post exposure prophylaxis -4 doses
211
Spumaviruses
Do not cause human disease Makes foamy structures inside the cell
212
Two families of retroviridae
Orthoretroviridae Spumaviridae
213
Retroviridae genome
+ssRNA Enveloped
214
Retrovirus Proteins
Reverse transcriptase (RNA—>DNA, DNA—>DNA) Integrate Protease
215
Retroviruses were character by ______ & ———-
Nucleocapsid structure Location in the particle
216
_____ now used to classify retroviruses as simple or complex
Genome contents
217
Simple retroviruses
Only encode the Gag, Pro, Pol and Env genes
218
Complex retroviruses
Encode Gag Pol Env and more genes
219
Retroviruses Replication Cycle
``` Attachment Entry Reverse Trasncritpion Integration Transcription from provirus Translation Assembly Release Maturation-protease activity ```
220
Reverse transcription
SsRNA genome to dsDNA
221
Retroviruse replication integration
Virus dsDNA into host making provirus
222
Reverse Transcription
Defining feature of retroviruses Initiates once nucleocapsid is in cytoplasm - need higher levels of NTPs present - Low NTP levels prevent reverse transcription Occurs within a large complex similar to nucleocapsid
223
Infection cannot progress if___________ does not occur
reverse transcription
224
Reverse transcription is ____ between genome copies
Promiscuous
225
Reverse transcription silent when
Copies are identical Many different recombination when different genomes are in the Virion
226
Retrovirus must access
The nucleus
227
Retrovirus access the nucleus during
Mitosis Importation can also infect non dividing cells
228
_____ end processing of dsDNA
3’ Attack target DNA, nick created Host repair
229
Retrovirus integration of virus DNA is
Permanent No mechanism to remove it
230
If retrovirus is integrated into the germ-line then ________ is inherited and is called ______
Provirus Endogenous
231
Retrovirus can also disrupt host genes to cause
Cancer or other diseases
232
Integration of retrovirus identified oncogenes (4)
Transcription factors Secreted Growth factors Growth factor receptors Cell signal transduction pathways
233
Defective retroviruses
Many defective viruses are made during replciation
234
Defective retroviruses are missing at least one of
Gag Pol Env
235
Retroviruses require _______ to make progeny
Complementary infection
236
Many retroviruses infections are
Benign Usually not cytopathic Little impact to cell replication and physiology
237
Viruses are never
Eliminated by the host response
238
Slow Retroviruses
Ex. Leukemia viruses Effect is like high level mutagenesis Eventually results in tumorigenesis
239
Cytopathic Retroviruses
Minority of retroviruses carry cytopathic genes Cause Tissue damage directly
240
Acute transforming Viruses
Induce rapid tumor formation Carry host genes Often replication defective because host gene replaces an essential gene
241
Human T cell Leukemia Virus (HTLV)
Four distinct types Deltaretrovirus
242
HTLV-1 Transmission: Person to Person
Mother-child via breastfeeding Sharing needles Blood transfusions Sexual transmission
243
HTLV-1 Transmission: Within Host
Highly cell associated | Primary mode for spread is contact between infected and naive cells
244
HTLV-1 Disease
Adult T cell Lymphoma/leukemia Latent period of 30-50 years Infects memory T cells, antigen activation triggers transcription of provirus. Virus Tax protein and others stimulate cell proliferation. Cells become transformed generating tumors -with or without protein expression
245
HTLV-1 infected T cells enter
The CNS Activate astrocytes microglial cells Recruit inflammatory cells cause further tissue damage
246
HTLV-Assocaiated Myeolopathy (HAM)/(TSP) Tropical paraperisis
Shown to be the same Onset typically 3 years after infection Starts with bladder control issues Proposes to lower back pain, leg weakness or stiffness in hips or knees Men impotent
247
HAM/TSP treatment
Corticosteroids interferon yield temporary relief of symptoms
248
ATLL treatment
Treat the lymphoma with chemotheratpy regardless of HTLV infection
249
HIV
Two many types in humans Lentivirus
250
HIV Disease
Latent Period for AIDS: 6 months to 25 years Infection begins virus containing blood or bloody fluid to a mucosal surface or blood
251
HIV targets
memory T-cells (CD4+)
252
HIV initial acute infection
2 weeks after infection Mucocutaneous ulceration and weight loss more indicative of HIV infection GALT seeded as a result
253
HIV Chronic infection established
Ongoing virus replciation and T cell depletion
254
Influenza
Orthomyxoviridae Segmented (-)ssRNA Enveloped
255
Adenovirus
Adenoviridae DsDNA Non-enveloped
256
Rhinovirus
Picornavirus +ssRNA Nonenveloped
257
Three types of influenza virus
A, B, C Type A is most common and associated with greatest concerns
258
Influenza Proteins
``` HA-hemagglutinin, cell attachment NA-Neuraminidase, viral budding and release M1-Matrix M2-Ion Channel PB1,2, PA-Transcription complex ```
259
Influenza virus identified by
Surface antigens HA and NA 16 HA serotypes 9 NA serotypes
260
Avian vs Human Influenza Strains
HA major determinant and for human to human transmission
261
Influenza A uses a ____ ___
Animal reservoir
262
Influenza Type A attachment
Attachment by HA brings cell and virus membranes into proximity Conformation change triggered after Cell attachment by pH change in endosome Causes membrane fusion (B) Model for all enveloped viruses
263
Influenza replication
Transcription and replication take place in nucleus Protected genome escapes nucleus and buds from cell surface NA critical to budding
264
Current circulating strains of influenza
H3N2 H1N1
265
Highly Pathogenic Avian Influenza
HPAI strains have multi basic residences at HA cleavage site allowing replciation throughout the body Skin lesions Necrotic and swollen combs Systemic infection H5 or H7 strains
266
H5 and H7 strains can mutate to
HPAI strains
267
Adenovirus
Adenoviridae dsDNA Nonenveloped Proteins Fiber-cell attachment Penton base-cell entry Hexon-capsid
268
Adenovirus entry
Entry via coxsackie adenovirus receptor PH triggered capsid disassembly Moves to nucleus
269
Adenovirus Gene expression 3 stages
Immediate-early: Early Later
270
Adenovirus Gene expression: Immediate
E1A portion of genome - 2 transcriptional regulators - necessary to reach early stage
271
Adenovirus Gene expression: Early
5 genome sections E1B E2 E3 E4 and L1 DNA replciation and post transcriptional events
272
Adenovirus Gene Expression: Late
Take over of cellular mRNA synthesis
273
Adenovirus genome replication
Initiated on either end, indentical end sequences Replication in 5->3 direction, one strand displaced Displaced strand circulations to allow template copy to be made Primed by the protein pTP unusual priming strategy
274
Adenovirus cell regulation
DNA replciation occurs during S phase Not all cells are actively replciation
275
E1A inactives _______ leading to ___ _____ gene expression
PRb S phase
276
E1B inactivates ______ leading to _ __ and preventing ____
P53 S phase Apoptosis
277
Adenovirus E3 gene
Produces proteins important to evasion Blocks MHC class I expression reducing CTL cell killing Blocks TNF induced apoptosis Blocks IFN-a IFN-b action keeping protein translation active
278
Rhinovirus
Frequent cause of mild upper respiratory infections Large antigenic diversity - over 100 serotypes - makes vaccine development impractical Humans only known reservoir
279
Rhinovirus attaches to
Intercellular adhesion molecule 1 (ICAM-1) or the very low density lipoprotein VLDL receptor
280
Ebola
Filovirus Polymorphic particle enveloped RNA genome Helical nucleocapsid
281
Herpes Simplex Virus Type 1
Aphaherpesviridae DsDNA Enveloped
282
Herpes Simplex type 2
Alphaherpesviridae dsDNA Enveloped
283
Cytomegalovirus
Betaherpesviridae DsDNA Enveloped
284
Epstein Barr Virus
Gammaherpesviridae dsDNA Enveloped
285
Human Papillomavirus
Papillomaviridae DsDNA Nonenveloped
286
Alphaherpesvirus
Variable host range Short reproduction cycle Rapid spread in culture Efficient destruction of infected Cells Capacity to establish latency in sensory ganglia
287
HSV-1 Infection
Oral-oral Oral-genital Nearly 2/3 adults are seropositive
288
HSV-2 Infection
Primarily genital-genital oral-genital also possible 1/5 adults are infected
289
Alphaherpesvirus infects
Epithelial cells in the skin or mucosa Mucosa are more susceptible
290
Latency of alphaherpesvirus
Stationary cells, genome circulizes and stays as an episode in the nucleus Peripheral ganglia common site of laten infections Triggers: Sunburn, systemic infection, immune impairment, stress
291
Betaherpesvirus
restricted host range Long reproductive cycle Slow progression in cell culture Enlargement of infected cells
292
Gammaherpesvirus
Restricted host range Targets T and B lymphocytes Lyric infections Latency in lymphoid tissues Protypical member: Epstein Barr virus
293
Burkett’s lymphoma
Most common childhood cancer in Africa Tumor in jaw eye socket ovaries In all cases, tumor cells have monoclonal EBV episode Role of EBV unsure -spur B cell growth, mutations or genes transform cells
294
Hodgkins lymphoma
EBV associated carcinoma 3 types NL-modular sclerosing MC-Mixed cellularity LD-Lymphocyte Depleted
295
Beta/gammaherpesvirus immune evasion: Intrinsic
Blocks cell death inhibits apoptosis
296
Beta/gammaherpesvirus immune evasion: Innate
Decreases NK cell activity Inhibit NK receptor activation
297
Beta/gammaherpesvirus immune evasion: Adaptive
Decreased antigen presentation Degrades MHC class I and II Blocks MHC class II and T-Cell receptor interactions
298
CMV persistence
Persist in hematopoietic progenitor cells and macrophages in vitro Chronic persistent infection, not latency Controlled by healthy, active immune system
299
EBV persistence
Persistence of genome in memory B cells Virus proteins ensure B cell proliferation and EBV genome replication
300
Human papoillomaviurs proteins
L1-cell attachment | L2- Membrane penetration
301
HPV gain access
Through abrasion of the skin then establish an infection in the basal layer. Cell polymerase required for genome replication Virus production in differentiating cells Non-lyric virus, released wit dead cell shedding
302
HPV: Oncogenesis
E7 blocks retinoblastoma protein-continued cell proliferation E6 blocks the p53 tumor suppressor pathway HPV requires actively replicating cells to replicate and produce progeny
303
Antivirals block
Specific steps in the virus life
304
Antivirals must be active against
Virus replcaitions but not normal celllular function to reduce toxicity
305
Antivirals exploit
Structural function and genomic information to identify targets
306
Enfuvirtide-HIV
Blocks remolding of gp41, inhibits membrane fusion Prevents entry
307
Amantadine & Rimantadine-influenza
Blocks influenza ion channel preventing nucleocapsid release at the end of the cell entry process Prevents entry
308
Nucleoside analogs
Chain terminators Prevent genome replcaitions
309
Acyclovir
treatment of herpesvirus Prevent Genome Replication Most effective against HSV-1 and HSV-2
310
Ganciclovir
Effective against CMV more toxic due to interference with cellular kinases Prevent genome replication
311
Valganciclovir
Activity similar to acyclovir, improved oral biovalability Prevents genome replcaition
312
Foscarnet
Herpes virus treatment prevents genome replication Prevents viral polymerase activity IV administration Toxic
313
Nucleoside inhibitors of HIV and HBV
Good oral availability Toxicity is an issue Resistance often observed HIV therapy usually includes more than one, including one from a different class
314
Ribavirin
Inhibitor of RNA viruses prevent genome replication Triphosphate form inhibits polymerase Monophosphate form inhibits inosine monophosphate dehydrogenase lowering GTP in cell Impairs capping of mRNA
315
Maturation of progeny viruses often requires
Cleavage of virus polypeptide
316
Immature progeny are not
Infection
317
Ritonavir
HIV Treatment blocks cleavage of Gag-pol polypeptide Boosts activity of other protease inhibitors because it also blocks the action of cellular protease that act on other viral protease inhibitors
318
Antiviral challenges
Bioavailability Specificity Toxicity
319
Interferons
Natural antiviral | Effective against RNA viruses more than DNA
320
Active immunization
Administering all or part of a pathogenic agent to induce antibodies or cell mediated immunity
321
Passive Immunization
Administration of exogenously produced antibodies
322
Advantages of live attenuated
Easy to administer Produces immunity at site of first infection Induces antibody and cell mediate immunity Long lasting
323
Disadvantages of live attenuated
May revert during replciation | Not safe for immunodeficiency person
324
Advantages of killed vaccines
Safe for immunocompromised persons Cannot revert
325
Disadvantage of killed viruses
Usually injected Does not induce cell mediated immunity Protection is shorter
326
Three important immune cell types in vaccination
B Cells CD8+ T cells CD4+ T Cells
327
Vaccines utilizing B cells only
Pneumonococcal | HIB
328
Vaccines utilizing B cell and T cell immunity including secretory IgA
Influenza Polio Oral Typhoid
329
Innate Immunity Cells
``` Epithelial barriers Phagocytes Dendritic cells NK cells Plasma proteins ```
330
Viruses must reproduce within cells because
They cannot generate energy or synthesis proteins on their own
331
Viruses are
Obligate intracellular parasites
332
Protozoa
Microscopic single called eukaryotes
333
Helminths
Macroscopic multicellular worms of various length, possessing differentiated tissues and complex organ systems
334
Intermediate host
A host used by a parasite in the course of its life cycle and can multiply asexually bunt no sexually
335
Definitive host
Where sexual reproduction of a parasite takes place
336
Three groups of protozoan
Sarcodina Mastigophora Apicomplexa
337
Protozoan nucleus
A true membrane bound nucleus
338
Protozoan cytoplasm
Divided into inner endoplasm and thin outer ectoplasm
339
Endomplasm protozoan
Granular contains nutrients
340
Protozoan ectoplasm
Organized into specialized organelle of locomotion - pseudopods - flagella
341
Most Protozoa are hetertroiphic
Assimilate organic nutrients engulfing soluble or particular matter - pinocytosis - phagocytosis
342
Amoeba-Entamoeba histolytica
Microscopic Causes amebic dysentery 50 million people
343
Entameoba hystolytica principal host
Humans are principal host and reservoirs Transmitted by fecal-oral route directly or indirectly though water Highly infectious
344
Entameoba hystolitica: Cysts
Environmental form-resistant to heat, low pH and chlorine levels in municipal water supplies
345
Entameoba hystolitica: Trophozites
Dwell in lumen or wall of colon
346
Entameoba hystolitica cysts mature vs immature
Immature cysts have single nucleus Mature cysts have quadrincuclues Chromatid bodies are present in immature and get absorbed as cyst matures
347
Entameoba hystolitica trophozoites
Are microaerophilic Multiply rapidly in aneraobic environment of gut Feed on bacteria and tissue cells Amitonchodriate-no mitochondria
348
Entameoba hystolitica cysts turn to trophozites where
Distal small instestine which then invade intestinal mucosa
349
Amebic Dysentery
Most infections are asymptomatic Invasive Disease causes abdominal pain diarrhea bloody diarrhea and flatulence
350
Fulminating amebic dysentery
abrupt onset high fever, severe abdominal cramps, liver pain, and profuse diarrhea • 5% with symptoms have liver abscesses that can spread to pericardiu
351
Extraintestinal Disease
Can result in liver abscesses lung and brain involvement
352
Naegleria fowleri causes
Primary amebic meningoencephalitis
353
Naegleria fowleri enters through the
Nose, penetrate nasal mucosa, migrates to the brain via olfactory nears
354
Acanthamoeba causes
Keratitis (corneal ulceration) or Granulomatous embers encephalitis
355
Keratitis
Chronic progression ulcerative lesion of the eye may result in blindness Contact lens wearers at risk
356
Only _____ flagellates induce disease
4
357
Trichomonas Vaginalis exists only as
One morphological state —trophozoite
358
Trichomonas Vaginalis lacks
A mitochondria
359
Trichomonas Vaginalis causes
Trichomoniasis-very common sexually transmitted disease Spread by direct skin to skin contact
360
Giardia Lamblia infects
Humans and many mammals
361
Giardia Lamblia exists as
A dormonatn microbial cysts in contaminated water
362
Giardia Lamblia spread by
Fecal to oral route mainly through drinking water
363
Giardia Lamblia flagellated parasite colonize and reproduce
In the small intestines causing giardiasis | -not in blood or other GI
364
Giardiasis
1-3 weeks after infection Diarrhea Gas Floating stool
365
Leishmania spp. Type of parasite
Obligate intracellular flagellate parasite of mammals
366
Leishmania is transmitted by
Phlebotomine sandflies
367
Leishmania reservoirs
Rodents | Dogs
368
Leishmania organims 2 forms
Amastiogite Promastigote
369
Amastigote
Mononuclear phagocytes and bloodstream | -intracellular nonmotile form
370
Promastigote
Alimentary tract of sandflies Extracellular and motile form
371
Leishmania pathogenesis
Sandflies feed—ingest amastigotes from host—Promastigotes injected into next host—also inject peptides that inactivate macrophages—alters classical complement pathway-promastigote s get phagocytosis—amastigotes form within phagolysozome
372
3 diseases caused by leishmaniasis
Cutaneous leishmaniasis Mucocutaneous leishmaniasis Visceral leishamanisais
373
Localized cutaneous leishmaniasis
CD4+T cells of TH1 type secrete inf-gamma in response to antigens Macrophages produce nitric oxide to kill intracellular amastigotes
374
Visceral Leishmaniaisis
Pathogen causes dramatic inhibition of Th1 response-disseminate through bloodstream to visceral organs TH2 response and antibodies associated with visceral disease
375
Chagas’ disease caused by
Trypanosomiasis cruzi
376
Chagas’ disease spread by
Redivide insect kissing bug
377
T. Cruzi is in
Reduviid feces the poop after they feed
378
2 Phases of Chagas Disease
Acute Phase- a week after bite Fever fatigue headache rash Chronic Phase-decades later
379
Trypanosoma Brunei
Transmitted by tsetse fly African sleeping sickness
380
Sporozoa-Apicomplexa
Obligate intracellular parasite Apical complex structre This group included Plasmodium Toxoplasma Cryptosporidium Babesia
381
Oocyst
Sexual forms
382
Merozoite
Asexual form that can infect host cells
383
Plasmodium causes
Malaria
384
Plasmodium transmitted by
Anopheles mosquitoes Causes periodic fever and anemia when erythrocytes burst
385
Plasmodium reproductive stages
Sexual-mosquitoes Asexual -humans
386
Plasmodium life cycle
Almost the same for all 5 species Sporozoite in saliva gets injected by female mosquito into human Moves to liver Infects hepatocytes Merozoites are released from hepatocytes infect erythrocytes Inside erythrocytes-trophozoites form then schizont Erythrocytes ruptures releasing merozoites which invade new erythrocytes
387
Plasmodium falciparum
Causes falciparum malaria which is the worst type to have Cerebral malaria
388
Plasmodium vivax
Most frequent and widely distributed causing of recurring malaria Less virulent Splenomegaly
389
Malaria reason for fever
IL-1 and TNF produced by macrophages that ingest cell debris
390
Malaria anemia
Phagocytosis of infect earthy types and parasite induced cell rupture leads to reals of toxic products
391
Toxoplasma gondii
Toxoplasmosis Cats are the only definitive host Both sexual and asexual cycles take place in GI of felines Oocytes in feces ingested by humans Still births
392
Toxoplasmosis steps
Oocyst are excreted in cats feces Oocyst ingested Most people are asymptomatic Cervical nodes most often affected
393
Nematodes
Worms with bodies that are round in cross section
394
2 categories of nematodes
Intestinal nematode Tissue nematodes
395
Large round worms
Largest and most common intestinal helminth
396
Hookworms
One the most common intestinal nematodes worldwide
397
Pinworms
Common in children in US
398
Whipworms
Common soil transmitted in southern US
399
Strongyloides stercoralis
Similar to hookworm Greater risk for life threatening infections
400
Ascaris lumbriucoides
Large round worm Causes ascariais
401
Ascaris Infection: Life Cycle
Contracted through ingestion of eggs excreted in feces Eggs hatch in intestines larvae burrow through gut wall migrate to lungs via blood Break into alveolar walls-travel up the throat where they get coughed up and swallowed Upon reaching small insetting develop into adult worms and have a free constant supply of food Takes 3 months
402
Large round worm infection symptoms
Shortness of breath Abdominal swelling Diarrhea Slow growth Learning problems in children
403
Anyclostoma and NEcator
Hookworms Toothlike structures that allow attachment to small bowel -suck blood
404
Hookworms life cycle
Eggs deposited in soil hatch into Rhabditiform larvae then molt into filariform larvae (infectious form) Contact with human -penetrate skin carried through blood vessels to hear then lungs Travel to alveoli to throat Coughed then swallowed Larvae then reach small intestine’ Suck blood
405
Trichinella spiralis
Trichinosis Contracted from eating undercooked pork with encysted larvae Matured adult worms penetrate intestinal mucosae causing nausea Larva invasion of striated muscle begins 1 week later
406
trichonosis symptoms
Fever muscle pain Eyelid swelling Myocardial involvement and heart failure
407
Cestodes
Long ribbon like worms Tapeworm Beef tape worm Pork tapeworm Fish tapeworm
408
Beef tape worm
human is definitive host, cow intermediate host- cysts form in cow muscle
409
Pork tape worm
both pork and humans are intermediate hosts (may acquire cysts)
410
Fish tapeworm
Humans and fish eating mammals are definitive host- Crustacean and fish intermediate host
411
Taeniasis
Tapeworm infection After ingestion by animal, eggs hatch and oncospheres penetrates intestinal wall and circulate to muscles where they become cysticerci Humans ingest cysticerci from undercooked meat Adult tapeworm develops in humans small intestine over several months
412
Beef Tapeworm infection
Contracted by eating meat contains larval form-infection is in gut lumen of humans
413
Porktapeworm infection
Eggs can infect both pigs and humans Humans are an intermediate unlike beef Cysts from in muscles or in the brain
414
Cysticercosis of brain
Pork tapeworm ``` Can develop in Subcutaneous tissues Muscles Heart Lungs Liver Eye Brain ```
415
Fungi make up
Their own kingdom Fungi are eukaryotes
416
Fungi are mostly
Strict aerobes A few are facultative anaerobes
417
Fungi cause disease by
Inducing an inflammatory response or through direct invasion or destruction of tissues
418
Fungal cell membrane consists of
Ergosterol
419
Fungi cell walls are unique
Different from cell walls of plants and bacteria NO peptidogluycan, LPS, Glycerol or teichoic acid Fungal wall contains chitin, mannan and glucan
420
Fungi 3 medically important categories
Yeast Molds Dimorphic fung
421
Yeast is a ______ fungi
Unicellular Single cells-asexual reproduction
422
Molds are ______ fungi
Multicellular Both secula and asexual repodoctuion possible
423
Dimorphic fungi can exist as
Both mold and yeast
424
Molds reproduce two ways: Asexually
By conidia that form on the tips of growing hypahe
425
Molds reproduce two ways: sexually
Through development of spores
426
Hypahe of molds
Vary depending on species Septa may contain pores and incomplete walls-allow moment of nutrients organelles and nuclei between adjacent cells
427
Fungal asexual reproduction
Asexual form is call anamorph and forms stricter called conidia Involves mitosis division of haploid nucleus . No genetic recombination
428
Fungal sexual reproduction
Sexual from is called Teleomorph and forms specialized structures called spores, also called ascospores, zygospores, absidpores depending on struction -haploid nuclei of donor and receipting cells fuse to form a diploid nucleus which divides by classic meiosis. Genetic recombination can occur
429
Fungi dimorphism is
Reversible and is linked to virulence
430
Thermally dimorphic
Temperature determines whether mold or yeast
431
3 ways to encounter fungi
Incidental contact in environment Normal human flora Contact with infected individual
432
Most fungal infections are
Mild and self limiting
433
Primary barriers against fungal infections
Intact skin and mucosal surfaces are primary barriers Dedication epithelial cell turnover fatty accidents and low pH of skin
434
_______ compete with fungi and inhibit growth
Bacterial normal flora
435
_______ Immunity is required to elimante fungal infections
T cell mediated CD4+TH1/TH17 cell mediated immune response
436
Primary mechanisms for contains fungal infections
Phagocytosis and killing by neutrophils Some fungi are too large so secrete enzyme and reactive oxygen species that can digest or kill large fungi
437
Immunity to fungal infections is mediate by
T cells
438
CD4+ T cells Recogonize
Presented antigens in MHC complex on APC (dendritic Cell) through an interaction with their TCR This stimulates the resale’s of cytokines which activate neutrophils and macrophages
439
Azoles
Itraconazole Interfere with ergosterol synthesis Fungistatic
440
Polyenes
Amphotericin B Bind to cell wall ergosterol and forms channels
441
Polyenes must be administered
Intravenously as a colloidal suspension
442
Azoles target either
Yeast of mold forms of fungi Better tolerated than amphotericin B target enzymes that converts lanosterol to ergosterol resulting in defective membranes Toxic to liver Resistance can occur and arythmias
443
Superficial and Cutaneous Mycoses
Limited to epidermis and skin structure Dermatophytes Malassezia
444
Dermatohphyte Skin Infections
Most common fungal infections in humans Infect keratizned tissues
445
Dermatophytes clinical diseases called
Tineas (ringworm athletes foot jock itch) Microsporum Trichophyton Epidermophtyon
446
Dermatophytes Entry
Skin trauma is required
447
Dermatohphyte Hyphae grows
Outward in centrifugal pattern Systemic infections very rare
448
Tina Capitis
Hyphae invade hair shaft Hair can Brea at the root and fungus can plug hair follicle causing bald patches
449
Tina Unguium
Nail plate invasion leads to hyperkeratosis and discoloration-dislodges and distort nail
450
Seborrheic dermatitis
Patches with greasy scales in facial hair and scalp -dandruff
451
Tina versicolor
Hypopigmented or hyperpigmented patches on chest or neck with scaling
452
Subcutaneous mucosal usually enter skin via
Thorns or splinters
453
Sporothrix schenckii-subcutaneous mycoses
Thermally dimorphic fungus Sporotrichosis-rose pickers Disease Disseminated only in immunocompromised patients
454
Sporothrix Schenckii infection starts as
A painless applies developing a few weeks to a few months after inoculation. Papuans slowly enlarge and eventually ulcerate leaving open sores. Infection follows lymphatics**
455
Chromoblastomycosis
Scaly wart like lesions usually on feet or leg Amputataion required
456
Mycetoma
Caused by different species of environmental fungi, chronic infection with sinus tract nodules and discharged visible grains
457
Opportunistic fungal pathogens
Not considered tru pathogens Only cause disease when host defense are decreased
458
Candida Albicans
Most frequent opportunistic fungal pathogen Colonies grow rapidly
459
Candida Albicans reproduce by
Forming buds or blastocondidia Some form hyphae or pseudo in vivo Polymorphic fungus-not true dimorphism
460
Candida shift from
Yeast to hyphae associated with invasion
461
Candida hyphae
From strong attachment to epithelial cells Hyphae secrete proteinases and phospholipase that digest epitheal I cells-facilitate invasions Also forms biofilms on prosthetic surfaces
462
Candidiasis
INfection only when normal flora is disrupted Broad spectrum antibiotics biggest culprit Decreased T cell function
463
Mucosal Candidiasis
Mucosal (Thrush) thick white plaques on orophaygneal and vaginal mucosa
464
Cutaneous candidiasis
Warm moist areas of skin Diaper rash
465
Urinary tract infections
Candidiasis Ascending infections
466
Disseminated Candidiasis
Life threatening When gains access to bloodstream Enters through skin lesion, GI disruption, prosthetic devices, intravenous cat here’s , UT Once in blood stream-micro abscesses in multiple organs Disseminated candidiasis symptoms are similar to bacterial infections-however they often involve the eyes and can lead to blindness
467
_______ involved in defense against candida infection
Both humoral and cell mediated immunity
468
Osponziing IgG antibodies
Against yeast carbohydrate mannan-activate classical complement pathway
469
T cell mediated immunity: candida
Keep candida in check on mucosal surfaces (neutrophils)-main host defense against invasion through muscles
470
Th1 mediated immunity candida
IL2 INFy TNFa correlate with enhanced resistance to candida infection
471
Th2 candida
IL4 IL6 IL10 associated with chronic disease
472
Aspergillosis
Filamentous fungi Ubiquitous in soil INhaltion of spores
473
Aspergillosis reproduce by
Forming candidiasis and area conidiophores (sexual)
474
Aspergillosis Entry
Candidiasis are inhaled Germinate into hyphae Macrophages unable to kill hyphal form Neutrophils line up along hyphae and secrete reactive oxygen intermediates that kill the fungus
475
Aspergillosis pneumonia
Most common patients with emphysema and bropnchiectsia are at risk
476
Disseminated aspergillosis
Disseminated through bloodstream can occur and affect any organ system
477
Allergi respiratory disease aspergillosis
Occurs in people with allergies build up of mucous allows fungus to grown
478
Aspergillosis
Results in patients with prior lung infections with scarring and cavities Fungal spores germinate in cavities and fungal hypahe grow into balls
479
Zygomycetes
Colonize oral mucosa paranasal sinuses and pharyngeal mucosa Associated with diabetic ketoacidosis
480
Pneumocystis
Colonizer of human airway
481
Cryptococcosis
Environmental yeast Polysaccharide capsule
482
Cryptococcus virulence factors
Capsule Lactase engulfment Phospholipase s Urease
483
Cryptococcus capsule
Made of GXM glucuronaxulmannan
484
Lactase enzyme
Produces antioxidant melanin pigments
485
Cryptococcus
Are inhaled into alveoli producing lung infection In the lungs they produce polysaccharide capsule -t cell mediated immunity crucial
486
Cryptococcus most often presents as
Meningitis
487
Endemic mycoses
Dmorphic Fungi that infect heathy people Histoplasmosis Blastomycosis Coccidioidomycosis
488
Histoplasmosis
Dimorphic soil fungus In lungs transforms into yeast
489
Blastomycosis
Disease occurs when inhaled into the lungs Skin lesions also common occur dissematined spread by blood Granulomas can develop
490
Coccidioidomycosis
Dimorphic not temperature dependent
491
Coccidioidomycosis: Arthroconidia
Highly infection mold form inhaled into alveoli Phagocytosis
492
Coccidioidomycosis: Spherules
In lungs transform into spherules filled with endosomes Resist phagocytosis
493
Coccidioidomycosis life cycle
Desert climates Hyphae differentiate into arthrocondia which break loose and get suspended in the air Inhaled into lungs In humans differentiation produces cleavage planes and eventually huge spherules The spherules rupture releasing endosomes which can then repeat the in vivo cycle
494
Coccidioidomycosis cell mediated immunity
CD4 T cell is need to control infection and activate macrophages
495
Coccidioidomycosis can disseminate
Can spread to other organs Chronic meningitis possible
496
Active Immunity
The development of antibodies in response to antigenic stimulation
497
Passive immunity
Transferred protection through preformed antibodies produced by another individual
498
Active immunization
Vaccination - longer duration of protection - Delayed onset
499
Passive immunization
Preformed antibodies - immediate onset - shorter duration of protection
500
Disadvantages of passive immunization
No long term protraction Serum sickness Risk of infection Graft vs host disease
501
Natural passive immunity
Placental trasnfer of IgG Colostral transfer of IgA
502
Artificial passive immunity
Antibodies or immunoglobulins Immune cells
503
Vaccination
A process of induction of immunty to a pathogen by deliberate injection of a weakened modified or related form of the pathogen which is no longer pathogenic
504
Principal behind the smallpox vaccine
Cowpox and smallpox shave some surface antigens Immunization with cowpox induces antibodies against cowpox surface antigens Cowpox antidisestablishmentarianism bind to and neutralize smallpox virus
505
Immunologic adjuvants
Substances when mixed with an immunogenicity enhances the immune response
506
Immunologic adjuvants examples
Prolongs antigen persistence Enhances costimulatory signals Induces germinal center formation Stimulate lymphocyte proliferation
507
Enhanced co stimulators signals
Increases expresssion of MHC and B7 molecules Secretion of cytokines - >increased antigen presenting ability - >maximal activation of TH cells
508
Animal adjuvants
CFA Oil in water mullion Complete Freunds
509
Human Adjuvants
Alum (alumninum hydroxide )
510
Live Attenuated Vaccines
Contain a version of the living microbe that has been weakened in the lab so it cant cause disease - closet thing to a natural infection - lifelong immunity
511
Live attenuated vaccines induce
Robust immune responses CD4 CD8 strong cellular responses Strong antibody response long lived memory B cells
512
Live attenuated Disadvantages
Possibility of reversion to a virulent form Must be refrigerated Contraindications in very young Very old HIV patients
513
Attenuated Advantages
Easy to create Small number of genes Easier to control their characteristics
514
Viruses are attenuated in cells in
Which they do not reproduce well in. Hostile environment takes the fight out of viruses -they evolve to adapt to the new environment They become weaker with respect to their natural host
515
Why are bacteria difficult to attenuate
Bacteria have thousands of genes and thus are much harder to control -recombinant DNA technology to remove several key genes in various bacteria is one approach
516
Attenuated vaccine examples
Measles Mumps Chickenpox Influenza vaccines -A/H1ni A/H3N2 And inactivated vaccine
517
Influenza vaccine
A flu virus contains 8 gene segments Combine desired HA and NA genes from flu strain 1 with flu strain 2 grow in an egg
518
How are viruses inactivated to create inactivated vaccines
Chemicals Heat Radiation
519
Inactivated vaccines are ____ and ____ than live vaccines
Stable Safer Microbes cant mutate back to their disease causing state Don’t need refrigerated Can be freeze dried
520
Inactive vaccines stimulate
A weaker immune system response than live vaccines -usually take several doses
521
Killed Advantages
``` Safe Stable No refrigeration Nontranmissible Cannot multiply or rever ```
522
Killed disadvantages
``` Multiple doses Unnatural route High Ag concetration needed Variable efficacy Weak CMI responses Inadequate killing ```
523
Subunit Vaccines
Instead of the entire microbe, subunit vaccines include only the antigens that best stimulate the immune system -immunodominat epitope
524
Chances to adverse reaction in subunit vaccines
Lower No live microbes Less microbial particles
525
Subunit vaccines from 2 ways
Microbe broken down Antigen molecules manufactured using recombinant DNA
526
Toxoid Vaccines
Used when a bacterial toxin is the main cause of illness
527
Toxins can be inactivated by treating them with
Formalin - solution of formaldehyde and sterilized water - detoxed toxins are called toxoids are safe for use in vaccines
528
Toxoid vaccine example
Diptheria Tetanus
529
Conjugate Vaccines
Encapsulated bacteria may be more difficult for the immune system to detect -polysaccharide coating evade immune detection
530
A conjugate vaccine links
Antigens or toxins from a microbe to the outer polysaccharides -helps the immature immune system react to polysaccharide coating and defend against the disease causing bacterium
531
Conjugate vaccine example
Haemophilus influenza type B
532
Herd immunity
The more people that are vaccinated the fewer susceptible individuals will be exposed and the less likely person to person transmission will occur
533
Some components of the innate immune response are common to all pathogens
Phagocytosis and killing of microbes Antigen presentation Cytokines production to induce inflammation and reactive endothelium
534
NK cells produce
Cytokines
535
Both innate and adaptive immunity work to
Protect against infection and eradicate infection
536
IgG
Virus
537
IgA
Mucosal virus
538
PAMPS go to what receptors
Toll like receptors
539
Chemokines
Make chemical gradient specialized cytokines that tell cells where to go
540
Type I interferons
Interferon alpha | Interfereon beta
541
The most potent stimulus for IFNs are
Viral nucleus acids detected by pattern recognition receptors
542
Type I IFN does what
Inhibits viral replication and inhibits viral protein synthesis
543
How does the immune system deal with intracellular pathogens
Kill the infected host cell Cytoxic cell NK cell
544
NK cell
Kill cancer cells Viral infected cells Lymphocyte but not MHC Not capable of generating memory
545
NK cells kill target cells by 2 mechanisms
The death receptor Granule dependent pathways-contact dependent perpherin
546
What is immunologic memory
Specific to B and T lymphocytes Acquired after initial exposure to Ag
547
All T cells recognize Ag via
T cell receptor
548
Before TCR can recognize Ag it must be
Processed by APC -Ag broken down into shor fragments Presented by APC - MHC I - MHC II
549
B cells do not require
Ag to be processed/presented B cells via membrane bound Ig can recognize Ag in its native form
550
MHC I
On inside cell Endogenous Ag -critical to viruses Not on erythrocytes
551
MHC II
Always on -professional APCs Exogenous Ag Typically present Ag to helper T cells
552
Helper T cells function
Cytokines Secretion
553
Acationg of macrophages
Th cells make IFN gamma
554
Actaiviton and enchanted Ab production by B cells
Th cells make IL4
555
Activation and enchanted killing of TC cells
Th cells make IFN-gamma
556
What do TC cells do
Killing of infected of tumor transformed cells - perforn - Granzymes -Cytokine Secetefrion -IFN GAMMA -Tumor necrosis factor TNF alpha
557
Central tolerance
Occurs in generative lymphoid oranges involving immature self reactive lymphocytes recognizing self antigen
558
Peripheral Tolerance
In peripheral sites involving mature self reactive lymphocytes encountering self antigen
559
Immunological tolerance is NOT
Simply a failure to recognize an antigen
560
Immunological tolerance IS
An active response to a particular epitope and is just as specific as an immune response
561
Tolerance can be ______ or _______
Natural Induced
562
Immunological Tolerance
A state unresponsive for a particular antigen - LEARNED very specific and induce prior to exposure to antigen - INclude tolerances to non self
563
Self Tolerance
Physiological state in which the immune system does not react destructive against self tissue
564
Self tolerance my be induced in _____
Immature self reactive lymphocyte in generative lymphoid oranges Or in mature lymphocyte in peripheral sites
565
Response to self antigen
Anergy Deletion Change in specificity
566
Reactivity is prevented by processes that occur during
Development rath than being genetically pre-programmed
567
CD4/8- start in bone marrow and fetal liver travel to
Thymus
568
Lymphocytes that do not bind MHC through their TCR
Are destined to die by apoptosis
569
Positive selection and lineage commitment occur in
Cortical region of the thymus
570
Negative selection occurs
In the medullary region of the thymus
571
Positive selection uses what avidity
Low avidity
572
Negative selection uses what avidity
High avidity
573
During maturation in the thymus most immature T cells that recognize antigens with high adviity are
Deleted
574
Self reactive CD4+ T cells that see self antigens in thymus
Are not deleted but instead differentiate into regulatory T cells
575
Choice between lymphocyte activation and tolerance is determined by
The properties of the antigens State of maturation of the antigen specific lymphocytes Types of stimuli received when these lymphocytes encounter self antigens
576
Central Tolerance in B cells
Occurs in Immature B cells in the bone marrow
577
Potentially autoreactive cells can
Be eliminated or inactivated by contact with self Ag
578
________ and _______ of the self Ag detriments the fate of B cells
Nature Concentration
579
Multivatlent Ag
Induce B cell death
580
High concentrations of Ag
Induce B cell death
581
Lower concentrations of small soluble self Ag induce
Functional anergy Results in decreased membrane Ig Blocked signal transduction by membrane bound Ig
582
Peripheral tolerance
is the mechanism by which mature T cells that recognize self antigens in peripheral tissues become incapable of responding to these antigens
583
Colonial Deletion/apoptosis
Actual elimination from the cellular repertoire by activation induced cell death
584
Colonial anergy
Mature cell is present but is functionally inactivated
585
Suppression
Inhibitor of cellular activity through interaction with other cells Tregs (CD4+/CD25+ T cells, TGF beta or IL10 secreting reg T cells)
586
Ignorance
Co-existence of self reactive clones and antigen; cells do not respond to antigen
587
Factors determine which mechanisms are operative
Concentration of self antilnge in lymphoid organs Affinity of antigen receptor for antigen Nature of antigen Concentration and availability of co-stimulators molecules
588
Without helper T cells
Won’t get a full B cell response
589
B cell clonal expansion
Antibody secretion Isotype switching Affinity maturation Memory B cell
590
How to T cells affect the outcome of B cell activation in the periphery
2 signal hypothesis
591
Signal one
Generated though the Ag receptor
592
Signal two
Mediated by CD40 and CD40L B cell anergy results if one the signals is missing
593
IL4 | IL13
+ IFN-gamma =-
594
Anergic cells shopw a block in TCR induced signal tranduction
Lack of costimulation by B7 and B72 Costimulation by inhibitory receptors
595
CTLA-4 competes with _____ for b71 and b72
Cd28
596
CTLA4 keeps ______ in check
T cells
597
Knockout mice lacking CTLA4 develop
Uncontrolled lymphocyte activation Massively enlarged lymph nodes and spleen Fatal multiorgan lymphocytic infiltrates
598
Self reactive cells may be deleted from repertoire
Activation in the absence of IL2 can lead to death Persistent Ag Activation induced cell death
599
Capsase 8/9
Apoptosis
600
Caspase 9
Passive cell death
601
Caspase 8
Induced cell death
602
How does ignorance happen
Antigen is expressed in a privileged site/sequestered T cells cannot get to the antigen across an endothelial barrier Perhaps the antigen is not expressed in the context of MHC molecules
603
Oral administration of Ag favors
Tolerance induction
604
A state of immune _______ follows oral administration of an antigen
Hyporepsoiveness
605
T cells
Cell mediated response Recognize processed antigen in the context of MHC to irradiate infection -effector functions include cytokine productin adn release of cytotoxin factors
606
B cells
Humoral responses Recognize free antigen via Ig receptor to irradiate infection -effector functions include antibody mediated destruction of antigen
607
Autoimmune disease occurs when
The immune system becomes dysregulated and attacks the very organis it was designed to protect
608
Autoimmunity results when
Central and peripheral tolerance is broken
609
Factors that can predispose an individual to various auto immune diseases
MHC association Familial concordance Gender Climate Chemical angers Infections agents Immune dysregulation
610
What initiates an autoimmune response
Incomplete deletion of self reactive cells Aberrant stimulation of normally anergic self reactive cells Altered regulation of anergic self reactive cells
611
Systemic Autoimmune Diseases
Immune cells target multiple organ systems and tissues Thought to be due to aberrant regulation of many clones of lymphocytes
612
Organ specific autoimmune disease
Immune cells target specific organs or tissue Thought to be due to failure of self tolerance in only a few clones of cells which react to a limited number of antigens
613
MS
Immune systems targets central nervous system via myelin specific T cells
614
Systemic Lupus erythematosous
A systemic disorder in which a variety of autoantibodies (DNA, nucleoproteins, platelets, lymphocytes) can cause multisystem damage
615
Systemic AI diseases
Lupus | RA
616
Organ Specific AI
Insulin dependent diabetes mellitus Multiple sclerosis
617
SLE increased risk associated with
HLA DR2 and HLA DR3 Female
618
SLE symptoms
``` Fatigue Fever Alopecia Mucosal Ulceration Butterfly rash Joint and muscle pain ```
619
SLE Pathogenesis
Immune complex disease Type III Large amounts of autoantibodies produced a giants self antigens - DNA - Nucleoproteins - Platelets - Lymphocytes
620
MS
HLA DR2 ``` Impaired vision Ataxia Spasticity Bladder dysfunction Weakness Sensitivity to temperature Cognitive impairment ```
621
MS pathogenesis
T cell mediated autoimmune diseae in which T cells are specific for components for eh myelin sheath Also evidence of macrophage and microglial cell involvement in myelin degradation Damage to/loss of myelin impairs nerve conduction
622
Allergy
Deleterious effects of hypersensitivity to environmental antigens
623
Autoimmunity
Disturbance in immunologic tolerance of self antigens with damages to self tissue
624
Alloimmunity
Immune reaction to tissues of another individual
625
Type I hypersensitivity
IgE mediated
626
Type II hypersensitivity
Tissue specific reactions
627
Type III hypersensitivity
Immune complex mediated
628
Type IV hypersensitivity
Cell mediated
629
Alloimmunity is when the immune system reacts with
Antigens on tissue of other genetically dissimilar membranes of the same species - transplant rejection - Transient neonatal
630
Transient neonatal alloimmunity
Fetus expresses parental antigens not found in the mother
631
MHC molecules have a
Broad specificyt for peptides
632
Peptides associated with MHC have a
Slow on and slow off rate
633
MHC molecules do not discriminate
From self and foreign peptides
634
The MHC haplotype
Of an individual determines which peptides bind and how peptides bind
635
HLA
Human leukocyte antigen
636
MHC genes are
Highly polymorphic Hundred of alleles in human with 10^13 combination
637
How are MHC alleles expressed
Concomitantly The set of MHC alleles on an individual chromosome is termed the MHC haplotype
638
MHC haplotype can influence
How an individual responds to certain pathogens Susceptibility to certain diseases Transplant success
639
Graft Rejection according to time
Hyperactive Acute Chronic
640
Hyperacute rejection
Immediate a rare Preexisting antibody to The antigens of the graft
641
Acute rejection
Cell mediate response against unmatched HLA antigens Paraenchamhyl cell damage
642
Chronic Rejectgion
Months or years Inflammatory damage to endothelial cells of vessels due to a weak cell mediated reactions against minor HLA antigens
643
Graft Versus Host
Immunocompromised individuals are at risk for GVH T cells in the graft are mature and capable of cell mediated destruction tissues within the recipient Not a problem if patient is immunocompetent
644
AB blood type
Universal recipient No antibodies A and B antigen
645
O blood type
Universal donor Anti-a anti-b antibodies No antigens
646
ABO Blood system
A and B are codominat Individuals have naturally occurring antibodies to the A and B antigens they lack
647
blood antibodies are usually of the
IgM class
648
A blood group
Anti-B antibodies A antigen
649
Primary immunodeficiency
Congenital Genetic defects that result in an increased susceptibility to infection
650
Secondary immunodeficiency
Acquired Develop as a consequence of Malnutrition Disseminated cancer Treatment with immunosuppressive drugs INfection of cells of the immune system
651
Primary immunodeficiency may affect
One or more components of the immune system including T, B lymphocytes and Natruarla kIller cells as well as phagocytic cells and complement proteins
652
Immunodeficiency may result from defects in
Leukocyte maturation or activation or from defects in effector mechanism of innate and adaptive immunity
653
The types of recurring infections can
Predict the type of immunodeficiency
654
Deficient humoral immunity usually results in
Increased susceptibility to infection by pyogenic bacteria
655
XLA
All antibody isotype are very low Circulating B cells absent Pre B cells reduced in numbers in bone marrow Tiny tonsils and lymph nodes Thymus and T cell dependent areas are normal
656
XLA defect association with the loss of
Burton Tyrosine Kinase
657
X linked immunodeficiency with hyper IgM
Characterized by very low serum IgG IgA and IgE A high concentriaont of polyclonal IgM Pyogenic infections Lymphoid hyperplasia
658
Hyper IgM B cells are not
Signaled by T cell to go through isotype switching and only produce IgM
659
Deficient Cell-mediated immunity usually results in
Increased susceptibility to viruses and other intracellular pathogens
660
Severe Combined Immunodeficieny Diseae
Rare fatal syndrome profound deficient of T and B cell function Bubble boy Have B cells but don’t produce immunoglobulin

Micro/Immuno (3 decks)

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