Viruses Flashcards
1
Q
Viral Srutcture
A
Genome- either DNA or RNA
Capsomere- viral subunits- assemble into a capsid
Nucleocapsid- genome assembled into the capsid
Virus specific glycoproteins
Envelope- originates from the host membranes- covers the capsid
2
Q
Capsid symmetry & structure
A
Held together by non-covalent reversible bonds.
Cubic/Icosahedral symmetry- NA amount is limited by size of particle
Helical symmetry: no limit on amount of NA packaged
3
Q
Triple Shell Capsid
A
Seen in rotavirus- has outer coat, middle shell/capsid and inner layer.
4
Q
Bacteriophages
A
Bacterial viruses Head- NA and protein Tail and contractive sheath Tail fibers and tail pins Base/end plate
5
Q
Peplomers
A
Spike-like viral glycoproteins. Attach to receptors on host cell. Are on the capsid or envelope
6
Q
Matrix proteins
A
inside the envelope. Help assemble the nucleocapsid
7
Q
VAP: Viral attachment proteins
A
facilitate host cell entry
HA- on influenze binds RBCs
VAP on EBV binds C3d receptor on B cells
8
Q
HA (hemagglutinin)
A
VAP on influenza- binds RBCs and helps enter host cell.
9
Q
VAP on EBV
A
Binds C3d receptor (CR2) on B cells- facilitates entry into host cell.
10
Q
Viral Envelope
A
Lipoprotein membrane. Derived from host membrane
Poor in host cell proteins, rich in virus specific glycoproteins
Has peplomers on surface with viral origin.
Increases susceptibility to heat, drying, detergents and lipid solvent.
Fecal-oral transmission is more likely to be naked
Person-person contact transmission are more likely to be enveloped
11
Q
Rhabdovirus envelope
A
bullet shaped
12
Q
Poxvirus envelope
A
Complex structure. No simple symmetry.
Brick-like external shelf.
13
Q
Pseudovirions
A
wrong DNA is packed instead of the viral genome.
Can infect a host, but cannot repicate
14
Q
Viroids
A
Virus without a protein coat or envelope. Only have genome.
Replicated by host RNA pol II
HDV has viroid behavior, but codes for a protein
15
Q
Defective/Satelite virus
A
Cant replicate without helper virus (HDV needs HBV)
Cannot infect host on its own.
16
Q
Prions
A
Infectious proteins
Have no genome
Adopt modified structure to normal protein that causes damage
TSE
Can be acquired through infection, hereditary, or spontaneous.
PrPc will change to PrPsc–> chain reaction–> aggregated cause neuronal damage.
17
Q
Stages in viral synthesis
A
1- Attachment
2- Penetration and Uncoating
Includes latent period
3- Synthesis
4- Formation of viral mRNA and new genomes
5- Formation of new protein
6- Assembly: self-generated
7- Release: lysis or exocytosis
18
Q
Eclipse phase
A
Follows initial infection when all viral particles disappear.
Includes the latent period
19
Q
Latent period
A
“Building the army”
Viral genome takes over host cell machinery and directs production to viral components
20
Q
Early v. Late proteins
A
Early- responsible for preparing for replication of viral nucleic acid
Late- form the viral capsomeres
21
Q
Viral release by cell lyses
A
Common for non-enveloped viruses
Exocytosis more common for enveloped– requires the cell membrane to grab viral envelope
22
Q
Lytic bacteriophage
A
aka virulent
Kills host immediately
23
Q
Lysogenic phase of bacteriophage
A
phage genome becomes prophage by integrating into host chromosome, or existing and replicating independently.
Does not kill the host.
24
Q
Horizontal gene transfer
A
host genome transferred to a new host during packaging. Done by defective phage.
25
Cryptic virus
Those that get stuck in the genome and can't get out
Common in reverse transcriptase viruses.
26
C. diphtheriae and lysogenic prophage
diphtheria toxin is encoded by existent lysogenic prophage. Doesn't require activation of the bacteriophage or getting out of the lysogenic cycle.
27
Factors that determine viral tropism
VAPs in the outer coat--susceptibility
Txt factors present-- expressivity
Cell enzyme pathways to produce viral proteins-- permissivety
28
Receptor for Influenza A on epithelial cells
Sialic acid
29
HIV receptor
CCR5 or CXCR4 CD4+cells
30
Rabies receptor
Acetylcholine receptor on neurons
31
EBV receptor
CR2 (CD21; complement fragment C3d receptor) on B cells
32
Viruses have what kind of genome?
All are haploid except for retroviruses
33
Segmented viral genomes
Reoviruses- dsRNA
| Orthomyoviruses- -ssRNA
34
Diploid viral genomes
Retroviruses- +ssRNA
35
Ambisense viral genomes
Arenaviruses
Bunyaviridae
Both classified as -ssRNA (groupV) but part of the ssRNA is - and other part is +
36
RNA replicase
RNA dependent RNA polymerase
| Makes RNA from RNA
37
DNA replicase
DNA dependent DNA polymerase
| Makes DNA from DNA
38
Reverse transcriptase
RNA dependent DNA polymerase
| Makes DNA from RNA
39
dsDNA viruses
```
Pox
Herpes
Aden
Papilloma
Hepadna (partial)
```
40
ssDNA viruses
Parvo
41
Circular genome viruses
ds: Papillomaviridae
Polyomaviridae
ss: Circoviridae
partially ds: Hepadnaviridae
42
helical +ssRNA viruses
Corona
43
Icosahedral +ssRNA viruses
```
Toga
Flava
Picorna
Calici
Retro
```
44
Icosahedral dsRNA viruses
Reo-- segmented genome
45
helical -ssRNA viruses
```
Paramyxo
Rhabdo
Filo
Orthomyxo
Arena
Bunya
```
46
Group I viruses
dsDNA
47
Group II viruses
+ssDNA
48
Group III viruses
+dsRNA
49
Group IV viruses
+ssRNA
| directly infectious
50
Group V viruses
-ssRNA
| need RNA-dependent RNA polymerase (RNA replicase)
51
Group VI viruses
+ssRNA with RT
52
Group VII
dsDNA with RT
53
Only DNA virus not replicated in the nucleus
Poxviruses- replicated in the cytoplasm
54
IRES element
3D RNA structure- internal ribosomal entry site. Put in place of the 5'CAP on some viruses that replicate in the cytoplasm
55
Boceprevir
targets viral proteases in HCV
56
Saquinavir
targets viral proteases in HIV/AIDS
57
Only RNA viruses that don't replicate in the cytoplasm
Orthomyxo and retro
| both replicate in the nucleus
58
Viral classes that carry RNA replicase
III, IV and V
III and V need it to become +ssRNA
IV needs it after in the host to cope with the -ssRNA produced
59
Viruses with IRES elements
Picornavirus
60
What viruses can become tumorigenic?
Retroviruses
61
Complementation
when one or both viruses infecting a host have defective functions but at different gene location, so rescue each other
ex: HBV and HDV
62
Phenotypic mix
genome of one virus is coat with proteins from another virus genome mixed with the capsid from another virus.
Makes the new virus highly pathogenic
63
Viremia
transmission of virus by blood throughout the entire body
64
HSV1 transmission inside the body
through the trigeminal ganglion
65
HSV2 transmission inside the body
through lumbar and sacral ganglion
66
VZV transmission inside body
trigeminal or thoracic ganglion
67
Rabies transmission in body
Spreads from infected meninges or CSF to the CNS and brain
68
Paralytic poliomyelitis systemic transmission
```
Fecal oral path
Propagation in SI
Reaches the mesenteric lymph nodes
Initial bloodstream viremia
Secondary bloodstream viremia-- brings virus to CNS-- paralysis
```
69
Animal reservoir in Yellow and Dengue fevers
Monkeys
70
Transplacentally transmitted
CMV
parvo B19
Rubella
71
Transmitted at birth
```
HBV
HCV
HSV2
HIV
HPV
```
72
Transmitted by breast feeding
CMV
| Human T-cell lymphotropic virus
73
Congenital infection syndrome of rubella
```
Cataracts
Heart defects: PDA, pull a. stenosis
MR
Microcephaly
Deafness
```
74
Hemagglutination to Detect virus
The virus will cross link the RBCs-- agglutination =positive for the virus
75
Plaque assay
only applicable in lytic viruses
One vision infects one cell-- progeny infect surrounding cells-- several cycles leads to several killed cells and a plaque
76
Neuraminidase
Cleaves silica acid to release newly formed visions from the nucleus.
77
Reyes Syndrome
develops in children with viral illnesses who are given aspirin
May have fever, rash, vomiting, and liver problems
78
Th17 cells
Linked to fungal infections
79
Th1 cells
Linked to intracellular infections
80
Th2 cells
Linked to extracellular infections
81
Immunopathology of exotoxins
drive CD4 activation and the XS release of cytokines
82
Enterotoxins
subgroup of exotoxins that cause non-inflammatory pathology
83
Cytokine Storm
Infectious triggers massive release IFN a/B and of pro-inflammatory cytokines Il-1, IL-6 and TNF-a
Causes vascular leakages, neutrophil activation, fever, chills, coagulation, acute phase protein release, and septic shock
84
Toxic shock
Caused by super Ags. Triggered through endotoxins or cytokine storm.
85
What part of bacteria trigger the inflammatory rxn?
LPS from G-
| Lipoteichoic acid from G+
86
Here rxn
Associated with ant-bacterial tx of Spirochetes.
Seen in borreliosis (lyme disease) and T. palladium (syphilis) case, as well as bartonellosis and trypanosomiasis.
Occurs due to massive release of endotoxin-like products from dying bacteria from tx--> sxs worsen wishing first few hrs, may becomes life threatening
Resembles bacterial sepsis: fever, chills, HA, Myalg, HoTN, flu-like, itch and rashes
87
PANDAS
Pediatric AI Neuropsychiatric Disorders Assoc w/Strep. Infections
Neuropsych sxs linked to GAS (B-hemolytic) infections in children.
Believed to be AI damage of the basal ganglia-- leads to OCD and tics.
88
Sydenham's chorea
aka St. Vitus Dance with Tourette syndrome
Follows acute rheumatic fever.
Similar to PANDAS
89
Asplenic patients
Susceptible to encapsulated organism infections that would normally be cleared through opsonization with Abs.
Risk: pneumococcal, meningococcal, H. influenza infections.
Most serious infections are in 2 years post splenectomy
90
What drives the initial NK response?
Type I interferons, and IL-12
91
Who are more likely to experience cytoxicity from viral infections?
Adults, bc they have more developed immune systems
92
Viral exanthemas
Type III HS rxn.
93
Viral Immunopathogenesis
- Cytotoxicity
- Hypersensitivites
- Autoimmunity
94
Immunopathology of: SLE
Suppresses Treg fxn by cytokine storm
95
Immunopathology of: EBV
Polyclonal activation leading to AI
96
Immunopathology of: Hereditary Angioedema
Defect in regulatory proteins- C1-INH
97
Type I HS rxns
<30min onset
Ag-triggered IgE-dependent release of vasoactive mediators, followed by late-phase rxn.
Anti-parasitic effects and toxin neutralization
Localized Allergies, and Systemic anaphylaxis
98
Type II HS rxn
<8hr
Cell-bound Ab promotes complement mediated cytotoxicity.
Beneficial: lysis and phagocytosis of extra cell. bacteria
Pathologic: Destroys RBCs (in transfusions and Rh disease) Organ damage in some AI diseases (Goodpasture's)
99
Infectious Type II HS rxns
GBS- caused by c. jejuni
Dengue
Pika
CMV (HHV-5)
Ag mimicry in:
Acute RF (follows strep infection)
RBC lysis bc of ABO incompatibility
100
Type III HS rxn
<8hr
Ag-Ab complexes activate complement
Beneficial: Helps clear extracellular microbes, by inflam rxn at the site.
Path: Arthus rxn (localized), Serum sickness (generalized), systemic AI diseases
101
Infectious Type III HS rxns
```
Staph infective endocarditis
Strep glomerulonephritis
SLE
RA
Arthus rxn
Serum-sickness
```
102
Type IV HS rxn
24-72 acute
>1 week chronic
Phagocytized soluble Ag is presented to CD4 cells--> activates macros and inflammation
Beneficial: Protects against fungal infections, intracell bacteria and viruses
Path: acute- contact dermatitis, TB skin test
Chronic: granuloma formation
103
Examples of Type IV HS rxns
```
Bacterial:
TB
Leprosy
Parasitic:
Schistosomiasis
Unknown:
Sarcoidosis
Chron's
```
104
C1, C4, and C2 deficiencies
immune complex diseases
SLE
pyogenic infection (strep and staph)
105
C3 deficiency
Severe bacterial infections
106
Alternative pathway deficiencies
Properdin, Factor B and D
results in severe pyogenic infections
NO immune complex disorders
107
MAC complex deficiencies
Neisseria spp. infections
108
C1-Inhibitor deficiency
Hereditary Angioedema
109
Leukocyte Adhesion Def.
LAD-1- AR mutation in B2 integrin CD18- component of LFA-1 which mediated adhesion of T, B cells, macros and neutron to endothelial cells.
Neutron can't migrate to infected site-- pyogenic infections
Delayed umbilical cord separation.
110
CGD
impaired NADPH oxidase
Pathogens are phagocytyzed but not digested.
XL or AR
Granulomas form at site of infection
Common opportunistic infections: S. aureus, Aspergillus fumigatus and candida
111
Duncan Syndrome
aka XL lymphoproliferative syndrome
no sxs until infected with EBV!!!
in Males
Mutation of SH2 on SAP signaling protein impairs activation of T and NK cells.
T cells are incapable of killing EBV-infected B cells.
T cells proliferate-- increased risk of lymphoma other lymphoproliferative diseases
112
Sxs of Duncan syndrome
Fulminant infectious mononucleosis
Hypogammaglobulinemia
Lymphoma
Hemophagocytic lymphohistiocystosis
Poor prognosis- most die before 10
113
Ataxia-Telangiectasia
ATM gene mutation--codes for serine/threonine protein kinase involved in DNA repair.
Neurodegen disorder with telangiectasia (dilation of sm. BVs- seen in eyes mostly)
114
Immunopath of Ataxia Telangiectasia
Defect in repair of dsDNA breaks during VDJ recombination and class switch.
Affects:
T cells
B cell #s, with normal IgM, but vv. low IgG, E, and A.
Low blood lymphos
115
Wiskott-Aldrich
Triad in boys:
Pyogenic infections
Severe eczema
Thrombocytopenia
XL mutation in WASp gene expressed in hematopoietic stem cells. Responsible for actin cytoskeleton rearrangement
116
Ab profile in Wiskott-Aldrich
Reduced IgM
IgA and IgE elevated
IgG may be norm, elevated or reduced
117
What triggers outbursts of HSV-1
UV
Stress
Sickness
118
Persistent v. Latent Infection
Persistent- the virus is present and replicating. These pts can infect others even if they are asx
Latent- the virus is present, but not replicating. These pts cannot infect others until reactivated
119
Silent-subclinical
Life-long infection
| Can infect others
120
Progressive multifocal leukoencephalopathy
Presents after infection with JC polyomavirus.
121
JC polyomavirus
Has slow infection. Is latent for years and then later may present as PML in immunocompromised patients
122
CPE
the observed changes in the virus infected cell culture.
Rounded cell shape form
Darkening of cytoplasm
Eventual lysis or giant cells
Inclusion bodies
123
Negri bodies
Intracytoplasmic eosinophilic inclusion bodies in nerve cells infected with Rabies
124
Owl's eye
intranuclear basophilic inclusion bodies in CMV infected cells
125
Viruses that form syncytia
Herpesviruses
| Paramyxoviruses
126
Immune complex initiated arthritis
Caused by:
Early HBV infection
parvovirus B19
Rubella
127
6 childhood exanthems
```
1- Measles
2- Scarlet Fever
3- Rubella (German Measles)
4- Duke's disease
5- Erythema Infectiosum
6- Roseola
```
128
Viral immunopathogenesis assoc with CD8 T cells
Strong immune responses may be triggered and then worsen sxs or disease.
Immunocompetent may have exacerbation of sxs or disease bc of a strong immune response, where as compromised cannot mount a response and the virus continues to replicate without causing damage from the CD8 cells
Seen in lymphocytic choriomeningitis
129
Infections assoc w/AI diseases
HBV- MS
HCV- Mixed cryoglobulinemia
CMV- Scleroderma
130
Dengue Virus infection
Flavivirus
| High fever, myalgia, lymphadenopathy, bone and joint pain, HA, and MACULOPAPULAR RASH.
131
Dengue hemorrhagic fever/Dengue shock syndrome
Due to Ab-dependent enhancement- in previously infected patients who have pre-formed Abs to the virus-- get more intense immune response on second exposure.
132
Oncogenic viruses
```
HTLV-1
HBV
HCV
HPV 16 & 18 (32 and 33 too)
HHV-8
EBV
```
133
Burkitt Lymphoma
caused by EBV
134
Kaposi-sarcoma
caused by HHV-8
tumor of blood vessel walls
Common in HIV patients
Pink/red lesions on skin and mouth
135
Oncogenes of HPV
E6-- inhibits p53
| E7-- inhibits Rb
136
Oncogenes of Adenoviruses
E1A-- inhibits Rb
| E1B-- inhibits p53
137
HTLV-1
only human oncogenic retrovirus.
Cancer formation linked to TAX transactivator gene.
Has long latency period.
138
EBV/HHV-4 oncogenesis
Immortalizes B cells- produces potent B-cell mitogen and prevents apoptosis, produces inhibitory cytokines.
Linked to: Hodgkin lymphoma, Burkitt lymphoma, gastric ca. AIDS, nasopharyngeal ca, post-transplant lymphoproliferative disease
139
virokines
interfere w cytokine activity-- fxn exactly opposite of them.
140
Viral evasion
May infect immunoprivileged sites in body-- like HSV hiding in ganglia.
Direct infection of immune cells- causes immunosuppression.
Down regulation of molecules involved in immune recognition (LFA-3, ICAM-1 by EBV)
Down regulation of MHC-I expression (adenovirus)
141
HSV evasion from the immune system
Inhibits Ag presentation. HSV protein interferes with the TAP transporter
142
CMV evasion from the immune system
Inhibits Ag-presentation and proteasomal activity. Removes MHC-1 molecules from the ER.
143
EBV evasion from the immune system
Inhibits Ag-presentation and proteasomal activity. Produces IL-10 (inhibitory cytokine) to inhibit macrophage and DC activation
144
Pox virus immune evasion
Inhibits effector cell activation, and produces decoy-receptors to block cytokine activation of effector cells.
