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Pre-Midterm Micro > Viruses > Flashcards

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

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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

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3
Q

Triple Shell Capsid

A

Seen in rotavirus- has outer coat, middle shell/capsid and inner layer.

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4
Q

Bacteriophages

A 
Bacterial viruses
Head- NA and protein
Tail and contractive sheath
Tail fibers and tail pins
Base/end plate
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5
Q

Peplomers

A

Spike-like viral glycoproteins. Attach to receptors on host cell. Are on the capsid or envelope

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6
Q

Matrix proteins

A

inside the envelope. Help assemble the nucleocapsid

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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

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8
Q

HA (hemagglutinin)

A

VAP on influenza- binds RBCs and helps enter host cell.

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9
Q

VAP on EBV

A

Binds C3d receptor (CR2) on B cells- facilitates entry into host cell.

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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

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11
Q

Rhabdovirus envelope

A

bullet shaped

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12
Q

Poxvirus envelope

A

Complex structure. No simple symmetry.

Brick-like external shelf.

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13
Q

Pseudovirions

A

wrong DNA is packed instead of the viral genome.

Can infect a host, but cannot repicate

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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

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15
Q

Defective/Satelite virus

A

Cant replicate without helper virus (HDV needs HBV)

Cannot infect host on its own.

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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.

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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
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18
Q

Eclipse phase

A

Follows initial infection when all viral particles disappear.
Includes the latent period

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19
Q

Latent period

A

“Building the army”

Viral genome takes over host cell machinery and directs production to viral components

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20
Q

Early v. Late proteins

A

Early- responsible for preparing for replication of viral nucleic acid

Late- form the viral capsomeres

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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

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22
Q

Lytic bacteriophage

A

aka virulent

Kills host immediately

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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.

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24
Q

Horizontal gene transfer

A

host genome transferred to a new host during packaging. Done by defective phage.

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25
Q

Cryptic virus

A

Those that get stuck in the genome and can’t get out

Common in reverse transcriptase viruses.

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26
Q

C. diphtheriae and lysogenic prophage

A

diphtheria toxin is encoded by existent lysogenic prophage. Doesn’t require activation of the bacteriophage or getting out of the lysogenic cycle.

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27
Q

Factors that determine viral tropism

A

VAPs in the outer coat–susceptibility
Txt factors present– expressivity
Cell enzyme pathways to produce viral proteins– permissivety

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28
Q

Receptor for Influenza A on epithelial cells

A

Sialic acid

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29
Q

HIV receptor

A

CCR5 or CXCR4 CD4+cells

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30
Q

Rabies receptor

A

Acetylcholine receptor on neurons

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31
Q

EBV receptor

A

CR2 (CD21; complement fragment C3d receptor) on B cells

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32
Q

Viruses have what kind of genome?

A

All are haploid except for retroviruses

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33
Q

Segmented viral genomes

A

Reoviruses- dsRNA

Orthomyoviruses- -ssRNA

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34
Q

Diploid viral genomes

A

Retroviruses- +ssRNA

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35
Q

Ambisense viral genomes

A

Arenaviruses
Bunyaviridae
Both classified as -ssRNA (groupV) but part of the ssRNA is - and other part is +

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36
Q

RNA replicase

A

RNA dependent RNA polymerase

Makes RNA from RNA

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37
Q

DNA replicase

A

DNA dependent DNA polymerase

Makes DNA from DNA

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38
Q

Reverse transcriptase

A

RNA dependent DNA polymerase

Makes DNA from RNA

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39
Q

dsDNA viruses

A 
Pox
Herpes
Aden
Papilloma
Hepadna (partial)
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40
Q

ssDNA viruses

A

Parvo

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41
Q

Circular genome viruses

A

ds: Papillomaviridae
Polyomaviridae
ss: Circoviridae
partially ds: Hepadnaviridae

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42
Q

helical +ssRNA viruses

A

Corona

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43
Q

Icosahedral +ssRNA viruses

A 
Toga
Flava
Picorna
Calici
Retro
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44
Q

Icosahedral dsRNA viruses

A

Reo– segmented genome

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45
Q

helical -ssRNA viruses

A 
Paramyxo
Rhabdo
Filo
Orthomyxo
Arena
Bunya
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46
Q

Group I viruses

A

dsDNA

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47
Q

Group II viruses

A

+ssDNA

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48
Q

Group III viruses

A

+dsRNA

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49
Q

Group IV viruses

A

+ssRNA

directly infectious

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50
Q

Group V viruses

A

-ssRNA

need RNA-dependent RNA polymerase (RNA replicase)

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51
Q

Group VI viruses

A

+ssRNA with RT

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52
Q

Group VII

A

dsDNA with RT

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53
Q

Only DNA virus not replicated in the nucleus

A

Poxviruses- replicated in the cytoplasm

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54
Q

IRES element

A

3D RNA structure- internal ribosomal entry site. Put in place of the 5’CAP on some viruses that replicate in the cytoplasm

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55
Q

Boceprevir

A

targets viral proteases in HCV

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56
Q

Saquinavir

A

targets viral proteases in HIV/AIDS

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57
Q

Only RNA viruses that don’t replicate in the cytoplasm

A

Orthomyxo and retro

both replicate in the nucleus

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58
Q

Viral classes that carry RNA replicase

A

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
Q

Viruses with IRES elements

A

Picornavirus

60
Q

What viruses can become tumorigenic?

A

Retroviruses

61
Q

Complementation

A

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
Q

Phenotypic mix

A

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
Q

Viremia

A

transmission of virus by blood throughout the entire body

64
Q

HSV1 transmission inside the body

A

through the trigeminal ganglion

65
Q

HSV2 transmission inside the body

A

through lumbar and sacral ganglion

66
Q

VZV transmission inside body

A

trigeminal or thoracic ganglion

67
Q

Rabies transmission in body

A

Spreads from infected meninges or CSF to the CNS and brain

68
Q

Paralytic poliomyelitis systemic transmission

A 
Fecal oral path
Propagation in SI
Reaches the mesenteric lymph nodes
Initial bloodstream viremia
Secondary bloodstream viremia-- brings virus to CNS-- paralysis
69
Q

Animal reservoir in Yellow and Dengue fevers

A

Monkeys

70
Q

Transplacentally transmitted

A

CMV
parvo B19
Rubella

71
Q

Transmitted at birth

A 
HBV
HCV
HSV2
HIV
HPV
72
Q

Transmitted by breast feeding

A

CMV

Human T-cell lymphotropic virus

73
Q

Congenital infection syndrome of rubella

A 
Cataracts
Heart defects: PDA, pull a. stenosis
MR
Microcephaly
Deafness
74
Q

Hemagglutination to Detect virus

A

The virus will cross link the RBCs– agglutination =positive for the virus

75
Q

Plaque assay

A

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
Q

Neuraminidase

A

Cleaves silica acid to release newly formed visions from the nucleus.

77
Q

Reyes Syndrome

A

develops in children with viral illnesses who are given aspirin
May have fever, rash, vomiting, and liver problems

78
Q

Th17 cells

A

Linked to fungal infections

79
Q

Th1 cells

A

Linked to intracellular infections

80
Q

Th2 cells

A

Linked to extracellular infections

81
Q

Immunopathology of exotoxins

A

drive CD4 activation and the XS release of cytokines

82
Q

Enterotoxins

A

subgroup of exotoxins that cause non-inflammatory pathology

83
Q

Cytokine Storm

A

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
Q

Toxic shock

A

Caused by super Ags. Triggered through endotoxins or cytokine storm.

85
Q

What part of bacteria trigger the inflammatory rxn?

A

LPS from G-

Lipoteichoic acid from G+

86
Q

Here rxn

A

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
Q

PANDAS

A

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
Q

Sydenham’s chorea

A

aka St. Vitus Dance with Tourette syndrome
Follows acute rheumatic fever.

Similar to PANDAS

89
Q

Asplenic patients

A

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
Q

What drives the initial NK response?

A

Type I interferons, and IL-12

91
Q

Who are more likely to experience cytoxicity from viral infections?

A

Adults, bc they have more developed immune systems

92
Q

Viral exanthemas

A

Type III HS rxn.

93
Q

Viral Immunopathogenesis

A
  • Cytotoxicity
  • Hypersensitivites
  • Autoimmunity
94
Q

Immunopathology of: SLE

A

Suppresses Treg fxn by cytokine storm

95
Q

Immunopathology of: EBV

A

Polyclonal activation leading to AI

96
Q

Immunopathology of: Hereditary Angioedema

A

Defect in regulatory proteins- C1-INH

97
Q

Type I HS rxns

A

<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
Q

Type II HS rxn

A

<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
Q

Infectious Type II HS rxns

A

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
Q

Type III HS rxn

A

<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
Q

Infectious Type III HS rxns

A 
Staph infective endocarditis
Strep glomerulonephritis
SLE
RA
Arthus rxn
Serum-sickness
102
Q

Type IV HS rxn

A

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
Q

Examples of Type IV HS rxns

A 
Bacterial:
   TB
   Leprosy
Parasitic:
   Schistosomiasis
Unknown:
   Sarcoidosis
   Chron's
104
Q

C1, C4, and C2 deficiencies

A

immune complex diseases
SLE
pyogenic infection (strep and staph)

105
Q

C3 deficiency

A

Severe bacterial infections

106
Q

Alternative pathway deficiencies

A

Properdin, Factor B and D
results in severe pyogenic infections
NO immune complex disorders

107
Q

MAC complex deficiencies

A

Neisseria spp. infections

108
Q

C1-Inhibitor deficiency

A

Hereditary Angioedema

109
Q

Leukocyte Adhesion Def.

A

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
Q

CGD

A

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
Q

Duncan Syndrome

A

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
Q

Sxs of Duncan syndrome

A

Fulminant infectious mononucleosis
Hypogammaglobulinemia
Lymphoma
Hemophagocytic lymphohistiocystosis

Poor prognosis- most die before 10

113
Q

Ataxia-Telangiectasia

A

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
Q

Immunopath of Ataxia Telangiectasia

A

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
Q

Wiskott-Aldrich

A

Triad in boys:
Pyogenic infections
Severe eczema
Thrombocytopenia

XL mutation in WASp gene expressed in hematopoietic stem cells. Responsible for actin cytoskeleton rearrangement

116
Q

Ab profile in Wiskott-Aldrich

A

Reduced IgM
IgA and IgE elevated
IgG may be norm, elevated or reduced

117
Q

What triggers outbursts of HSV-1

A

UV
Stress
Sickness

118
Q

Persistent v. Latent Infection

A

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
Q

Silent-subclinical

A

Life-long infection

Can infect others

120
Q

Progressive multifocal leukoencephalopathy

A

Presents after infection with JC polyomavirus.

121
Q

JC polyomavirus

A

Has slow infection. Is latent for years and then later may present as PML in immunocompromised patients

122
Q

CPE

A

the observed changes in the virus infected cell culture.

Rounded cell shape form
Darkening of cytoplasm
Eventual lysis or giant cells
Inclusion bodies

123
Q

Negri bodies

A

Intracytoplasmic eosinophilic inclusion bodies in nerve cells infected with Rabies

124
Q

Owl’s eye

A

intranuclear basophilic inclusion bodies in CMV infected cells

125
Q

Viruses that form syncytia

A

Herpesviruses

Paramyxoviruses

126
Q

Immune complex initiated arthritis

A

Caused by:
Early HBV infection
parvovirus B19
Rubella

127
Q

6 childhood exanthems

A 
1- Measles
2- Scarlet Fever
3- Rubella (German Measles)
4- Duke's disease
5- Erythema Infectiosum
6- Roseola
128
Q

Viral immunopathogenesis assoc with CD8 T cells

A

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
Q

Infections assoc w/AI diseases

A

HBV- MS
HCV- Mixed cryoglobulinemia
CMV- Scleroderma

130
Q

Dengue Virus infection

A

Flavivirus

High fever, myalgia, lymphadenopathy, bone and joint pain, HA, and MACULOPAPULAR RASH.

131
Q

Dengue hemorrhagic fever/Dengue shock syndrome

A

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
Q

Oncogenic viruses

A 
HTLV-1
HBV
HCV
HPV 16 &amp; 18 (32 and 33 too)
HHV-8
EBV
133
Q

Burkitt Lymphoma

A

caused by EBV

134
Q

Kaposi-sarcoma

A

caused by HHV-8
tumor of blood vessel walls
Common in HIV patients
Pink/red lesions on skin and mouth

135
Q

Oncogenes of HPV

A

E6– inhibits p53

E7– inhibits Rb

136
Q

Oncogenes of Adenoviruses

A

E1A– inhibits Rb

E1B– inhibits p53

137
Q

HTLV-1

A

only human oncogenic retrovirus.
Cancer formation linked to TAX transactivator gene.
Has long latency period.

138
Q

EBV/HHV-4 oncogenesis

A

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
Q

virokines

A

interfere w cytokine activity– fxn exactly opposite of them.

140
Q

Viral evasion

A

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
Q

HSV evasion from the immune system

A

Inhibits Ag presentation. HSV protein interferes with the TAP transporter

142
Q

CMV evasion from the immune system

A

Inhibits Ag-presentation and proteasomal activity. Removes MHC-1 molecules from the ER.

143
Q

EBV evasion from the immune system

A

Inhibits Ag-presentation and proteasomal activity. Produces IL-10 (inhibitory cytokine) to inhibit macrophage and DC activation

144
Q

Pox virus immune evasion

A

Inhibits effector cell activation, and produces decoy-receptors to block cytokine activation of effector cells.

Pre-Midterm Micro (8 decks)

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