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Virology Flashcards

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1
Q

HPV (oncogenesis)

A

Localized infection - skin warts
Oncogenic: via E6 disabling host Rb and E7 acting on host’s p53
*can cause squamous cell carcinoma of cervix

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2
Q

Lysogenic (Temperate) Virus

A

Lysogenic cycle - host cell multiplies and daughter cells contain the prophage

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3
Q

Lytic (Virulent) Virus

A

Kills host immediately; particles released by host cell lysis or budding

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4
Q

EBV (oncogenesis and evasion mechanism)

A

Receptor: CR2
Cell: B cell
Evasion: produces IL-10 (anti-inflamm. cytokine)
*silent sub-clinical virus

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5
Q

HIV (tropism)

A

Receptor: CD4 (plus CCR5 and CXR4 on macrophage)
Cell: Th and Macrophages

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6
Q

Influenza A (tropism)

A

Receptor: Sialic acid (Neuraminidase on virus breaks down sialic acid in order for aggregated virions to bud out of the cell)
Cell: epithelial cell

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7
Q

Rabies (tropism and inclusions)

A 
Receptor: nicotenic ACh
Cell: neurons
Inclusions: Negri bodies
Mechanism: retrograde, affects CNS eventually 
"slow virus"
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8
Q

Viral Attachment Proteins (VAP)

A

Viral glycoproteins located on the outer leaflet (envelope for enveloped viruses OR the capsid for naked viruses)
*contributes to the viral “tropism”

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9
Q

RNA Dependent RNA-Pol (RNA Replicase)

A

Group IV codes for RR, Group III and V code for RR and also contains the enzyme in their virion

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10
Q

Antigenic Drift

A

Small change in a genome w/in specific strain, happens at slow rate compared to Ag Shift
*type of antigenic variation (e.g. - orthomyxo specifically influenza virus)

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11
Q

Antigenic Shift

A

Mix and match of chromosomes btwn 2 diff strains of virus - faster change than drift
*reassortment of genome (type of antigenic variation)

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12
Q

Phenotypic Mix

A

Genome of 1 virus is coated w/ proteins from another viral genome mixed w/ capsid from another virus

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13
Q

Viremia

A

Transmission of virus by blood throughout the entire body reaching distant organs

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14
Q

Paralytic Poliomyelitis

A

Fecal-oral path w/ initial propagation in SI followed by viral reach to mesenteric lymph nodes

  • initial viremia bloodstream brings virus to some organs
  • secondary viremia brings virus to CNS
  • IgG produced
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15
Q

Incubation Period

A

Pt is asymptomatic (virus enters host cell and is not detectable)

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16
Q

Prodromal Period

A

Non-specific sx’s present

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17
Q

Specific-illness Period

A

Specific sx’s signature of certain viral dz

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18
Q

Recovery Period

A

Healing of dz, or can move into chronic state or cause infection at a secondary site

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19
Q

Congenital Rubella

A

ROS: cataracts, patent ductus arteriosus (PDA), intellectual disability, microcephaly, deafness
*transplacental transmission

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20
Q

Cytomegalovirus (CMV)

A

Inclusions: “owl’s eye” in nucleus
Evasion: blocks MHC-I being presented
*can be transmitted trans-placental or breastfeeding
(Most common viral cause of death in BMT pt’s)

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21
Q

Virus eradicated by vaccine?

A

Smallpox

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22
Q

Type I Hypersensitivity

A

Mediator: IgE and vasoactive mediators (mast cell degranulation)
Benefits: anti-parasitic responses and toxin neutralization
Pathologic effects: localized allergies, systemic anaphylaxis

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23
Q

Microbes involved in Pulmonary Type I Hypersensitivity

A

Molds: leads to asthma

G-ve: leads to organic dust toxic syndrome or Asthma

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24
Q

Type II Hypersensitivity

A

Mediator: IgG w/ Ag
Mechanism: complement mediated cytotoxicity, or modification of cell surface receptor function
Benefit: lysis/phagocytosis of extracellular microbes
Pathologic effect: RBC destruction, tissue damage

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25
Examples of Type II Hypersensitivities
Infectious cause: Guillan-Barre, Dengue and Zika, CMV (HHV-5) Ag mimicry: acute RF following strep throat infection, RBC lysis due to ABO incompatibility Drug induced: penicillin allergy
26
Type III Hypersensitivity
Mediator: IgG w/ soluble Ag (immune complex) Mechanism: complement activation Benefit: acute inflamm @ site of extracellular microbes Pathologic effect: Arthus rxn, serum sickness and generalized drug rxn's
27
Infectious cause of Type III Hypersensitivity
Staph infective endocarditis, strep glomerulonephritis, Arthus Rxn, Serum Sickness-like post-infectious Rxn (viral infections) *SLE and RA
28
Type IV Hypersensitivity
Mediator: Cell-mediated, Ab independent Mechanism: phagocytized soluble ag presented to CD4+ T cells activates macrophages and inflammation Benefit: protects against fungi, intracellular bacteria and viruses Pathologic effect: acute - contact dermatitis, Tb skin test; chronic - granuloma formation
29
Granuloma
Aggregate of cells aiming to wall-off and isolate structures that cannot be otherwise killed/expelled E.g. - TB, leprosy, schistosomiasis, sarcoidosis and Crohn's dz
30
C5-C9 deficiency
Present with recurrent Neisseria infections (MAC can't form)
31
Titer
Amount of dilution of virus until no hemagglutination occurs (and the RBCs sediment in the bottom)
32
Hepatitis D Virus (HDV)
Satellite virus, requires HBV as helper virus | Cell entry: requires HD antigen from HDV and HB antigen from HBV to allow host cell entry
33
Eclipse phase
After initial infection the viral particles enter host cells so they "disappear", this is the latent period until new visions are assembled (which is done by self-assembly)
34
Early Proteins
Responsible for initial behavior of the virus and prep for replication of viral nucleic acid (non-structural proteins)
35
Late Proteins
Participate in formation of the viral capsomeres such as structural proteins
36
HCV and HIV drug targets
Viral proteases as targets
37
Latent Viral Infection
Varicella-Zoster (HHV3) presents as chicken pox (varicella) but in secondary presents as herpes zoster aka shingles *trigeminal or thoracic ganglion
38
Latency in HSV-1
Resides in trigeminal ganglion, the first/acute infection is worse *reactivation by UV, stress, illness and the sores are not as bad as the first time
39
Chronic Viral Infection
HBV and HCV - can lead to HCC eventually
40
Silent Subclinical Viruses
Life-long infection | E.g. - CMV and EBV
41
Slow Infections
Long incubation period effort dz presentation | E.g. - JC virus and prions
42
JC Virus
Family: polyoma Dz: can present as Progressive Multifocal Leukoencephalopathy (PML)
43
BK Virus
Family: polyoma Dz: BK nephropathy
44
Measles (latency)
Aka German Measles Family: paramyxo Dz: Subacute Sclerosing Panencephalitis (SSPE) Latency: 1-10 years
45
Rubella (latency)
Family: toga Dz: Progressive Rubella Panencephalitis Latency: 10-20 years
46
HIV (latency)
Family: retro Dz: AIDS Latency: 5-10
47
Rabies (latency)
Family: rhabdo Dz: rabies Latency: 3-12 weeks *Negri bodies inclusions in neuron cytoplasm
48
HTLV (latency)
Family: retro Dz: leukemia/lymphoma of T cells Latency: 10-30 years
49
Syncytial Formation
Instead of killing host cell, virus stimulates host cell to fuse with other cells leading to multinucleated giant cells (syncytia) E.g. - paramyxo (RSV, measles, mumps), HSV-1, HSV-2, HIV
50
Rotavirus (symptoms)
Mechanism: initiates stimulation of enteric nervous system ROS: cause diarrhea likely due to excessive cytokine production and fluid release
51
Arthritis caused by viruses
Early HBV, parvo B19, rubella
52
Viral Exanthemas
Abrupt appearance of skin rash affecting several areas simultaneously E.g. - measles, rubella (German measles), parvo B19, HHV-6 and HHV-7
53
Enanthema
Mucous membrane eruption
54
Viral Immunopathogenesis (cause)
Attributed to or driven by cytotoxic CD8+ T cells or Ab production
55
Dengue
Family: flavivirus (4 serotypes) ROS: high fever, lymphadenopathy, myalgia, pain, HA, maculopapular rash Complication: hemorrhagic fever due to ADE *antibody dependent enhancement (ab to a diff serotype enhances the pathogenicity of the new serotype infecting the host)
56
Ab-Dependent Enhancement (ADE) in Dengue
Initial infection with stereotype 1, and subsequent infection with stereotype 2 the Ab's will be produced for 1 and only partially block serotype 2 *does not enhance killing but facilitates infection by serotype 2
57
Oncogenic Viruses
HTLV, HBV, HCV, HPV 16 and 18, EBV, HHV-8 | *DNA viruses are more common drivers of tumorigenesis in humans
58
HTLV-1 (oncogenesis)
Family: retro Oncogenesis: linked to TAX transactivator gene which works on activating viral transcription and on promoters in terminal viral LTR region Dz: adult T cell lymphoma
59
HHV-8 (oncogenesis)
Susceptibility of developing Kaposi Sarcoma when immunocompromised *most frequent tumor in AIDS pt's
60
EBV (HHV-4) ...oncogenesis
Oncogenesis: immortalizes B cells by producing a potent B cell nitrogen and by preventing apoptosis Dz: Hodgkin lymphoma, Burkitt lymphoma, gastric ca, nasopharyngeal carcinoma
61
Negri Bodies
Inclusion bodies in cytoplasm of nerve cells infected w/ rabies
62
Owl's Eyes
Inclusions in nucleus of CMV infected cells
63
Pox Virus
Structure: complex Replication: cytoplasm Inclusions: intracytoplasmic acidophilic inclusions Evasion: produces decoy receptors
64
Reovirus (inclusions)
Perinuclear cytoplasmic acidophilic inclusions
65
Virokines
Viral products that interfere with host cytokine activity | E.g. EBV produces IL-10 (anti-inflammatory cytokine)
66
HSV
Pathogenesis: initiates apoptosis leading to fragmentation of host genome then cell lysis Evasion: fucks with TAP transporter
67
Poliovirus (pathogenesis)
Inhibits cellular Initiation Fator (IF) in protein synthesis in neurons
68
Adenoviruses
Pathogenesis: round, swollen cells that can climb together Oncogenesis: through E1A and E1B
69
Measles
Aka Rubeola Family: Paramyxo *"Three C's": cough, coryza, conjunctivitis *Koplik spots: gray-white spots on buccal mucosa

Microbiology (14 decks)

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