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Virology Flashcards

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Biology 101 flashcards
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
Q

Examples of Type II Hypersensitivities

A

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

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26
Q

Type III Hypersensitivity

A

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

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27
Q

Infectious cause of Type III Hypersensitivity

A

Staph infective endocarditis, strep glomerulonephritis, Arthus Rxn, Serum Sickness-like post-infectious Rxn (viral infections)
*SLE and RA

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28
Q

Type IV Hypersensitivity

A

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
Q

Granuloma

A

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
Q

C5-C9 deficiency

A

Present with recurrent Neisseria infections (MAC can’t form)

31
Q

Titer

A

Amount of dilution of virus until no hemagglutination occurs (and the RBCs sediment in the bottom)

32
Q

Hepatitis D Virus (HDV)

A

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
Q

Eclipse phase

A

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
Q

Early Proteins

A

Responsible for initial behavior of the virus and prep for replication of viral nucleic acid (non-structural proteins)

35
Q

Late Proteins

A

Participate in formation of the viral capsomeres such as structural proteins

36
Q

HCV and HIV drug targets

A

Viral proteases as targets

37
Q

Latent Viral Infection

A

Varicella-Zoster (HHV3) presents as chicken pox (varicella) but in secondary presents as herpes zoster aka shingles
*trigeminal or thoracic ganglion

38
Q

Latency in HSV-1

A

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
Q

Chronic Viral Infection

A

HBV and HCV - can lead to HCC eventually

40
Q

Silent Subclinical Viruses

A

Life-long infection

E.g. - CMV and EBV

41
Q

Slow Infections

A

Long incubation period effort dz presentation

E.g. - JC virus and prions

42
Q

JC Virus

A

Family: polyoma
Dz: can present as Progressive Multifocal Leukoencephalopathy (PML)

43
Q

BK Virus

A

Family: polyoma
Dz: BK nephropathy

44
Q

Measles (latency)

A

Aka German Measles
Family: paramyxo
Dz: Subacute Sclerosing Panencephalitis (SSPE)
Latency: 1-10 years

45
Q

Rubella (latency)

A

Family: toga
Dz: Progressive Rubella Panencephalitis
Latency: 10-20 years

46
Q

HIV (latency)

A

Family: retro
Dz: AIDS
Latency: 5-10

47
Q

Rabies (latency)

A

Family: rhabdo
Dz: rabies
Latency: 3-12 weeks
*Negri bodies inclusions in neuron cytoplasm

48
Q

HTLV (latency)

A

Family: retro
Dz: leukemia/lymphoma of T cells
Latency: 10-30 years

49
Q

Syncytial Formation

A

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
Q

Rotavirus (symptoms)

A

Mechanism: initiates stimulation of enteric nervous system
ROS: cause diarrhea likely due to excessive cytokine production and fluid release

51
Q

Arthritis caused by viruses

A

Early HBV, parvo B19, rubella

52
Q

Viral Exanthemas

A

Abrupt appearance of skin rash affecting several areas simultaneously
E.g. - measles, rubella (German measles), parvo B19, HHV-6 and HHV-7

53
Q

Enanthema

A

Mucous membrane eruption

54
Q

Viral Immunopathogenesis (cause)

A

Attributed to or driven by cytotoxic CD8+ T cells or Ab production

55
Q

Dengue

A

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
Q

Ab-Dependent Enhancement (ADE) in Dengue

A

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
Q

Oncogenic Viruses

A

HTLV, HBV, HCV, HPV 16 and 18, EBV, HHV-8

*DNA viruses are more common drivers of tumorigenesis in humans

58
Q

HTLV-1 (oncogenesis)

A

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
Q

HHV-8 (oncogenesis)

A

Susceptibility of developing Kaposi Sarcoma when immunocompromised
*most frequent tumor in AIDS pt’s

60
Q

EBV (HHV-4) …oncogenesis

A

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
Q

Negri Bodies

A

Inclusion bodies in cytoplasm of nerve cells infected w/ rabies

62
Q

Owl’s Eyes

A

Inclusions in nucleus of CMV infected cells

63
Q

Pox Virus

A

Structure: complex
Replication: cytoplasm
Inclusions: intracytoplasmic acidophilic inclusions
Evasion: produces decoy receptors

64
Q

Reovirus (inclusions)

A

Perinuclear cytoplasmic acidophilic inclusions

65
Q

Virokines

A

Viral products that interfere with host cytokine activity

E.g. EBV produces IL-10 (anti-inflammatory cytokine)

66
Q

HSV

A

Pathogenesis: initiates apoptosis leading to fragmentation of host genome then cell lysis
Evasion: fucks with TAP transporter

67
Q

Poliovirus (pathogenesis)

A

Inhibits cellular Initiation Fator (IF) in protein synthesis in neurons

68
Q

Adenoviruses

A

Pathogenesis: round, swollen cells that can climb together
Oncogenesis: through E1A and E1B

69
Q

Measles

A

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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