Microbiology Virology

Front 1

3 outcomes of a viral infection?

Back 1

1. Abortive/failed
2. Cell death (lytic)
3. Virus production w/o death (nonlytic). These are presistent.

Front 2

3 categories of persistent infections.

Back 2

1. Chronic.
2. Latent.
3. Transforming.

Front 3

5 characteristics of viruses.

Back 3

1. Obligate intracellular parasites.
2. Lack ATP synthetic machinery.
3. Lack protein synthetic machinery.
4. Lack complex enzymes for metabolism.
5. Rely on host cells for most of replication.

Front 4

6 ways viruses can affect the host cell.

Back 4

1. Shut down host cell protein translation, causing cell death.
2. change growth properties of cell.
3. Change stability/regulation of hot proteins.
4. Change host RNA synethesis.
5. Change host DNA replication.
6. Change host anti-viral response.

Front 5

Describe virus structure.

Back 5

Contains:
1. Capsid = protein shell surrounding genome. Either icosahedral or helical.
2. Envelope = makes nonstable b/c requires aqueous environment.

Front 6

6 steps in viral life cycle.

Back 6

1. Attachment.
2. Entry.
3. Uncoating
4. Replication.
5. Assembly.
6. Release.

Front 7

Describe how virus enters the cell:
a. naked
b. enveloped

Back 7

a. Naked via receptor-mediated endocytosis;

b. Enveloped by either:
1. Receptor-mediated endocytosis, or
2. Membrane fusion w/cytoplasmic membrane.

Front 8

What is the eclipse period?

Back 8

Time when nucleic acid is inside the cell,but is not infectious.

Front 9

How does replication/translation of DNA & RNA viruses differ?

Back 9

DNA - use host RNA/DNA polymerase.
RNA - use viral transcriptase.

Front 10

Where do nonenveloped DNA viruses replicate? nonenveloped RNA viruses?

Back 10

DNA in nucleus.
RNA in cytoplasm.
(CHECK ON THIS INFO)

Front 11

What is a serotype?

Back 11

Different antigens on the capsid. Neutralizing Ab differ for each serotype.

Front 12

3 factors that affect the extent of a viral disease.

Back 12

1. Host range (what types of cells are injected)
2. dose/pathogenicity
3. State of host.

Front 13

List 3 small DNA viruses.

Back 13

1. Adenovirus
2. Parvovirus
3. Papovavirus

Front 14

Characteristics of Adenovirus

Back 14

Linear, ds DNA.
Nonenveloped c spikes for attachment.
Causes:
1. Respiratory infection.
2. Conjuctivitis.
3. GI tract (u. subclinical)
4. ARD (crowding/stress)

Front 15

Characteristics of Parvovirus.

Back 15

Small, ss DNA.
Non-enveloped.
Two viruses:
1. B19 - infects immature erythroid cells. 5th disease (erythema infectiosum).
Polyarthritis in adults. Can cause severe anemia.
2. AAV - no known diseases.

Front 16

Characteristics of Papovavirus.

Back 16

Circular, ds DNA.
Non-enveloped.
3 viruses to know:
1. Papillomavirus.
2. Polyomaviruses: (both cause mild respiratory but may be carried latently in kidney/tonsil.)
a. BKV- multiples in urinary tract. Kidney tranplant failure.
b. JCV - progressive multifocal leukencephalopathy.

Front 17

List 2 large DNA viruses.

Back 17

1. Herpes.
2. Pox (Variola & Vaccinia).Variola caused smallpox.

Front 18

Characteristics of Smallpox.

Back 18

Large, Very complex ds DNA.
Enveloped, but stable.
Caused by Variola virus of Pox family.
There is no animal reservoir for smallpox.

Front 19

Describe pathogenesis of small pox.

Back 19

Virus in respiratory secretions & skin lesions. Hu-Hu contact leads to RT infection → to regional lymph nodes → 1 viremia → internal organs → 2 viremia → skin eruptions.
Death: organ failure.
2° complications: pneumonia.

Incubation period: 2 weeks. Symptom free but infectious.

Front 20

Structural characteristics of Herpes Virus.

Back 20

ds linear DNA.
Enveloped.
Have glycoprotein spikes used for penetration.
Icosahedral capsid.
*Between nuclear capsid & envelope is e- dense tegument which contains proteins that are ready to be released after fusion.

Front 21

Name 3 common properties of productive herpes infections.

Back 21

1. cytolytic.
2. viral DNA synthesis occurs in nucleus, carried out by virus-encoded enzymes.
3. Nucleocapsids assemble in the nucleus & gain an envelope.

Front 22

What are the 3 herpes subfamilies?

Back 22

1. alpha (1,2,VZV)
2. beta (CMV,6,7)
3. gamma (EBV, 8)

Front 23

Characteristics of alpha subfamily of herpes.

Back 23

Variable host range.
Rapid repro cycle.
Latency established in neurons.
Members: 1,2,VZV.

Front 24

Characteristics of beta subfamily of herpes.

Back 24

Restricted host range.
Slow repro cycle.
Latency established in lymphocytes, monocytes.
Cytomegalic.
Members: CMV, 6,7.

Front 25

Characteristics of gamma subfamily of herpes.

Back 25

Restricted host range.
Latency established in lymphoid cells.
Members: EBV, 8.

Front 26

2 requirements for latency to be established:

Back 26

1. Supression of cytolytic activities.
2. Avoidance of host antiviral defenses.
It doesn't kill the cell and the cell doesn't kill it.

Front 27

Characteristics of Herpes Simplex Viruses infections.

Back 27

Infection via epithelium of oral/genital/ocular or by break in skin.
HSV1- usually oral/ocular.
HSV2 - usually genital.
Primary oral infection mostly asymptomic & occur b/w 6 mon. & 3 yrs.
Primary genital causes vesicular, ulcerative lesion, fever, malaise, dysuria, localized lymphadenopathy.
Primary oral infection: keraconjuncitivit with vesicles & dendritic corneal ulcerations.

Front 28

How is latency established by Herpes Simplex virus?

Back 28

Neurons of PNS infected with virus released from epithelial cells.
Retrograde spread within axons.
Latency ion cell bodies of DRG.
Note: Latency in non-dividing cells so that they don't need to replicate their genome.

Front 29

What are HSV Latency-Associated Transcripts (LAT)?

Back 29

A transcript spliced to generate a stable intron encoded w/i the HSV genome. LATs appear to maintain HSV in transcriptionally inert, latent stage and prevent apoptosis.

Front 30

Describe the neuroinvasiveness of HSV infections.

Back 30

Low neuroinvasiveness.
Highly neurovirulent.

Front 31

What is recurrent herpetic stromal keratitis?

Back 31

Autoinflmmatory reaction (T-cell dependent) that is assoc with HSV.
Underlying mechanisms:
1. Molecular mimicry - Ab destroy host.
2. Bystander activation - T cells respond to antigen X and end up responding to antigen Y.
3. Inflammatory cells release cytokines, chemokines & GF that dirupt balance b/w angiogenic and antiangiogenic activity.

Front 32

How does reactivation from latency occur (HSV)?

Back 32

1. Viral Fc-gamma receptor (a dimer of gE +gI) inhibits Ab-dependent cell-mediated cytotoxicity & C1q blinding,& attachment of granulocytes.
2. Viral complement receptor (gC): Binds C3b & prevents binding of properdin and C5.
CHECK THIS ANSWER.

Front 33

How TAP/ICP47 is involved in HSV reactivation form latency.

Back 33

CHECK THIS ANSWER.

Front 34

Treatment of HSV infections:

Back 34

Acyclovir & Ganciclovir
(Guanosine analogues)
Triphosphorlated form is incorporated into growing DNA chain for that DNA replication terminates prematurely.