Microbiology Exam Iii - Viruses

Front 1

What are viruses? what are the basic ingredients for a virus?

Back 1

viruses = obligate intracellular parasites - not really living

genetic material - DNA or RNA, single or double stranded, in pieces or one molecule

shell to house the genetic material = nucleocapsid

proteins - for dock and exit onto host cells, and for manipulation of host cell response

Front 2

What is the difference between an eveloped and naked virus?

Back 2

naked = capsid forms outer protein shell

enveloped = lipid membrane surrounds the capsid - glycoproteins in the membrane

Front 3

flaviviridae - West Nile Virus
-infection
-transmission
- structure

Back 3

infection:
- most - asympomatic
- some - West Nile fever - lymphodenopathy + joint pain - flu like
- few (1%) - West Nile encephalitis - less conscious, poor movement, coma

Transmission:
- infects birds, dogs cats rabbits humans
- mosquito vector
- humans are dead end hosts - cannot propagate disease\

structure: + RNA, icosahedral capsid, enveloped

Front 4

members of flaviviridae

Back 4

West nile - birds and humans
Yellow Fever - primates and humans
Dengue - mosquito vector - primates and humans

Front 5

Filoviridae
- types - from where?
- structure
- pathology and symptoms
- success

Back 5

- ebola from congo, marburg from african green monkey testing in germany

- enveloped - neg strand RNA

- very quick reproduction - produces huge cytokine storm - causes hemorrhagic fever (liquefication from inside)

- inefficient virus - kills 90% of patients - kills before spreads

Front 6

What is the basic function of interferons?

Back 6

interfere with viral reproduction

Front 7

specifically, what do interferons do? (what steps)

Back 7

a. interferon binds
b. induces antiviral state - antiviral proteins produced
c. antiviral proteins activated when in contact with dsRNA
d. cascade produces 2 effects

1. stops protein synthesis (PKR phosph of eIF - 2 alpha)
1. degrades mRNA (ribonuclease L)

Front 8

why is dsRNA only found in virus infected cells? how is this helpful in immune response?

Back 8

usual route in cells: DNA --> RNA --> proteins, so never dsRNA in normal cell

but virus: RNA -> RNA template --> RNA copy, so dsRNA are present

dsRNA is targeted by interferon-beta to produce an antiviral response

Front 9

What is the difference between pos and neg strand RNA?

Back 9

+RNA -----> proteins
or
+RNA -----> -RNA template --> +RNA

-RNA --> +RNA --> proteins
or
--> -RNA

Front 10

Why must -RNA bring its own polymerase, and +RNA does not need to?

Back 10

+RNA can encode for an RNA polymerase

-RNA cannot - so must carry own RNA polymerase

Front 11

What are the general steps in the life cycle of adenoviruses?

Back 11

one night stand
1. get in
2. get loose
3. get busy
4. get your stuff
5. get out

Front 12

Describe how adenoviruses enter host cell.

Back 12

Get in

1. fiber binds receptor (CD46, CAR = coxsackievirus adenovirus receptor, MHC)
2. base protein of receptor interacts with integrin for actin mediated endocytosis
3. virus is taken via Clathrin coated pits

Front 13

What happens directly after an adenovirus enters the cell?

Back 13

Get loose
1. endosome containing virus acidifies, altering structure
2. capsid dissociates - frees DNA
3. viral DNA enters host nucleus thu nuclear pore

Front 14

Describe viral replication of adenovirus.

Back 14

Get busy

1. Early Genes -host manipulation
E1A and E1B - stim cell growth and block apop
E2 - encodes DNA polymerase
E3 - blocks inflammation
VA-RNA (?) - blocks PKR activity

2. Late genes - makin babies
Capsid proteins (II - penton base; IV - fibers)
Core proteins = DNA binding proteins (V, VII)

Front 15

What advantage does adenovirus have for an error prone replication?

Back 15

creates mutation rate - strong resistance against antiviral agents

Front 16

What happens during last two stages of adenovirus - get yo stuff and get out!

Back 16

4. get yo stuff - capsid migrates to nucleus - assembly - DNA enters capsid through small opening

5. get out - multiply until lysis of host
slower replication = latency, persists until time is right to attack

Front 17

How do adenoviruses establish latency?

Back 17

slower replication = latency
persist until time is right to attack

Front 18

what is a practical use for adenoviruses in medicine?

Back 18

to target malignant cancerous tissue - can be used in removal of tumors

how -
1. telomerase activation causes cancer
2. viruses engin with hTERT promoter + GFP gene
3. viruses will replicate in malignant tissue (with telom activ) and express GFP

Front 19

how is latency est. with adenovirus?

Back 19

slow replication usually in adenoid cells and lymphoid cells

Front 20

what are the stages of transcription and protein synthesis of herpesvirus?

Back 20

1. immediate early - transcription and cell takeover
2. early - enzymes and DNA polym
3. late - structural proteins (after dna replication)

Front 21

describe infection cycle of herpesvirus.

Back 21

1. bind to host cell - fusion and release of nucleocapsid
2. nucleocapsid travels to nuclear memb (immed early protein synth)
3. viral DNA delivered - transcription and replication of genome (early protein synth)
4. Naked capsid with DNA synth and released from nucleus (late protein synth)
5. out to ER and golgi body - membrane and glycoprotein maturation
6. lysis or exocytosis

Front 22

name the kinds of herpersviruses

Back 22

alpha - HSP 1 and 2, Varicella-zoster virus

gamma - epstein barr - kaposi's sarcoma

beta - CMV - HHP 6&7

Front 23

what causes kissing disease?

Back 23

epstein barr virus - infects B cells
(gamma herpersvirus)

Front 24

what causes viral infections from tissue transplants or transfusions?

Back 24

cytomegaly (CMV)

Front 25

are antibodies to glycoproteins of herpesvirus effective?

Back 25

the only kill extracellular virus

but not intracellular viruses - persistent infection

Front 26

how does herpesvirus maintain latency?

how is it reactivated?

Back 26

LAT genes transcribed (not transl)
LATs (RNA) - regulate apoptosis
- in HSV they inhibit lytic genes

triggered by:
UV, stress (emo phys), immunosuppression, menstru, foods, fever

Front 27

herpes viral infection in fingers?

Back 27

whitlow - HSV?

Front 28

hepres virla infection - encephalitis?

Back 28

HSV-1 -- often hides out in trigeminal ganglion

Front 29

herpes infection in eye?

Back 29

keratitis

Front 30

disease caused by HSV-2 shedding by mother

Back 30

HSV neonatal infection

Front 31

What is used to treat HSV diseases?

what does it do?

Back 31

acyclovir

1. first activated by HSV- TK - becomes Acyclo-GTP
2. binds to DNA polym (has great affinity for it)
3. prevents vDNA replic