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Group #1 = 49.4 #2 = 49.4 #3 = 49.2 #4 = 49.8 #5 = 49.0 #6 = 48.3 #7 = 48.4 #8 = 49.8. Group #9 = 49.6 #10 = 49.5 #11 = 47.6 #12 = 49.3 #13 = 49.3 #14 = 49.8

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group case study presentation evaluation 50 points
Group #1 = 49.4

#2 = 49.4

#3 = 49.2

#4 = 49.8

#5 = 49.0

#6 = 48.3

#7 = 48.4

#8 = 49.8

Group #9 = 49.6

#10 = 49.5

#11 = 47.6

#12 = 49.3

#13 = 49.3

#14 = 49.8

#15 = 48.7

Group Case Study Presentation Evaluation: 50 points
family retroviridae
Family Retroviridae
  • “backward” nucleic acid synthesis
  • Convert genomic viral (+)RNA -> cellular dsDNA (provirus)
  • Uses RT (reverse transcriptase), RNA-dependent, DNA polymerase (also DNA-dependent, DNA polymerase)
sub family spumavirinae
Sub-Family: Spumavirinae
  • “foamy” vacuoles in cell culture
  • Mammals, primates
  • Human foamy virus – first retrovirus found in humans
  • “orphan virus” - no associated disease
sub family oncovirinae
Sub-Family: Oncovirinae
  • “tumor”
  • infection leads to cell transformation
  • RNA tumor virus
  • Avian, reptile, mammals, primates
  • Human T-cell leukemia virus (HTLV)
sub family lentivirinae
Sub-Family: Lentivirinae
  • “slow”
  • Persistent chronic infection
  • Chronic disease of CNS, lung, immune deficiency
  • No cell transformation
  • Mammals, primates
  • Human immunodeficiency virus (HIV)
lentivirus hiv
Lentivirus: HIV
  • Envelope (env) - 120 nm, glycoprotein spikes
  • Matrix protein (gag)
  • Capsid -icosahedral, wedge-shape
  • Nucleoprotein (gag) – group-specific antigen
  • Genome – two copies (+)RNA
  • Enzymes (prot:pol:int) – protease, polymerase (RT, RNAse-H), integrase
hiv genome rna
HIV Genome: (+)RNA
  • Two RNA molecules associate by dimer linkage site
  • 10 kb; 5’ cap, 3’ polyA tail
  • Three major genes -(gag, pol, env)
  • Complex overlapping genes found in Lentivirus - regulatory, accesory

(vif, tat, rev, vpu, vpr)

hiv genome 5 end region
HIV Genome: 5’ End Region
  • R – terminal repeat, important for reverse transcription
  • U5 – unique 5’ end sequence (becomes 3’end of proviral DNA, signal for poly-A addition to mRNA)
  • PB – primer binding site of cell tRNA
  • Leader – recognition sequence for packaging genome RNA, donor site for all spliced subgenomic mRNAs
hiv genome major genes
HIV Genome: Major Genes
  • gag (“group-specific antigen”) - code for structual proteins; capsid, matrix, nucleoprotein (RNA-binding)
  • pol (prot:pol:int) – code for enzymes
    • Protease cleaves viral polyprotein
    • RT/RNase for reverse transcription
    • Integrase cuts cell DNA to insert proviral DNA
  • env– code for envelope glycoproteins; surface, transmembrane
hiv genome 3 end region
HIV Genome: 3’ End Region
  • PP – polypurine (A-G) tract, initiation site for viral (+)DNA synthesis
  • U3 – unique 3’ end sequence (becomes 5’ end of proviral DNA), regulatory sequences for mRNA transcription & DNA replication
  • R – terminal repeat, for reverse transcription
hiv provirus dsdna replication
HIV Provirus (dsDNA) Replication
  • Uncoat in cytoplasm, viral genome (+)RNA with RT -> (-)DNA -> (±)DNA, transport into nucleus
  • Evidence for viral DNA:
    • Virus replication inhibited by actinomycin-D (blocks DNA->mRNA)
    • Infected cells have DNA complimentary to viral RNA
    • Discovery of viral RT
reverse transcription ssrna to dsdna
Reverse Transcription (ssRNA to dsDNA)
  • Cell tRNA primer at PB internal site
  • (-)DNA synthesis, simultaneous RNA degradation by RT
  • “strong stop” at end, reinitiate DNA synthesis by “jumping” to other end
  • PP (short RNA sequence of genome) primer for (+)DNA strand synthesis
  • “strong stop” at end, “jumping” to other end
  • Proviral dsDNA with novel ends, Long Terminal Repeat (U3, R, U5)
reverse transcription 1st jump
Reverse Transcription: “1st Jump”
  • 1. Primer tRNA anneals to PBS (genome RNA); RT makes (-)DNA (R U5) copy of 5’ end; RNase H removes hybridized RNA (R, U5)
  • 2.“(-)DNA strong stop”
  • 3. “First Jump” – (-)DNA R hybridizes to RNA R sequence at 3’end
  • 4.(-)DNA extended and completed (to PBS); most RNA removed, except PP tract
reverse transcription 2nd jump
Reverse Transcription: “2nd Jump”
  • 5.PP primer for (+)DNA (5’ end U3RU5) synthesis; RNase H degrades PP tract
  • 6.“(+)DNA strong stop”
  • 7. “2nd Jump” – (+)DNA binds to PBS near 3’ end of (-)DNA
  • 7a. RNase H degrades PBS/tRNA of (-)DNA
  • 8. Both strands extended & Provirus completed:
    • dsDNA
    • LTR at ends
hiv provirus integration into cell dna
HIV Provirus Integration Into Cell DNA
  • Requires viral LTR on ends of DNA
  • Viral integrase (endonuclease) nicks cell DNA at random sites
  • Viral DNA ligated into cell DNA
  • Integration required for retrovirus infection
  • Free viral RNA / DNA degraded by host cell
hiv provius gene expression
HIV Provius Gene Expression
  • Uses host cell RNA pol II
  • Genome length mRNA:
    • Translates for gag or gag-pol proteins (by translational frame shift)
    • Genome for progeny virus
    • Multiple splicing for subgenomic mRNAs
hiv spliced mrnas
HIV Spliced mRNAs
  • Translates for env proteins
  • Translates for regulatory & accessory proteins
    • Switch for subgenomic, genomic mRNAs
    • Down-regulate (nef)
    • Activate (tat)
    • Infectivity (vif)
hiv assembly release
HIV Assembly/Release
  • Viral genome mRNA in cytoplasm associates with viral nucleoprotein and viral pol proteins
  • Capsid formation, insert genome RNA, migrate to matrix protein at cell plasma membrane
  • Capsid picks up envelope by budding through plasma membrane, exits cell
hiv pathogenesis
HIV Pathogenesis
  • Infects macrophage (phagocytic defense) & helper T cell (regulates both humoral & cell-mediated immunity)
  • Persistent chronic infection in lymphoid tissue (clinical symptom of PGL = persistent generalized lymphadenopathy)
  • Virus held in low level by host defense
  • Over time, virus replicates to high level, destroys T cells, host immunity impaired
  • Clinical AIDS disease, opportunistic infections, and death
  • Follow course of infection by: CD4+T cells, HIV (RNA), clinical disease in patient
retrovirus oncogene
Retrovirus Oncogene
  • Oncogene: gene encoding the proteins originally identified as the transforming agents of oncogenic viruses, some of which were shown to be normal components of cells (growth control proteins)
  • v-onc is viral version of an oncogene
  • c-onc is cellular version of same gene
  • Most likely v-onc subverted from cell
oncornavirus three mechanisms for cell transformation
Oncornavirus: Three Mechanisms for Cell Transformation
  • 1. Oncogene Transforming Protein
  • 2. Alter Host Cell Regulation
  • 3. Stimulate Host Cell Growth
  • Useful models in study of cell regulation and cell transformation
  • Most human cell cancers due to chemical carcinogens
oncornavirus 1 oncogene transforming protein
Oncornavirus: 1. Oncogene Transforming Protein
  • Rapid transforming
  • Rous sarcoma virus in chickens
  • “src” (v-onc)
  • Gene product - tyrosine kinase, up-regulates cell metabolism
  • Leads to rapid cell transformation
oncornavirus 2 alter host cell growth regulation
Oncornavirus: 2. Alter Host Cell Growth Regulation
  • Slow transforming
  • Virus does not have oncogene
  • Murine leukemia virus integrates into cell DNA
  • Turns on c-onc, up-regulates host cell
  • Continued cell activation, over period of time, leads to cell transformation
oncornavirus 3 stimulate host cell growth
Oncornavirus: 3. Stimulate Host Cell Growth
  • Slow transforming
  • Virus does not have oncogene
  • Human T-cell leukemia virus (HTLV)
  • Infects T lymphocyte, release of cytokines, stimulates growth of neighboring T cells
  • Continued T cell activation, over time leads to cell transformation
cellular retrovirus like genetic elements
Cellular Retrovirus-Like Genetic Elements
  • 1940’s - Barbara McClintock propose “moveable genes” by genetic studies of maize
  • Remove & insert circular genetic elements
  • Allow for genetic diversity
    • Bacterial transponsons: drug resistance
    • Retrotransposons: yeast, drosophila
    • Retroposons: humans
reading questions
Reading & Questions
  • Chapter 19: Retroviruses: Converting RNA to DNA
  • Omit Chapter 20: Human Immunodeficiency Virus Type 1 (HIV-1) and Related Lentiviruses
  • Questions: 1, 2, 8, 9
class discussion chapter 12
Class Discussion – Chapter 12
  • 1. How does reverse transcriptase (RT) synthesize RNA into DNA utilizing three different enzyme activities?
  • 2. Why must the retrovirus DNA replication complex make two “jumps”? How is it able to “jump”? Seriously, does DNA really “jump”?
  • 3. Is reverse transcription unique to viruses?
micr 401 final exam
MICR 401 Final Exam
  • Tuesday, Dec. 4, 2012
  • 1:30 – 3:00pm
  • Papovavirus thru Hepadnavirus
  • Case Study and Questions #9-15
  • Lecture & Discussion Questions, Reading & Chapter Questions
  • Exam:
    • Objective Questions (MC, T/F, ID)
    • Short Essay Questions
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