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35 Cards in this Set
- Front
- Back
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What is the morphology of retroviruses?
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enveloped - dipliod ss+RNA
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What is contained inside the nucleocapsid of retroviruses?
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2 identical copies of ss+RNA
10-50 copies of RT 10-50 copies of integrase 2 copies of tRNA |
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What is at the ends of the retrovirus genome?
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LTR sequences that contain promoter and enhancer elements
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What proteins do all retroviruses encode?
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gag, pol, env
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What is the function of gag, pol and env?
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gag = internal structural proteins (capsid, matrix and nucleic acid binding protein - p24 & p17)
pol = RT, integrase and protease env = envelope glycoproteins (gp120 and gp41) |
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What are the 2 subfamilies of retroviridae?
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Orthoretrovirinae
Spumaretrovirinae |
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What disease does spumavirus cause?
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Human foamy virus.
First retrovirus isolated in humans but has never been associated with human disease. --> vacuolated "foamy" cytopathology |
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What are the two types of orthoretrovirinae?
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Type 1: encode proto-oncogenes = DIRECTLY cause cell transformation (fast & direct)
Type 2: encodes Tax (promotes growth factor genes) --> INDIRECTLY promotes cell growth (slow & indirect) |
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Describe Type 1 acute leukemia or sarcoma viruses.
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Infect birds, mice and other animals. No human acute leukemia viruses know at the present.
--> rapid onset of cellular changes after viral infection. HIGHLY oncogenic |
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Describe Type 2 Leukemia viruses.
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Produce Tax (transcripitonal regulator) that indirectly promotes cell growth.
Associated with malignancy AND neurological disorders. Includes HTLV. |
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How is HTLV-1 transmitted? where is it endemic?
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Blood transfusion
sexual intercourse breast feeding Endemic in S. Japan, Caribbean, parts of central America |
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HTLV-1 has a tropism for what kinds of cells?
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CD4+ and Neurons
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When does clinical disease usually occur in HTLV-1 infeted persons?
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Long latency period before clinical disease which appears in 1 in 20 people.
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What clinical disease is seen with HTLV-1 (a deltavirus)?
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Adult Acute T-cell Lymphocytic Leukemia (ATLL) = neoplasia of CD4 cells; usu monoclonal and usu fatal.
Tropical Spastic paraparesis |
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What clinical diseases are HTLV-2 and HTLV-5 implicated in?
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HTLV-2 : atyplical forms of hairy cell leukemia
HTLV-5 : isolated from malignant cutaneous lymphoma |
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Describe lentiviruses.
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Slow onset of disease.
Cause neurologic disorders and immunosuppression Include HIV 1 & 2, visna virus (sheep) and caprine encephalitis virus (goats) |
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What are some other accessory genes encoded in the lentivirus genome that are not found in simple retroviruses?
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tat: transactivator of trxn (similar to tax in HTLV-1)
*Don't need to know the proteins below. nef: alters T-cell signaling; essential for pathogenicity (neg. factor) vif: promotes assembly and maturation vpu: enhances virion release vpr: gives virus growth advantage |
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How does HIV infectio differ from HTLV infection?
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HIV = lymphocytosis
HTLV = lymphoproliferative |
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What are the three steps for entry of HIV into a cell?
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Recognition: gp120 binds CD4
Attachment: to accessory protein on host cell (ex. CCR5) Fusion: gp41 |
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What happens after the nucleocapsid is released into the cytoplasm?
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Nucleocapsid is uncoated and RT transcribes dsDNA from the +ssRNA in cytoplasm
*tRNA serves as a primer **RT is VERY error prone. |
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What are the 2 modes of replication for retroviruses after they are integrated into the genome?
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1. Viral genome replicated passively as the host cell grows and divides.
(clinical latency phase) 2. During lytic growth when the provirus is transcribed. |
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When was AIDS syndrome first described?
When was HIV-1 first isolated? |
1981 - described
1984 - isolated HIV-1 |
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How is HIV transmitted?
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Requires direct contact with mucosal surfaces or fluids = sexual contact, perinatally, exposure to blood and body fluids
*virus is NOT stable outside the host |
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What kinds of cells does HIV bind to?
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CD4+ cells
CD4 lymphocytes, monocytes, macrophage |
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What is HIV illness due to?
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Destruction and eventual depletion of CD4 cells and the opportunistic infections from depleted T cell immunity.
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What is the disease progression in HIV infection?
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1. Acute infection: seroconversion illness = flu-like symptoms within weeks of exposure; chronic lymphadenopathy
2. Clinical Latency: reflects body's ability to produce new CD4 cells; NOT a true viral latency! 10 billion viral particles produced daily 3. AIDS: median time progression is 10 years; CD4 count below 200 |
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What are lab tests for HIV infection?
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ELISA for routine screening of HIV Ab
--> may take up to 6 mo for seroconversion Western Blot for confirmation - detects Ab to certain viral Ag - Positive test requires 2/3 proteins (p24, gp120/160, gp41) |
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What is testing of HIV RNA in serum used for?
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To test the viral load.
NOT diagnostic! Only used to provide information about prognosis and therapeutic efficacy. |
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FDA approved rapid tests are available but what must they be followed up with?
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Confirmatory testing is essential after the + rapid test.
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What are some opportunistic diseases seen with HIV infection above 200 T cell count?
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Between 200 - 500 CD4 count:
MTB Varicella zoster virus HHV-8 (KS) Candidiasis and PCP @ 200. |
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What are some infections seen with CD4 count less than 200?
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T. gondii
Cryptococcus CMV MAC JC virus EBV Crytptosporidium parvum (diarrhea) |
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How is HIV treated?
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Combination therapy is essential!
Resistance common because RT has a high mutation rate! |
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What are the classes of drugs used to treat HIV?
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Nucleoside analog RT inhibitors
Non-nucleoside RT inhibitors Protease inhibitors Fusion inhibitors |
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What are some common examples of NRTIs?
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AZT = Retrovir
*side effects --> anemia, GI ddI = Videx *side effects --> pancreatitis |
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What is the MOA of fusion inhibitors, ex. Fuzeon?
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Blocks the action of the transmembrane protein, gp41
--> prevent HIV entry into the cell --> HIV can mutate gp41 to become resistant Administered as subcutaneous injections twice a day. |
