HLTB21H3 Chapter Notes - Chapter 5: Electron Microscope, Rous Sarcoma Virus, Luc Montagnier

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3 Jun 2012

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Cause fever and lung congestion may lead to respiratory failure. Usually found in children with leukemia or adults with lymphomas or those on immunosuppressive drugs. Appearance of a rare cancer of the skin by a red-purple blotching called kaposi"s sarcoma. Robert gallo named hltv iii (human lymphotropic t-cell virus) Today known as hiv human immunodeficiency virus. Hic virus is a spherical shape (can only be seen with electron microscope) They are not cells but able to reproduce by taking over the machinery of a living cell. It must subvert the cell"s machinery to copy viral rna into dna. Found a virus that causes a cancer named rous sarcoma virus (rsv) In rsv was able to make a dna copy from the virus"s rna.

Related Questions

Ms. C.A., a 38-year-old dancer, went to the emergency department one night after work. She reported a worsening condition of shortness of breath with an unproductive cough, mild chest pain, and tiredness. She also reported persistent diarrhea for the past 6 weeks and weight loss (without dieting) of 16 pounds.

She had no history of smoking or of previous respiratory illness. Her medical history included genital herpes and gonorrhea within the past 2 years. She has had unprotected intercourse with numerous sexual partners.

A complete blood count (CBC), electrocardiogram (ECG), and chest radiograph were ordered. Subsequent to the chest film report of diffuse, bilateral, interstitial shadowing, a bronchoscopy with bronchoalveolar lavage (BAL) was performed.

Laboratory Data

Assay Patient Result Reference Range

Hemoglobin 11.5 g/dL 13.5-17.5

Hematocrit 38% 39-51

Total WBC 5.8 Ã 10⁹/L 4.5-11.0

Absolute lymphocyte count 0.75 Ã 10⁹/L 1.6-3.5

T lymphocytes

CD4+ 0.13 Ã 10⁹/L 0.7-1.1

CD8+ 0.42 Ã 10⁹/L 0.5-0.9

B lymphocytes 0.10 Ã 10⁹/L 0.2-0.5

BAL Positive for Pneumocystis carinii

Questions:

Is this patient considered to be immunodeficient? (3 pts)

2. What further diagnostic assays would be useful in establishing a diagnosis? (5 pts)

3. What opportunistic pathogens are typically associated with patients who have an immunodeficiency? (2 pts)

a. Cryptococcus neoformans

b. Cytomegalovirus

c. Hepatitis B virus

d. Both a and b

It was all over the news this morning (March 29, 2018) that a new cancer âvaccineâ was about to begin human trials after a 97% success rate in mouse trials against both blood cancers (lymphomas) and solid tumors such as breast and colon cancer. I will excerpt a description compiled from several scientific and news sources. Based on what we talked about in Bio 221, you should be able to understand this. Answer each of the questions about this exciting new âvaccine.â

T cells are present in most tumors by infiltration. These include CTLA4-expressing Treg cells, as well as CD4- expressing TH cells and CD8-expressing cytotoxic T-lymphocytes. Once cancer is well established, the balance between these inputs is tipped toward immunosuppression. We found that a Toll-like receptor 9 (TLR9) ligand, CpG, induces the expression of OX40, an alternate costimulatory receptor, on CD4 T cells when it is injected into the tumor microenvironment. This is an indirect induction, in which CpG induces cytokine secretion by myeloid cells which in turn induces OX40 expression on T cells. Then OX40 can be activated using anti-OX40 antibodies, thereby activating TH cells in the tumor.

A. What is CTLA4 and how does it establish immunosuppression?

B. What is a costimulatory receptor, and why is an alternate one required here?

C. How does a TLR ligand such as CpG induce cytokine expression by myeloid cells? What myeloid cells are involved here?

D. How do antibodies that recognize OX40 help to stimulate TH cells? (Hint: think about autoimmune diseases. There is one we didnât talk about, called Gravesâ disease, that you might want to look up, too.) What else is required for the TH cells to become activated? E. How does all of this kill the cancer cells? What other cells in the tumor also must become activated? How? F. How does this differ from the CAR-T cell therapy?

greylocust179

A. What is CTLA4 and how does it establish immunosuppression?

B. What is a costimulatory receptor, and why is an alternate one required here?

C. How does a TLR ligand such as CpG induce cytokine expression by myeloid cells? What myeloid cells are involved here?

E. How does all of this kill the cancer cells? What other cells in the tumor also must become activated? How?

F. How does this differ from the CAR-T cell therapy?

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HLTB21H3 Chapter Notes - Chapter 5: Electron Microscope, Rous Sarcoma Virus, Luc Montagnier

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