Immunology Exam 6 Chapters 11 And 12 Study Guide Essay examples

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PCB Fall 14 Study guide

Chapter 11
1) Which T-cells decline in an HIV patient? What is the significant # of those cells for a transition to AIDs?
a. Massive reduction in CD4 T cells
b. Less than 200 CD4 T cells per ul.
c. HIV doesn't kill patient but cell mediated immunity is compromised and patient can die from infection
2) Know gp 120 and 41 and what they do? What is the precursor polypeptide these are created from?
a. One nucleocapsid protein is a protease used to cleave gp41 and gp120 envelope glycoproteins from a larger precursosr protein.
b. cleave a large precursor polyprotein (protein gp160)
c. binding and fusion of HIV into target cell takes place by interaction with 2 membrane glycoproteins (GP)
i. gp120- binding
ii. …show more content…
With hemagglutin/neuraminidase encoded by avian RNA molecules. Avian very different from those recognized by human protective immunity.
12) What confers protective immunity against influenza?
a. What is principal “protective immunity” to influenza?
i. Antibodies- Abs that bind to hemagglutinin and neuraminidase glycoproteins of the viral envelope.
b. Where do these Abs get made?
i. Primary (1) immune response
c. Your protective immunity to influenza is determined by the strain of virus to which you were first exposed!
13) How many genes are usually affected in inherited immunodeficiencies? Are they typically recessive or dominant?
a. 2 in female, 1 in male?
b. Have to be homozygous for it, so they are recessive.
c. Single gene; recessive; IFN-gamma receptor defect - example of a dominant
14) What is the central dogma of molecular biology? What is a retrovirus? Does the central dogma apply to retroviruses?
a. Retrovirus- viruses that use an RNA genome to direct the synthesis of a DNA intermediate
b. Central dogma- DNARNAProtein
c. Retrovirus starts with RNA (RNADNAprotein)
15) Do note cards on:
a. Toxic shock syndrome
i. Toxic shock syndromemassive cytokine release IL-1, IL-2, TNF-a ii. Antigen bridges MHC class II and TCRs iii. Caused by bacterial toxins (superantigens)
b. X-linked hyper-IgM syndrome
i. Defect in gene coding for CD40L on T cells ii. B cells cannot switch isotypes iii. Lack germinal centers iv. Susceptible to infection with pyogenic bacteria
v. T
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