a. gene conversion
b. epidemics
c. primary immunodeficiency disease
d. secondary immunodeficiency disease
e. seroconversion
c. primary immunodeficiency disease
a. hemagglutinin and neuraminidase
b. variable surface glycoproteins
c. EBNA-1
d. protein toxins
e. gp41 and gp120
a. hemagglutinin and neuraminidase
a. superantigen products
b. ability to fix complement
c. rates of gene conversion
d. capsular polysaccharides
e. variable surface glycoproteins
d. capsular polysaccharides
a. age
b. error-prone replication of its DNA genome
c. co-infection with avian and human influenza viruses
d. recombinant strains
e. the phenomenon of Ôoriginal antigenic sinÕ
b. error-prone replication of its DNA genome
a. Salmonella typhimurium
b. Trypanosome brucei
c. Treponema pallidum
d. Neisseria gonorrhoeae
e. None of the above
c. Treponema pallidum
a. pilin
b. flagellin
c. variable surface glycoproteins (VSGs)
d. hemagglutinin
e. neuraminidase
c. variable surface glycoproteins (VSGs)
a. latency
b. antigenic shift
c. antigenic drift
d. seroconversion
e. gene conversion
a. latency
a. Because sensory neurons express low levels of MHC class I molecules, they provide appropriate sites for viral dormancy.
b. Reactivation of herpesviruses follows stressful incidents.
c. Cold sores develop as a consequence of CD8 T-cell killing.
d. In a person lifetime, periodic episodes of reactivation are common.
e. Herpes simplex virus infects B lymphocytes.
e. Herpes simplex virus infects B lymphocytes.
a. hormonal fluctuations
b. antibody deficiency
c. bacterial infection
d. immunosuppression
e. ultraviolet radiation
b. antibody deficiency
a. varicella-zoster
b. Epstein-Barr virus
c. herpes simplex virus
d. cytomegalovirus
e. All of the above are herpesviruses
e. All of the above are herpesviruses
a. Epstein-Barr virus
b. Staphylococcus aureus
c. herpes zoster
d. Candida albicans
e. Listeria monocytogenes
c. herpes zoster
a. CD4
b. MHC class II alpha chain
c. CD28
d. T-cell receptor Vbeta chain
e. B-cell receptor
d. T-cell receptor Vbeta chain
a. effective at minuscule concentrations
b. nonspecific activation of 2-20% of CD8 T cells
c. processing to peptides is not required for T-cell activation
d. massive production of IL-2, IFN-gamma, and TNF-alpha
e. activate alpha:beta T cells
b. nonspecific activation of 2-20% of CD8 T cells
a. NK-cell activating receptors
b. C5 complement protein and Fc region of IgA
c. B-cell receptor
d. CD8 co-receptor
e. T-cell receptor Vbeta chain
b. C5 complement protein and Fc region of IgA
a. leukocyte adhesion deficiency
b. chronic granulomatous disease
c. hereditary angioedema
d. Chediak-Higashi syndrome
e. Listeria monocytogenes
c. hereditary angioedema
a. When it acts on target cells, it enhances the engulfment and killing of bacteria.
b. It is the major activating cytokine of macrophages.
c. It activates the JAK-STAT signal transduction pathway after binding to its cognate receptor.
d. It is secreted by CD8 cytotoxic T cells, CD4 Th1 cells, and NK cells.
e. It is secreted and functions as a monomer but facilitates the dimerization of its receptor.
e. It is secreted and functions as a monomer but facilitates the dimerization of its receptor.
a. they are recycled by endocytosis more quickly than the normal receptor
b. the cytoplasmic tail is truncated
c. they are able to form stable dimers with the normal form
d. they cause less severe immunodeficiency than do the homozygous recessive forms
e. they are unable to transduce signals when bound to the normal form
a. they are recycled by endocytosis more quickly than the normal receptor
a. Streptococcus pneumoniae
b. Haemophilus influenzae
c. Streptococcus progenies
d. Mycobacterium tuberculosis
e. Staphylococcus aureus
d. Mycobacterium tuberculosis
a. WiskottÐAldrich syndrome caused by deficiency of WASP
b. hyper IgM syndrome caused by deficiency of CD40 ligand
c. lymphoproliferative syndrome caused by deficiency of SH2D1A
d. Chediak-Higashi syndrome caused by deficiency of CHS1
e. agammaglobulinemia caused by deficiency of Bruton tyrosine kinase
d. Chediak-Higashi syndrome caused by deficiency of CHS1
a. a profound deficiency of neutrophils
b. leukocytosis
c. immune-complex deposition in tissues
d. defects in recruitment of phagocytes to infected tissues
e. complement-mediated lysis of erythrocytes
e. complement-mediated lysis of erythrocytes
a. possible death by suffocation
b. overproduction of vasoactive C2a fragment and peptide bradykinin
c. hyporesponsiveness of classical complement pathway
d. subepithelial edema
e. C1 inhibitor deficiency
c. hyporesponsiveness of classical complement pathway
a. classical; alternative pathways of complement
b. T-cell-dependent antibody responses; cell-mediated immune responses
c. innate; acquired immune responses
d. MHC class I; MHC class II molecules
b. T-cell-dependent antibody responses; cell-mediated immune responses
a. Artemis
b. purine nucleoside phosphorylase (PNP)
c. DNA-dependent protein kinase (DNA-PK)
d. RAG-1
e. RAG-2
b. purine nucleoside phosphorylase (PNP)
a. adenosine deaminase (ADA)
b. class II transactivator (CIITA)
c. TAP1 or TAP2
d. RAG1 or RAG2
e. Janus 3 kinase (Jak3)
e. Janus 3 kinase (Jak3)