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85 Cards in this Set
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Type of Vaccine
HepB |
Subunit
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Type of Vaccine
RotaTeq |
Live attenuated
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Type of Vaccine
DTaP |
Toxoid, Acellular Pertusis
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Type of Vaccine
HIb |
Conjugated
Haemophilus Influenza (meningitis) |
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Type of Vaccine
PCV |
Conjugated
Streptococcus pneumoniae (23 serotypes) |
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Type of Vaccine
PPV |
No protein
Pneumococcal Polysaccharide Vaccine. Contains 23 serotypes of Strept bacteria. |
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Type of Vaccine
IPV |
Killed, Whole inactive
(United States) |
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Type of Vaccine
OPV |
Live Attenuated = Sabin
(herd immunity) |
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Type of Vaccine
Influenza |
Killed, Whole inactive
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Type of Vaccine
MMR |
Live Attenuated
Live vaccines are generally required for enveloped viruses! Paramyxo and Togaviruses are enveloped. |
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Type of Vaccine
Varicella |
Live Attenuated
Herpes are enveloped. Enveloped tend to require live vaccines. |
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Type of Vaccine
HepA |
Killed, Whole inactive
Killed vaccines are sufficient for naked viruses. |
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Type of Vaccine
MCV4 |
Conjugated
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Type of Vaccine
HPV |
Subunit, Recombination
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Type of Vaccine
Gardasil |
Subunit, Recombination
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Coomb's Test
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Used for Rho-antibody; antibody binding cells; crossmatch blood transfusion donors
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Immunofluorescence
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Direct Fluorescent Antibody - detects antigen on tissue.
Indirect Fluorescent Antibody - detects pathogen-specific antibodies on tissue. |
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Class I compatibility testing, as it relates to Organ Transplantation
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Microcytotoxicty;
Lymphos are mixed with antisera. If antibodies recognize their specific epitope on the cells, they will be bound there and addition of complement will result in cell lysis. A dye is used to show leaky cells. |
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Monoclonal Antibodies (mAbs)
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Hemocyte antibodies to target cell antigens; HER2; Campath (CD52)
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IgE, Mast Cells, Eosinophils, Histamine, Leukotrienes, SRSA, IL-4, IL-5, Eotaxin, C3a, C5a
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Type I
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Antibodies (IgG)
Attacking cells, tissues (must be particulate) |
Type II
Goodpasteur’s Syndrome Grave’s Disease Myasthenia gravis Autoimmune Anemia |
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Autoimmune hemolytic anemia
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Abs bind to rbc and lyse (Type II) rbc is a cell
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Rheumatic Fever
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Detect Abs cross-reacting with Streptococcus pyogenes and cardiomyocytes (Type II)
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Grave’s Disease
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Abs that activate the TSH receptors (Hyperthyroidism) (Type II)
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Masthenia gravis
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Abs bind to Acetylcholine Receptors (Type II)
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SLE
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Multiorgan, Immune Complex, Anti-DNA Abs
Type III Classic! |
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Diabetes
type I |
Juvenile, T cells destroy Beta cells in Islets of Pancreas, Usually Th1 T cells; Delayed hypersensitivity (IV)
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Autoimmune destruction of myelin in CNS, T-cell mediated and Ab involved (Type II, IV). Organ specific autoimmune disease, involves loss of tolerance. T-cells recognize myelin antigen.
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Multiple Sclerosis
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Hypothyroidism; Destruction by antibodies and T cells specific for thyroid antigens.
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Hashimoto’s Thyroiditis
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AIRE deficiency involved in Central Tolerance. These patients develop several severe autoimmune diseases
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APECED
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No T or B (common receptor for the cytokines IL-2, IL-4, IL-7, IL-9 IL-15)
IL-7 is the important cytokine. Girls can inherit this from carrier parents. |
X-Linked SCID
(Boys) detected early by Pediatricians. |
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Adenosine Deaminase (ADA), PNP, Jak3, RAG1/RAG2
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SCID
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Pathology: Class I, TAP No CD8
Class II no CD4 T cells |
Bare Lymphocyte Syndrome
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Hypoplasia or aplasia of thyroid; Associated with tetany; Cardiac problems
22q11.2 |
DeGeorge Syndrome
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X-Linked Lymphoproliferative Disease
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SAP (Slam-Associated Protein)
Abnormal response to EBV. Uncontrolled CD8 and B Cells. Hemophagocytosis. |
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X-linked Agammaglobulinemia
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Pre-B cell receptor signaling. Will do heavy chain gene arrangement, but not light.
Decreased IgG Absence of germinal centers Absence of plasma cells Therapy is passive immunization with IVIG (ISG). Immune Serum Globulin. BTK Deficiency. Bruton's. |
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Malignancies, Rash, Eczema, Thrombocytopenia
Cytoskeletal Remodeling Defect in lymph activation and trafficking to inflammation. Progressive decrease in T-Cells Inability to produce Ab in response to T-cell independent polysaccharide antigens. Vaccines that are polysacc based will not make antibody for. |
Wiscott-Aldrich Syndrome
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Ataxia Telengectasia
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Autosomal Recessive
Defect in DNA repair for maintaining genome stability. Decreased T-cells Decrease in IgA, IgG2 Normal B-cells Prone to Infections and Malignancies, Balance problems (cerebellum) |
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APECED
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Many Autoimmune Diseases, Central Tolerance; AIRE
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Dysregulated T cell proliferation, T cells don’t die through FAS/FASL
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Autoimmune Lymphoproliferative Disease (ALPS)
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Treg cells are not present to regulate other cells. (Peripheral Tolerance). Patients develop Th1-mediated autoimmune diseases
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IPEX
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Neutrophil killing defective (prone to Aspergillis, Staph, Strep)
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Chronic Granulomatous Disease (CGD)
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Adhesion defect, migrate out of blood vessels, APC-T interaction; Leukocytosis in blood (they can’t migrate out of the blood-no homing)
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Leukocyte Adhesion Deficiency
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Big Granules. Lysosome defect, and the neutrophils can’t kill
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Chediak Higashi
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Neisseria infections
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MAC (C5b-C9)
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Paroxysmal Nocturnal Hemaglobineuria (PNA)
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DAF Deficiency
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Take a couple weeks (immune response). First phase rejection, followed by a second phase rejection (memory)
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Acute
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Not really a rejection, just a dead organ. May be drug-related or bad surgery. Complement, B cells, T cells. Lots of dead cells
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Chronic
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Type IV. T cells from graft are attacking the recipient’s tissues. Want to kill the mature T cells from the bone marrow donor (the graft) before transplantation.
Only in a Bone-Marrow Transplant into an Immunocompromised recipient |
GvHD
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Antigenic Variation due to a Shuffling of Exons
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Trypanosome
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Capsule, Antigenic Variation
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Streptococcus (23)
Neisseria capsule and serotype, too |
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Toxic Shock Syndrome
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Superantigen
Binds Beta-chain outside peptide groove. 20% of T-Cells will be activated by superantigen. |
(T cells gone wild)
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Has 23 different serotypes, Capsular
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Streptococcus (23)
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Protein A Binds IgG (the Fc portion) to inhibit phagocytosis.
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Staphylococcus aureus
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Contains LPS, O-side chains inhibit complement (MAC)
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E. Coli, Neisseria
Gram-negative organisms |
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Complicated Life Cycle, Latency?, Hides in rbcs
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Malaria
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Binds to CD21/CR2 on B cells, Persists inside B cells in latent form; Viral IL-10 competes with body's IL-10.
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Epstein-Barr Virus
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Antigenic Drift and Antigenic Shift
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Influenza
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Has an IgA Protease that cleaves IgA
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Neisseria (Gram -)
Haemophilus S. pneumoniae |
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Latency and reactivation causes Shingles
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Varicella zoster
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Intracellular in phagocytes, Granuloma formation, hard to access, avoids lysosomal killing inside macrophage
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Mycobacterium tuberculosis,
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Uses antigen variation, Infects CD4, macrophages, and dendritic cells. Latent infection; Downregulates MHC I expression; Destruction of mucosal CD4+ permits bacterial entry.
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HIV
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Defective maturation of T, B, and myeloid cells.
Defect at hematopoietic stem cell level. Marked decrease in T and B cell numbers. Autosomal recessive. Associated with pancytopenia. |
Reticular Dysgenesis
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Genetic SAP adaptor protein defect.
Prone to abnormal EPV response, which binds CD21 of B-cells causing lymphoma. Uncontrolled CD8 T cell proliferation and B cell proliferation. Uncontrolled hemophagocytosis. |
X-linked Lymphoproliferative Disease (Purtilo’s or Duncan’s)
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Similar pathogenesis as X-linked Purtilo’s or Duncan’s
Inappropriate and ineffective CD8 T Cell activation Hemophagocytosis Anemia Pancyopenias Perforin gene mutation (can’t kill target cell) G-protein regulation of granule exocytosis NK cell cytotoxicty will also be affected |
Familial Hemophagocytic Syndrome
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No granule fusion or enzyme deficient
Neutrophils, macrophages, dendritic, NK Cells Defective granules of NK Cells Defect in adherence and killing Manifestations: Pyogenic bacterial reinfection Albinism Melanosomes (hair or skin pigmentation) Organomegaly cytophagocytosis |
Chediak-Higashi Syndrome
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Autoimmune Polyendocrinopathy Candidiasis Ectodermal Dystrophy
Autoimmune Polyglandular Syndrome type-1 AIRE gene mutation Central Tolerance defect |
APECED; APS-1
Increase incidence of Autoimmune Disorders |
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Immune Dysregulation
Polyendocrinopathy Enteropathy X-linked syndrome FOXP3 mutation TF for development of Treg Cells CD4+ CD225+ |
IPEX
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25% of all SCID disorders
↓ B-Cells (progressive) ↓ T-Cells (progressive) T-Cells respond poorly ↓ IgG Purine degradation salvage pathway Accumulation of deoxyadenosine and dATP toxic purine metabolites inhibits DNA synthesis lymphocytes particularly sensitive! |
SCID (adenosine deaminase deficiency)
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↓ IgG
↓ IgA Normal B-Cell numbers Delayed T-Cell maturation Resolves around 1.5 – 2 years of age |
Transient Hypogammaglobulinemia of Infancy
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E. coli and its flagellum bind to macrophage via ?
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Toll-Like Receptor (TLR) on the macrophage.
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...have a thin peptidoglycan with a layer of Lipids, and Polysaccharides collectively known as Lipopolysaccharide (LPS). LPS contains side chains that radiate off called O-antigens.
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Gram - bacteria
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is the biologically active component and causes the toxicity of LPS.
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Lipid A
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The ____ of LPS prevent Complement C3b binding to the cell surface and MAC forming. This is an immune evasion mechanism of Gram-ve bacteria
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O side chains
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Skin Abscesses
Food poisoning Pneumonia Toxic Shock Syndrome |
Staphylococcus
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.....is a major component of the Staphylococcus aureus cell wall. It binds to the Fc domain of IgG molecules.
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Protein A
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Strep Throat
Tonsilitis Scarlet Fever Rheumatic Fever Cellulitis |
Streptococcus
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Causes sore throat and skin infections. Secretes Exotoxin A-C that acts as a superantigen to cause fever, rash and inhibit liver clearance of endotoxin.
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Streptococcus pyogenes (Group A)
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The conjugate meningococcal vaccine (MCV4) was introduced in the U.S. in 2005.
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Neisseria meningitis
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The characteristic skin rash of meningococcal septicemia, caused by ...
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Neisseria meningitidis:
Gram (-) diplococci Polysaccharide capsule prevents phagocytosis (most important virulence factor) Also has IgA protease. LPS endotoxin is overproduced, causing abrupt signs. |
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Both meningococcus and gonococcus produce ..
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an IgA protease that cleaves IgA.
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Antibody & Complement opsonize yeast and activation of macrophages by Th1 cells help kill ...
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Candida
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Variable Surface Glycoprotein (VSG) of Trypanosoma cruzi undergoes ...
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programmed antigen variation.
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IFN, TNF, IL-12, NK, Th1, CTLs
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Immune Control of Viruses
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...binds to CD21 on B cells and transforms B cells to become malignant.
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EBV
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