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55 Cards in this Set
- Front
- Back
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Neoplasia
-defintion |
-abnormal mass of tissue, excessive tissue growth, lack responsiveness to control mechanisms even after removal of stimulus
-malignant tumor |
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Epithelial neoplasia
-aka |
-carcinoma
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Mesenchymal neoplasia
-aka |
-sarcoma (connective tissue, blood vessels, lymphatics)
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How is cell growth controlled and regulated?
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Different proteins:
-growth factors -growth factor receptors -intracellular transducers -intracellular transcription factors |
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Growth factors
-examples |
-hormones
-cytokines |
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Major growth factor source from T-helper cells
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-IL-2
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Growth factor receptors
-types |
-cell surface
-intracellular |
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Major growth factor receptor for IL-2
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-targets cytotoxic T-cells via IL-2 receptor
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Intracellular transducer
-function |
-interactions on the cell surface (via growth factors) influence cell growth activity through intermediary molecules in the cytoplasm
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Intracellular transducer
-examples |
-cAMP
-Ca -intracellular proteins -others |
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Intranuclear transcription factors
-function |
-proteins in the nucleus that are involved in regulating transcription
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Neoplasia etiology
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-inflammation
-radiation -chemicals -genetic |
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Cellular genes and viral genes that result in neoplasia are known as...
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-oncogenes
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Oncogenes
-transmission |
-can be passed from parents to offspring
-can be acquired from viruses |
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Important DNA tumor viruses
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-Papilloma viruses
-Polyoma virus -Adenoviruses |
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Important RNA tumor viruses
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-Retroviruses
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Retrovirus
-characteristic genes |
-pol (polymerase: reverse transcriptase)
-env (envelope) -gag (group antigen/core protein) |
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Retrovirus
-cell infection |
-receptor envelope binding to cell surface
-fusion and entry -reverse transcription in the cytoplasm -viral genome integrated into the host genome -transcription forming viral genomic RNA -translation -assembly of proteins -budding -maturation |
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Feline Leukemia virus
-pathogenesis |
-oronasal contact with the virus
-replication in the tonsils and local lymphoid tissues -infection of monocytes -systemic replication -replication in highly active cells (bone marrow, intestinal crypt epithelium, megakaryocytes) -enters marrow and infects mucosa and glandular epithelium |
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Feline leukemia virus
-transmission |
-bites
-grooming in saliva -oronasal contact |
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Feline Leukemia Virus
-infection types |
-none
-progressive -regressive |
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what has to occur for any virus to be considered infectious or to be considered a viral infection?
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-viral replication
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FeLV
-progressive infection tissues where replication occurs |
-lymphoid tissues
-hematopoietic tissues -mucosal/glandular epithelium |
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FeLV
-how is the progressive infection characterized? |
-ineffective anti-viral response by the host
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FeLV
-how is the regressive infection characterized? |
-virus is present but with minimal incidence of disease because of early curtailment of viral replication
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Why might FeLV be present but not causing a problem in the host?
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-errors in copying
-where it is placed in the host genome -packaging of virus particles |
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FeLV Persistent infection
-occurs when |
-when there isn't sufficient FeLV immune response
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Forms of FeLV that can occur with a progressive infection
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-Neoplastic (proliferative)
-Blastopenic (degenerative) |
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FeLV
-neoplastic diseases |
-lymphosarcoma
-leukemia/myeloproliferation |
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FeLV
-blastopenic diseases |
-dysfunction of the immune system (autoimmune disease, impaired phagocytosis)
-thymic atrophy -immune complex deposition |
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FeLV
-types of lymphosarcomas |
-thymic
-alimentary -multicentric |
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FeLV
-types of leukemias |
-lymphoblastic
-erythroleukemic -myelogenic |
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FeLV
-main effect of the degenerative form |
-increased susceptibility to secondary infection
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FeLV
-largest cause of illness and death in domestic cats |
-Blastopenic disease
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FeLV
-describe the antigenically distinct subgroups |
-Subgroup A: all naturally infected cats infected with this group
-Subgroup B: not transmitted naturally between cats, result of recombination between type A and endogenous feline retrovirus sequences Subgroup C: recombinant of type A with host cell oncogene sequences (proto-oncogenes) |
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FeLV
-subgroup found in cell free fluids |
-Subgroup A
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FeLV
-subgroup infection most likely to cause persistent viremia |
-Subgroups A & B
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FeLV
-subgroup that is rapidly fatal |
-Subgroup C
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Feline Sarcoma Virus
-describe |
-mutant of FeLV that contains proto-oncogenes
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FeSV
-requirement for infection |
-requires simultaneous infection of replicating FeLV to replicate and produce FeSV capable of infecting other cells
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FeSV
-diagnosis |
-history
-(+) FeLV -histological confirmation of fibrosarcoma |
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FeLV
-prognosis |
-avg. 3.5 yr life expectancy from progressive infections that lead to fatal proliferative or degenerative FeLV disease
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FeLV
-detection |
Detect the GAG protein (capsid)
-IFA (indirect fluorescent antibody) -ELISA (pos. in 2-3 wks; may become neg. in regressive infections) Detect Virus neutralizing antibody (env protein) -not routine (need tissue culture) Detect FeLV-specific genomic RNA or Proviral DNA -PCR |
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FeLV
-prevention |
-infection rate related to cat population density
-attempt to avoid transmission via testing -don't really need to test single cat households, but test all others (multicat, history of FeLV, adoption, vaccination) |
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FeLV
-most important way to prevent infection |
-prevent exposure
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FeLV
-vaccine |
-only use in cats at very high risk of exposure
-Live vaccine with canarypox vector -Killed vaccine |
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Killed vaccine
-description |
-humoral response
-requires booster -not all viral infections respond to humoral immunity |
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Live Vaccine
-description |
-CMI and humoral response
-booster not needed -effectiveness related to potential for viral stability and ability to activate effective immune response |
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Cell mediated immunity
-definition |
-immune response that does not involve antibodies but rather involves the activation of macrophages, natural killer cells, CTLs, and the release of cytokines (not always present) in response to an antigen
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Cell Mediated Immunity
-affects what cells |
-microbes that survive in phagocytes and microbes that infect non-phagocytic cells
-most effective at removing virus infected cells |
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Do CTLs play a role in eliminating FeLV in infected cats?
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-yes
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Experiment to understand levels of FeLV-specific CTLs in infected cats
-results |
-cats with high levels of FeLV-CTL showed recovery from FeLV infection and the CTL activity preceded the appearance of serum neutralizing antibody
-cat with low FeLV-CTL response had persistence of FeLV infection and silencing of cell mediated and humoral immune responses |
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Adoptive transfer
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-recover uninfected lymphoblasts from popliteal LNs from unifected cat
-co-incubate uninfected lymphoblasts with FeLV infected fibroblasts for 7-10 days -reintroduce actived lymphocytes back into infected cat |
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Can specific FeLV CTL activity be demonstrated in infected cats by adoptive transfer of activated lymphocytes?
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-yes
-adoptive transfer reduced FeLV #s in blood |
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Ways FeLV infection can be monitored
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-virus isolation
-ELISA (detection of p27 antigen in blood) -PCR (detection of proviral DNA in blood) -Cr Release Assay (specific CTL response) |
