Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
270 Cards in this Set
- Front
- Back
|
Therapeutic Vaccines
|
Treat or moderates persistent infections through immune stimulation.
Lentivirus and Herpevirus |
|
|
T Herpesvirus
|
Used to vaccinate against Marek's disease, a neural lymphoma
|
|
|
Advantages of MLV
|
1. Host amplifies immunogen so you don't have to inject alot
1.Evokes humoral, secretory, and cell mediated immunity 3. rapid onset with long duration and only have to give one dose 4. less $ |
|
|
Disadvantages of MLV
|
1. Can cause dz by mutation back into the wild type thus virulent
2. Latent at gene level 3. hard to differentiate wild type because no genetic markers 4. May be contaminated with foreign virus 5. May change genetic plasticity meaning it can mutate |
|
|
What is the basis for RLV
|
Viral virulence genes are deleted and favorable genes are added
|
|
|
How are RLV made
|
Thymidine kinase and other noncoding regions are deleted and then genes coding for other viruses are inserted, ex. HA of influenza, and HN of parainfluenza
|
|
|
What is the principle for creating a RLV vaccine
|
Virus is penetrated, DNA unwound, certain gene sequences like those for replication and virulence are deleted and others like a lactate marker are inserted and then the DNA is recombined
|
|
|
What are the advantages of RLV that differ from MLV
|
Some virulence factors are removed thus it is non-pathogenic.
It CAN be identified by genetic markers No reversion to virulence so its safe in the environment |
|
|
What is a disadvantage of RLV
|
Retains gene plasticity so mutations and recombinations can occur
Possible latency at gene level |
|
|
Name 2 viruses that have high teratogenic effects if use MLV
|
Blue tongue
BHV aka infectious bovin rhinotrachetitis |
|
|
What type of cells are used to make MLV
|
diploid cells, normal karyotype, free of viral infections, not oncogenic
|
|
|
Who made the killed virus?
|
Pasteur
|
|
|
What is the principle of killed viral vaccines?
|
Inactivate infectivity but preserve antigenicity
|
|
|
What are the advantages of killed vaccines?
|
If properly inactivated they are incapable of replicating and thus incapable of causing disease
|
|
|
What are the disadvantages of killed vaccines?
|
1. 2 doses needed to stimulate humoral immunity becasue the host isn't amplifying
2. poor stimulation of secretory and cell mediated immunity because it isn't replicating 3. Short onset of immunity and duration is short, boosters needed 4. more $ because entire immunizing mass of antigen has to be injected 5. Foreign anitgens lead to allergic infections with repeated vaccination |
|
|
What is the basis for Subunit Viral Vaacines?
|
Using Influenza as a model, select antigens with highest potential for induction infectivity neutralizing AB which is the HA structural protein
|
|
|
What are the advantages of Subunit Viral Vaccines?
|
Incpable of causing disease
More purified than killed so ther are less sever local reactions and fewer allergic reations |
|
|
Diadvantages of subunit viral vaccines?
|
Same as those of Killed.
|
|
|
What is the basic principle behind recombinant subunit viral vaccines?
|
The immunizing antigen(vaccine) is made by expressing the respective gene in an appropriate expression system. We are still injecting the vaccine only we have the bacteria make it for us
|
|
|
What are examples where recombinant subunit viral vaccines are used?
|
Feline Leukemia prevention
Hepatitis B vaccine |
|
|
What is the biotechnology of making DNA viruses that are recombinant subunit vaccines?
|
Clone genes encodiing immunizing AG of ds-DNA viruses into vectors such as bacterial plasmids or viral vectors such as vaccinia virus
|
|
|
What has to be done the the genome of RNA viruses in making RSVV?
|
The RNA genome region encodign for immunizing antigen has to be reversely transcribed with revere transciptase of retrovirus into cDNA then the desired gene in dsDNA can be clones into vector
|
|
|
What virus is used in making RSVV and what in particular from that virus?
|
Reverse transcriptase from retrovirus.
|
|
|
What is E. coli's role in making RSVV?
|
Transform it with the plasmid that bears the inserted gene. The gene can thus be amplified with the growth of the transformed bacteria.
|
|
|
What are actually used as the RSVV?
|
Expressed proteins are glycoproteins that are purified.
|
|
|
What are the advantages of RSVV that differ from killed?
|
1. Better and longer lasting immunity becasue of concentrated immunogen
|
|
|
What is the disadvantage of RSVV?
|
The protein type is restricted meaning it must be produced in a prokaryote or eukaryote thus it isn't immunogenic in all cases.
|
|
|
Category 1 vaccines
|
Killed or recombinant Subunit
|
|
|
Category 2 vaccines
|
MLV or RLV without certain virulance genes
|
|
|
Category 3 vaccines
|
RLV with gene deletions and insertion of foreign genes
|
|
|
Category 4 vaccines
|
Gene based vaccines
|
|
|
How is an animal given the MLV vaccine protected?
|
the animal actually produces the antigenic mass needed to stimulate the immune response.
|
|
|
Which vaccines are use in pregnant animals?
|
Temperature-sensitive viral vaccines and Killed viral vaccines
|
|
|
What are viruses containing purified viral subunits called?
|
Subunit viral vaccines
|
|
|
What are vaccines containing temperature sensitive mutant virues called?
|
MLV vaccines
|
|
|
What do subunit viral vaccines contain?
|
Specific antigenic viral proteins that induce protective immunity.
|
|
|
Where do Subunit viral vaccines replicate?
|
Not in the host animal!
|
|
|
What can a multiple vaccine consist of?
|
Viral, Bacterial, OR fungal components.
|
|
|
Are attenuated virus strains used in genetic vaccines?
|
NO
|
|
|
MLV vaccines in regards to pregnant animals...
|
should not be used UNLESS the package insert states it is safe
|
|
|
What do RLV vaccines consist of?
|
viruses in which virulence genes are removed and or desirable genes are inserted.
|
|
|
Explain why stimulation of the immune response to the HA protein is important in influenza virus vaccines?
|
HA is the most immunogenic
(antigenic) protein on the envelope of influenza virus and as such, once vaccinated the host will mount a stronger immune response than if the response was to the neurominidase protein. |
|
|
Why do all vaccines against influenza virus contain the HA protein?
|
HA is the most anigenic and is involved in virus neutralization.
|
|
|
Why are killed vaccines the best to use in pregnant animals?
|
they don't replicate.
|
|
|
Are temperature sensitive viral vaccines attenuated?
|
YES.
|
|
|
Which type are attenuated viral strains used in?
|
MLV
|
|
|
Where should MLV vaccines be stored?
|
In the fridge.
|
|
|
A RLV vaccines used to prevent psuedorabies in sows caused by herpesbirus suis has what properties?
|
Virluence genes are deleted from its genome.
Productively replicates in cell cultures and in cells of vacinated swine. Contains an inser tof a genetic marker. |
|
|
What do Subunit viral vaccines contain?
|
A specific viral peplomere and capsomere AG inducing protective immunity.
|
|
|
What is essential for the use of multiple viral vaccines with MLV?
|
Each component of the differnet modified viruses must replicate independently each producing sufficient immunogenic mass.
|
|
|
Name a disadvantage to the widely used MLV vaccine.
|
Viral genomes of some vaccines may persist and remain associated with certain cells of the host after vaccination = LATENCY
|
|
|
What is Amantadine used clinically in the prevention of?
|
INFLUENZA VIRUS INFECTIONS.
|
|
|
What is Amantadine?
|
It is a lysosomotropic agent taken up by the cells into endosomes are prevents early events in orthomyxovirus replication.
|
|
|
What specific effect does Amantadine have on Influenza virus?
|
Interferes with uncoating thus preventing replication.
|
|
|
What are the side effects of Amantadine?
|
Insomnia and dyspepsia.
|
|
|
What does Zanamivix do?
|
Inhibits the spread of Influenza virus in mucous membranes - NANAase.
|
|
|
When does replication peak?
|
When clinical signs develope.
|
|
|
How does Iodo-deoxyuridine work?
|
I replaces thymidine causing nonfunctional DNA, only works in DNA viruses.
|
|
|
How do Ara-A and Ara-C work?
|
interfere with nucleotide phosphokinase thus inhibiting DNA synthesis.
|
|
|
What effect does Ara-A have on retrovirus?
|
transient.
|
|
|
Treatment using Ara-C...
|
Topical for conjunctival and genital herpes
Enchephalitis and hep B requires systemic. |
|
|
What is Ribovirin's mode of action?
|
Interferes with biosynthesis of purines.
|
|
|
What does Acyclovir do?
|
Interferes with herpesvirus replication.
|
|
|
What does AZT do?
|
Inhibits retrovirus replication.
|
|
|
What is the mechanism of action of AZT?
|
Induces cDNA chain termination of reverse transcriptase.
|
|
|
What is AZT used as?
|
A chemotherapeutic agent in lentivirus infections to reduce viral load.
|
|
|
What can inhibit proteases of lentiviruses?
|
Crixivan
|
|
|
What does Mitomycin C do?
|
inhibits DNA replication of host cells and of DNA viruses and RETROVIRUSES.
|
|
|
What is the mechanism of action of Actinomycin D?
|
inhibits mRNA transcription.
|
|
|
What was Rifampicin initially used to treat?
|
TB
|
|
|
What is the mode of action of Rifampicin?
|
Modulates specificity for viral polymerases - RETRO, REO, ROTA
|
|
|
What does Puromycin/Cycloheximide do?
|
Inhibits eukaryotic protien synthesis - viral proteins are thus not synthesized in infected cells
|
|
|
Whic virus types do Puromycin inhibit?
|
BOTH DNA and RNA
|
|
|
How do synthetic things work?
|
Mimic receptor determinants and bind to virus ligands thus inhibiting infection of cells.
|
|
|
What is the action of antimetabolite drugs?
|
They mimic nucleotides so they can be incorporated into the viral genome.
|
|
|
When do signs and symptoms of diseases for most viral infections occur?
|
When titers reach their max and continue after the virus has been cleared.
|
|
|
Amantadine
|
INFLUENZA
|
|
|
Acyclovir
|
GUANOSINE ANALOG - HERPESVIRUS
|
|
|
Oncornavirus replication can be suppressed but not eliminated by treating with what drug?
|
ACTINOMYCIN D
|
|
|
Antimetabolites are useful in treating viral infections because they are what?
|
nucleic acid derivatives that can be incorporated into viral nucleic acids precenting elongation.
|
|
|
Crixivan
|
LENTIVIRUSES
|
|
|
8 major aspects of disease induction.
|
Entry, mulitplication, spread, multiplication, cell reaction, interferon, humoral and cell immune, egress
|
|
|
Viruses that only cause Localized infections.
|
Influenza and Rhino
|
|
|
Local spread within epithelial cells of mucous membrane or skin.
|
POXVIRUS and PAPILLOMAVIRUS
|
|
|
How can Poxvirus spread within the infected host?
|
Epithelial cells, subepithelial, lymphatic, hematogenous.
|
|
|
Which viruses can replicate in the MAC's that engulf them?
|
DISTEMPER, HERPES, EIA
|
|
|
Though what are viruses released into general cirulation?
|
Throraci duct
|
|
|
Viruses associated with cell-associated viremia.
|
ORBIVIRUSES,LENTIVIRUSES
|
|
|
Plasma associated viremia
|
PICORNAVIRUS
|
|
|
EIA and feline immunodeficiency virus
|
Macrophage or Lymphocyte associated
|
|
|
Viremia associated with DISTEMPER
|
mixed.
|
|
|
What are ways viruses can penetrate body junctions?
|
1. space bt swollen endothelial cells
2. infect endothelial cells and "growth through" blood vessels 3. infected migrating leukocytes 4. penetration with infected lymphocytes |
|
|
Multiplication of viruses in target organs.
|
Hepatocytes, Neorons, cells of bloof and hemolymphatic system
|
|
|
Where does canine hepatitis induced by adenovirus multiply?
|
Hepatocytes in the liver.
|
|
|
How do interferons modulate viral infections?
|
Limit replication both locally and systemically.
|
|
|
How is virus cleared?
|
Humoral and cell mediated immune reations.
|
|
|
How can the virus us the immune system to persist?
|
Uses the AB to get into the immune cells.
|
|
|
What can AB-virus complexes cause?
|
Immune mediated pathogenic reactions.
|
|
|
Interferon alpha production.
|
Leukocytes.
|
|
|
Interferon beta produciton.
|
Fibroblasts.
|
|
|
What is the type 2 interferon?
|
Gamma or immune interferon.
|
|
|
Immune interferon production?
|
t-lymphocytes.
|
|
|
When is gamma interferon production induced?
|
During antigenic stimulation, viral infections represent antigenic stimulation.
|
|
|
How can interferons be differentiated?
|
Through specific antibodies.
|
|
|
What are inducers of type 1 interferons?
|
Infectious and Inactivated viruses.
|
|
|
How do INF inhibit translation?
|
Oligonucleotide polymerase activates a cellular endoribonuclease which hydrolyses viral mRNA which means it breaks it down.
|
|
|
How do INF inhibit protein synthesis?
|
Protein kinase phosphorylates an initian factor (eIF-2).
|
|
|
MLV vaccines and INF.
|
MLV vaccines are good inducers of INF and can be used when facing a viral outbreak of unknown etiology.
|
|
|
What is the molecular weight of type 1 INF?
|
20,000 Daltons
|
|
|
How does INF act?
|
By producing an antiviral state in the cells which take it up.
|
|
|
INF vs. AB
|
INF is innate viral resistance and AB is adaptive mechanisms.
|
|
|
What type pf proteins are INF?
|
They are ALL acidic.
|
|
|
How would you characterize the antiviral and species specificity of INF?
|
Broad antiviral specificity and strict species specificity.
|
|
|
What produces gamma interferons?
|
Natural killer cells.
|
|
|
Interferons interfere with...
|
Penetration, Uncoating,
|
|
|
What is the immunologic mechanism that inhibits viral replication at the level of mRNA?
|
alpha interferons.
|
|
|
What is the means of communication between cells in the body?
|
Cytokines and Lymphokines.
|
|
|
What is a unique feature of gamma interferons?
|
It is glycosylated.
|
|
|
Where is the action of INF?
|
Intracellular, AFTER induction of resistance in cells.
|
|
|
Where so viral infections induce INF?
|
At the site of infection.
|
|
|
How do INF inhibit translation?
|
Oligonucleotide polymerase activates a cellular endoribonuclease which hydrolyses viral mRNA which means it breaks it down.
|
|
|
How do INF inhibit protein synthesis?
|
Protein kinase phosphorylates an initian factor (eIF-2).
|
|
|
MLV vaccines and INF.
|
MLV vaccines are good inducers of INF and can be used when facing a viral outbreak of unknown etiology.
|
|
|
What is the molecular weight of type 1 INF?
|
20,000 Daltons
|
|
|
How does INF act?
|
By producing an antiviral state in the cells which take it up.
|
|
|
INF vs. AB
|
INF is innate viral resistance and AB is adaptive mechanisms.
|
|
|
What type pf proteins are INF?
|
They are ALL acidic.
|
|
|
How would you characterize the antiviral and species specificity of INF?
|
Broad antiviral specificity and strict species specificity.
|
|
|
What produces gamma interferons?
|
Natural killer cells.
|
|
|
Interferons interfere with...
|
Penetration, Uncoating,
|
|
|
What is the immunologic mechanism that inhibits viral replication at the level of mRNA?
|
alpha interferons.
|
|
|
What is the means of communication between cells in the body?
|
Cytokines and Lymphokines.
|
|
|
What is a unique feature of gamma interferons?
|
It is glycosylated.
|
|
|
Where is the action of INF?
|
Intracellular, AFTER induction of resistance in cells.
|
|
|
Where so viral infections induce INF?
|
At the site of infection.
|
|
|
What provides the virus with high avidity interaction with target cell?
|
Highly repetitive antigens.
|
|
|
Which virus AG get packaged into the virion?
|
Proteases, and Polymerases. Only structural ones.
|
|
|
Which viral antigens are NOT packaged in the virion?
|
Precursor proteins, enzymes, and regulatory proteins.
|
|
|
What does the presense of an antibody in an animal mean?
|
That it has been exposed either through an infection or through vaccination.
|
|
|
How can an active infection be determined?
|
Replicating genome in the infected ceels, anf free virions.
|
|
|
How do RNA and DNA PCR assays differ?
|
DNA= polymerase chain reaction
RNA = reverse transcriptase. |
|
|
How is an Antibody "neutralizing"?
|
It blocks the specific binding site OR by neutralizing enzyme functions by using hemagglutinin.
|
|
|
How are viruses selected?
|
By replication.
|
|
|
Broadly compare and contrast innate and adaptive.
|
innate does not need previous exposure and adaptive does. Innate is non-specific and adaptive is specific.
|
|
|
Which INF is involved with Innate immunity?
|
INF gamma.
|
|
|
What is the humoral component of innate?
|
Complement, Interferon, acute phase proteins, cytokines.
|
|
|
What are the cellular components of innate?
|
Macrophages and NKC.
|
|
|
How do INF inhibit transcription and translation?
|
Inducing MX protein.
|
|
|
How do INF inhibit viral uncoating?
|
Induces Nitic Oxide synthase.
|
|
|
How do INF prevent viral penetration?
|
Alter membrane dynamics.
|
|
|
How do INF directly augment the immune response?
|
1. Increase phagocytosis by MAC
2. increase cytokine production by T cells 3. increase NK cell and CTL cytotoxicity. |
|
|
How do viruses make cells suceptible to NK cells?
|
Down regulation of MHC class 1 production.
|
|
|
Once activated, what do NK cells do?
|
Produce IL-2 and INF gamma which increases T cell proliferation and activated macrophages.
|
|
|
What are the functions of the adaptive immune response?
|
Clear virus and virus infected cells from the body and prevent reinfection by the virus or similar viruses.
|
|
|
Which viral antigens to T-cells recognize?
|
Those presented in the context of MHC class 2.
|
|
|
T cells respond by producing what?
|
Cytokines
|
|
|
Example of virus from over response.
|
FIPV- Coronavirus
|
|
|
Which viruses lead to immunosupression?
|
FIV, canine distemper virus, bursal disease of chickens.
|
|
|
What causes the primary immunodeficiency in Infectious Bursal disease of chickens?
|
Bursal necrosis and atrophy from the bursa of fabricius being infected.
|
|
|
What happens in primary immunodeficiency?
|
No new B cells and no antibody response.
|
|
|
FIV
|
retrovirus/lentivirus. RNA virus with REVERSE TRANSCRIPTASE
|
|
|
In the first 12 hours after a naive puppy is infected with Canine hepatitis virus or adenovirus, what controls the spread?
|
NK cells killing the infected cells.
|
|
|
In the first 12 hours of an immune dog, what controls the viral spread?
|
Activation of complement though classical pathways and neutralizing antibodies
|
|
|
In the naive dog, which cells kill infected tonsil cells after the first 6 hours of infection?
|
NK cells
|
|
|
In naive dog, which cells kill infected kidney cells 10 days after inital infection?
|
CD8 + T cells recognizing MHC class 1
|
|
|
Following immunization, protection is most likely mediated by what?
|
CAV-specific antibodies
|
|
|
An adaptive immunological mechanism that neutralizes the ability of a virus to enter the cell is what?
|
Antibodies
|
|
|
An innate immunological mechanism that slows the virus spread by lysis of infected cells is what?
|
NK cells
|
|
|
What does Riboviron interfere with?
|
Biosynthesis of purines
|
|
|
Gamma interferons...
|
Are made by NK cells following viral exposure and inhibits virus infection of cells. It is important in regulating the immune response
|
|
|
MHC class 2 is...
|
Found on macrophages and B cells and binds to CD4
|
|
|
What is an example of a cellular effector mechanism involves in innate resistance to viruses?
|
NK cells
|
|
|
Which effector mechanism plays the most important role in clearing primary viral infections?
|
CD8 T cells
|
|
|
Which virus causes immunopathology by directly attacking the cells of a primary lymphoid organ?
|
Bursal disease virus
|
|
|
MHC class 1 is...
|
Found on all nucleated cells and binds to CD8
|
|
|
Give an example of an effector cell involves in innate resistance to viruses
|
NK cells
|
|
|
What does a viral neutralization assay measure?
|
The ability of antibodies to inhibit virus replication
|
|
|
Give examples of humoral effectors involved in innate resistance to viruses.
|
complement, alpha, beta, and gamma interferons.
|
|
|
What are examples of viruses that cause immunosuppresion by attacking and destroying lymphocytes?
|
FIV, distemper, and infectious bursal disease virus
|
|
|
What must the virus produce in order to use a serum neutralization assay?
|
CPE in tissue
|
|
|
Following immunization, protection is most likely mediated by what?
|
CAV-specific antibodies
|
|
|
An adaptive immunological mechanism that neutralizes the ability of a virus to enter the cell is what?
|
Antibodies
|
|
|
An innate immunological mechanism that slows the virus spread by lysis of infected cells is what?
|
NK cells
|
|
|
What does Riboviron interfere with?
|
Biosynthesis of purines
|
|
|
Gamma interferons...
|
Are made by NK cells following viral exposure and inhibits virus infection of cells. It is important in regulating the immune response
|
|
|
MHC class 2 is...
|
Found on macrophages and B cells and binds to CD4
|
|
|
What is an example of a cellular effector mechanism involves in innate resistance to viruses?
|
NK cells
|
|
|
Which effector mechanism plays the most important role in clearing primary viral infections?
|
CD8 T cells
|
|
|
Which virus causes immunopathology by directly attacking the cells of a primary lymphoid organ?
|
Bursal disease virus
|
|
|
MHC class 1 is...
|
Found on all nucleated cells and binds to CD8
|
|
|
Give an example of an effector cell involves in innate resistance to viruses
|
NK cells
|
|
|
What does a viral neutralization assay measure?
|
The ability of antibodies to inhibit virus replication
|
|
|
Give examples of humoral effectors involved in innate resistance to viruses.
|
complement, alpha, beta, and gamma interferons.
|
|
|
What are examples of viruses that cause immunosuppresion by attacking and destroying lymphocytes?
|
FIV, distemper, and infectious bursal disease virus
|
|
|
What must the virus produce in order to use a serum neutralization assay?
|
CPE in tissue
|
|
|
Where are receptor determinants(NANA) located?
|
Glycoconjugates of the mucous
|
|
|
NANAase function
|
Breaks down the determinants that attach to the HA antigen, liquifing the mucous and facilitating mucous penetration and virus spread
|
|
|
Equine Flu' s greatest replication
|
Upper respiratory tract
|
|
|
Disease of Equine Flu
|
Lower respiratory tract, loss of cilia from trachea leads to superinfections in lung
|
|
|
Influenza type most important in human and animal infections
|
Influenza A
|
|
|
Determines subtypes of influenza A
|
H and N peplomers
|
|
|
antigenic drifts
|
point mutations on the genome piece of H or N
|
|
|
Antigenic shifts
|
abrupt and major changes in H or N through reassortment of genome pieces in mixed infections.
|
|
|
Group most respiratory causing Herpeviruses belong to
|
Alphaherpes
|
|
|
Alphaherpes characteristics
|
Fast replication, induce inclusions, and are highly cytocidal
|
|
|
Feline Herpesvirus Infection
|
Feline viral rhinotracheitis
|
|
|
Equine Herpesvirus infection
|
Rhinopneumonitits
|
|
|
Equine Herpes 4
|
Major cause of equine rhinopneumonitis
Replicates equal in upper and lower but causes most severe changes in upper |
|
|
BHV 1
|
upper respiratoty tract with occular involvment
|
|
|
Other reults of BHV 1
|
enchephalitis
infectious pustular vulvovaginitis balanophosthitis |
|
|
How do BHV repiratory strains differ from the others?
|
In the restriction fragment analysis of their DNA genomes
|
|
|
BHV 1 incubation
|
2-4 days
|
|
|
Feline Panleukopenia
|
Parvovirus
|
|
|
Transmissible gastroenteritis of swine
|
Coronavirus
|
|
|
Coronavirus induced gastroenteritis, site of entry and innoculum size
|
Oral
Large innoculum fast disease onset |
|
|
What forms a functional entity for intestinal epithelial cell multiplication, differentiation,and function?
|
Crypts and villi
|
|
|
Entherohepatic Mechanism Type 1
|
affects mature cells at the villi
|
|
|
What effects do the cytopathic changes have on enterocytes?
|
Digestive capacity decreaes,
Nutrient absorption is bad Loss of transport proteins so no transporting of the food |
|
|
Loss of total body water is drawn from the extracellular space and plasm, this results in...
|
Hemoconcentration and peripheral vasoconstriction
|
|
|
Electrolyte loss and imbalance
|
sodium bicarb leaves then there's not enough blood for the kidney so then we have a bunch of K in the plasma
|
|
|
Acidic conditions in the body are reults from...
|
Cellular and metabolic acidosis
|
|
|
Why dose loosing sodium bicarb lead to cellular acidosis?
|
Because cells in tissues exchange K for H to maintain pH properly in the fluid around the brain
|
|
|
How is the lactic acidosis made?
|
peripheral vasocontriction doesn't let the muscles and stuff get and o2. lactic acid build up in these tissues because the liver can't do its metabolizing thing
|
|
|
Coronavirus shedding
|
Excretion starts right away, as soon as the diarrhea starts. Large viral loads are shed in the beginning
|
|
|
Virulance of coronavirus
|
Causes syncitia becase its enveloped, has a spike protein on its surface which must be cleaved by trypsin to become infective
|
|
|
Cytocidal effects
|
Enteropathogenic viruses are highly cytocidal in vivo but not so much in cultures
|
|
|
what is trypsins role in coronavirus?
|
enhances cytocidal action, cell fusion and infectivity
|
|
|
Parvovirus induced diarrhea - feline panleukopenia
|
Enterhepatic mechanism 2
|
|
|
Parvo-induced diarrhea pathogenesis
|
takes the hemotagenous route and becomes a viremia. Oral innoculations act faster than IV but recovery from oral is easier
|
|
|
Once you isolate the virus then what can you do?
|
serotyping(eliza)
immunoflouresent RNA fingerprinting could put on a cell culture but the problem with that is bacteria from the gut |
|
|
Piglet passive immunity
|
Lactogenic enteromammary IgA pathway
|
|
|
Protection
|
immune exclusion
|
|
|
Enterohepato-billiary pathway
|
Large amounts of IgG are provided from the colostum and are absorbed through the gut before it closes.
The circulating AB are continuously translocated though liver and bile and gut coating gut mucosal surfaces |
|
|
Immunization of the Dam
|
Must have previously been exposed to the infection or immunized to it in order to transfer specific antiodies to the baby
|
|
|
active immunity in intestinal inections
|
Local mucusal immunity is induced by local production of secretory IgA
|
|
|
Vaccines for intestinal stuff
|
oral and parenteral vaccine
maternal vaccine |
|
|
transmitted by insects
|
Toga Flavi Bunya
|
|
|
Distemper and HIV enter the CNS how?
|
mononuclear leukocytes that migrate through walls of cappillaries
|
|
|
Togaviruses get to the CNS how?
|
Into the parenchyma of CNS through migrating lymphoid cells, or viral replication in vascular endothelial cells or invasion of spinal fluid
|
|
|
How does Poliovirus spread?
|
in neural tissues
|
|
|
Porcine Polioenchephalomyelitis
|
TESCHEN
ENTEROVVIRUS PICORNAVIRIDAE |
|
|
Primary sites of replication for Teschen
|
tonsils of pharynx and intestinal cells
|
|
|
What route does Teschen take to the CNS
|
Extra- Neuronal
|
|
|
Western Equine Enchephalitis
|
ALPHAVIRUS
ARBOVIRUS |
|
|
Western Equine's viremia type
|
cyclic
|
|
|
Western Equine's route to CNS
|
Hematogenous
|
|
|
What cells are suseptible to western equine?
|
Cells of chorpid plexus
Meninges CNS blood vessesl NOT neurons |
|
|
How does rabies get to the CNS?
|
travels centripetally within axons
|
|
|
Where does rabies actually replicate?
|
in the nreve cell body itself
|
|
|
When does Rabies viral release occur?
|
At the same time the virus is replicating in the CNS
|
|
|
What characterizes the furious form of rabies?
|
Limbic system
Loss of cortical control |
|
|
Dump Rabies
|
Neocortex
Paralyisis of nerves |
|
|
Which vaccine type used in rabies?
|
Killed
|
|
|
Scrapie
|
Spongiform Enchephalopathies
|
|
|
Scrapie's major transmission route?
|
Oral but its not the most effective
|
|
|
Scrapie Prions
|
Scrapie-associated fibrils
|
|
|
How do cellular prions differ from scrapie prions?
|
Scrapie are very resistant to proteases and have configurational changes
|
|
|
What determines the type of adaptive resonse that will develope?
|
The nature of the innate reponse
|
|
|
Do all viruses induce inclusions?
|
NO
|
|
|
Do +ssRNA viruses carry their own polymerases?
|
NO
|
|
|
Why is Amantadine useful in treating influenza
|
It is a lysosomotropic agent which prevents viral uncoating
|
|
|
What 2 important molecules are on the surface on influenza?
|
HA and NA
|
|
|
What type of entigen would hepatocytes infected with a hepatic virus present?
|
Processed enfogenously and presented in the context of MHC class 1
|
|
|
Is cancer the result of single or multiple hits?
|
Multiple
|
|
|
Oncogene
|
any genetic element associated with cancer induction
A gene capable of transforming a normal cell into a cancerous one |
|
|
DNA virus families associated with cancer induction
|
Hepadnavirus
POlyomavirus Papillomavirus Adenovirus Herpesvirus Poxvirus |
|
|
Viral Transformation
|
Changes in the biological function of a cell that result from regulation of the cell's metabolism by viral genes and that confer on the infected cell certain properties characteristic of neoplasia - these changes often result from the integration of viral genome into the host cell DNA
|
|
|
pRB and p53 proteins
|
Involved in the negative regulation of cellular growth
|
|
|
How do DNA viruses inactivate tumor suppressor proteins?
|
Physically bind to them and inactivate them.
|
|
|
Protooncogenes
|
A cellular(host) gene that is homolougous with a similar gene that is found in a transforming virus
A cellular oncogene can only induce transformation after mutation |
