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;
26 Cards in this Set
- Front
- Back
|
Why do we grow cells in vitro?
|
They represent the best experimental models for in vivo situations.
They express characteristics seen in different tissue organs, e.g. epithelial cells with beating cilia. Best system for growing viruses, besides growing virus in a natural host. |
|
|
Where are primary cell cultures obtained from? How many divisions in vitro can they go through?
|
They are explanted directly from a donor organism (white blood cells or tissues: such as Liver, Kidney, Spleen, and Brain).
They can divide one or two divisions in vitro (up to 4 to 10 passages), but they do not continue to grow and eventually senesce and die. |
|
|
Where are secondary cells obtained from?
How many divisions in vitro can they go through? |
They are explanted from a donor organism.
Under the correct culture conditions, they can divide and grow for some time in vitro (50-100 generations). |
|
|
How long can cells lines divide in vitro? What is another name for cell lines?
Are they cancerous? |
They can continue to grow and divide indefinitely in vitro for as long as the correct culture conditions are maintained.
They are also known as transformed cells Growth properties have been altered. They may or may not be "cancer" or "tumour" cells. |
|
|
What is a permissive cell?
|
Permissive: the infected cells support complete replication of a particular virus.
|
|
|
What is a non-permissive cell?
|
Non-permissive: viral replication may be blocked at any point from viral attachment to the final stages of virion assembly and release.
|
|
|
What does viral tropism depend on?
What are examples of viral tropisms? |
Viral tropism depends on viral and host factors!
Receptors (attachment) Viral enhancers (are short, often tandem-repeated sequences of nucleotides) can regulate tissue-specific transcription (Papillomavirus in keratinocytes). Viral transcription activator (works in specific cells) Tissue specific promoter |
|
|
What happens when the Brain tissue is permissive to a virus?
|
Nothing happens
Headache Neurological symptoms Encephalitis |
|
|
What is the difference between acute, persistent and latent infections?
|
Acute infection: an infection is resolved within a short time (about 2 week)
Persistent infection: an infection last for long time (month) Latent infection: the virus or its genome is maintained indefinitely in the cell, either by the integration of the viral nucleic acid into the host cell DNA or by carriage of the viral nucleic acid in the form of an episome |
|
|
What is an episome?
|
An episome is a portion of genetic material that can exist independent of the main body of genetic material (called the chromosome) at some times, while at other times is able to integrate into the chromosome.
|
|
|
What are the4 primary effects of viral infection?
|
No apparent cellular pathology or morphological alteration
Replication may cause cytopathology (cell rounding, detachment, syncytium formation, etc.) [the only way that we know that the virus is present] Malignant transformation Cell lysis (death) |
|
|
Describe cytocidal, noncytocidal, productive, nonproductive and latent viral infections.
|
Cytocidal (cytolytic, cytopathic)
Noncytocidal Productive infection: infections lead to the production and release of new virions Nonproductive ( abortive): no mature virions produced Latent (genome present without viral antigen) |
|
|
What is the cytopathic effect (CPE)?
What are the 10 types? |
When a monolayer of cultured cells is inoculated with a cytopathic virus, virus replication cause cell damage, known as a cytopathic effect (CPE), which can be observed by light-microscope
CPE (cytopathic effect) can occur in both permissive and nonpermissive cells 1 Altered shape 2 Detachment from substrate 3 Lysis 4 Membrane fusion 5 Syncytia 6 Inclusion bodies 7 Apoptosis 8 Altered membrane permeability 9 Cytoskeleton Change 10 Ultrastructural changes in virus-infected cells Cellular destruction |
|
|
One of the CPE's is syncytia. What is that?
What viruses use it? |
It is results of fusion between an infected cell with neighboring infected or uninfected cells.
It is a conspicuous feature of infection of cell monolayer by: Lentivirus Paramyxoviruses Morbillivirusws Pneumoviruses Some herpesvirus |
|
|
One of the CPE's is inclusion bodies. What is that?
How can they be used to differentiate viruses? |
It is characteristic morphological change in cells infected by certain viruses, and could be seen under light microscope.
It could be: intranuclear or intracytoplasmic single or multiple large or small round or irregular in shape acidophilic or basophilic Different viruses form diferent types |
|
|
What is an inclusion body?
What viruses form inclusion bodies? |
Factory of virus replication, where viral replication occurs.
Poxvirus Reovirus Paramyxoviruses Rabies virus Herpesvirus Adenovirus Parvovirus |
|
|
What are some viruses that induce apoptosis?
|
Adenoviruses
Alphaviruses Chicken anemia virus FIV Herpesvirus |
|
|
One of the CPE's is cytoskeleton change. What are two things that can be depolymerized during this process? Any ideas as to what viruses might cause each?
|
Depolymerization of actin-containing microfilaments
Canine distemper virus Vesicular stomatitis viruse Vaccinia virus Herpesvirus Depolymerization of microtubules Enterovirus |
|
|
What are some ultrastructural changes in virus-infected cells?
|
Proliferation of various cell membranes (neclear membrane, endoplasmic reticulum)
Proliferation of vesicles in the cytoplasm Fusion of cytoplasmic membranes Disruption of cytoskeletal elements Nuclear , organelle condensation Destruction of nuclear and organelle |
|
|
Once the virus gets into the host cell, what are five mechanisms of cell damage?
|
1. Inhibition of cell nuclei acid synthesis
Pox: DNase degrades cellular DNA because it replicates in the cytoplasm, so it doesn't need the DNA; Herpes: displace host cell DNA systhesis 2. Inhibition of host cell RNA transcription 3. Inhibition of processing of host cell mRNAs Herpes: suppress cellular RNA splicing 4. Inhibition of host cell protein synthesis Viral products induce cellular mRNA degradation Viral factors bind to ribosomes and inhibit cellular mRNA translation 5. Cytopathic effects of toxic viral proteins Large amounts of viral products trigger self-destruction mechanism (apoptosis). These viruses are very hard to catch and ID because the viral genome will be degraded as well. |
|
|
What is the HA effect?
What are some viruses with HA? |
Hemadsorption: is due to the incorporation of viral glycoprotein peplomers (proteins on the surface of the viral envelope) into the plasma membrane of infected cells where they serve as receptors for ligands on the surface of erythrocytes.
Viruses with hemadsorption: Orthomyxovirus Paramyxovirus Togavirus calicivirus |
|
|
What happens in noncytocidal change? What type of viruses is this usually seen in?
|
Noncytocidal virus usually do not kill the cells in which they replicate.
They often cause persistent infection, in which infected cell produce and release virions but overall cellular metabolism is little affected Effects on specialized cells: Organs or tissues function Hormonal levels Enzyme activity Chemical and electrical neurotransmitter function They are often seen in cells infected with RNA viruses, such as: Pestivirus Arenaviruses Retroviruses paramyxoviruses |
|
|
Some infections cause behavioral changes - what type of infection is this and what kinds of changes are induced?
|
Noncytocidal viral infection
Borna virus induce behavior change in rats, cats, and horse Possible cause of depression and bipolar neuropsychiatric illness in human |
|
|
What kind of infection does lymphocytic choriomeningitis virus cause?
|
Noncytocidal viral infection
-Decrease the growth hormone mRNA production: delayed growth -Replicating in B cell of the islet of Langerhans: hyperglycemia |
|
|
What happens in viral interference? What two mechanisms mediates it?
|
It occurs when a virus-infected cell resists super-infection with the same or different virus.
It is mediated by two mechanisms: -Defective interfering mutants (only against the homologueous virus) -Interferons |
|
|
What happens when the virus causes no CPE?
|
no morphologic change, but could have subtle functional changes: reduced hormone response, reduced enzymatic activity, blocking neurotransmitter release, behavior changes, metabolic dysfunction or change.
|
