Viro - Lecture 4

drraythe's version from 2015-08-30 15:36


Question Answer
What is oncogenesis?The process of developing tumors
Which DNA virus did we focus on that was oncogenic?HERPES
What is an episome?A self-replicating genome (potential to cause dysregulation in the cell)
Which RNA virus did we focus on that was oncogenic?RETRO
What is an oncogene?Any genetic element associated w/ cancer induction
How are oncogenes activated?Via insertional mutagenesis, via transposition, via gene amplification, via mutation
What are C-oncogenes? (fxn)CELLULAR-oncogene. They are involved in the regulation of cell growth, division, & differentiation
What are V-oncogenes? (fxn)VIRAL-oncogenes. These usually act as growth factors, growth factor receptors, & hormone receptors, intracellular signal transducers, nuclear transcription factors (aka all growth stuff, all CANCER potential)
What do V-oncogenes usually code for? What are they usually under the control of?Usually code for exons (region of genome that will be expressed), & are under the control of LTRs (long terminal repeats)
What are ways that V-oncogenes escape from regulation?They may undergo mutations which affect protein-protein interactions, or they may join other viral genes which redirects them to another location
How does a DNA virus produce a tumor in a non-productive infection?They can integrate their genome into the cellular DNA or acting as an episome (plasmid).
If you were a retrovirus, what would you say the down-side of having a v-oncogene is?They are usually replication defective, which means they needed a replication-competent virus to help the replicate.
Viruses produce tumors (oncogenesis) by?(1) Transducing (phage xfers genetic material from one cell to the next)
(2) Cis activating (I think this means changing the cell's DNA) MY NOTES SAID: viruses bring an oncogenic gene (v-onco) OR change a cellular onco
Explain the "cis-activating" picture in this sectionA replication-competent virus replicates, & has LTRs which allow it to insert in the host genome. When the virus inserts, the host's oncogene is triggered or disrupted, which can cause the tumor
Explain the "transducing" picture in this section (transducing oncogenes)A replication-INCOMPETENT virus is carrying a v-oncogene, but it cannot replicate. However, if another replication-competent virus is able to help the incompetent one replicate, then there is an extremely rapid production of the oncogenes
Which immunity plays the major role in clearing a virus infection? Which immunity protects against re-infections?Clearing is done by Cellular immunity. Prevention/protection is done by humoral immunity.
What is the most important host factor in fighting a virus?Their IMMUNE SYSTEM!
list some examples of when the body's immune system hurts more than it helps(1) An Ab binds to cell surface Fc receptors, but the ab hasn't neutralized the virus, so the infection then spreads to the cell it bound to
(2) Immune complex deposition can damage organs
(3) Specific ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity) or complement mediated cell lysis starts killing more cells
(4) Increased secondary response to cytotoxic T-cells
What is passive immunity? How long does this last?Transfer of maternal antibodies from dam to fetus or newborn, protects them for the first few months against diseases the dam has experienced/been vaccinated (important for vaccination schedule)
What is translocation cutoff time? How long is it usually?The infants have limited time where their gut wall is open to absorb the maternal antibodies in the colostrum (GUT CLOSURE!). It is 2 days for most species we care about
Even if the colostrum only provides partial protection for the infant, what is the good news?Viral replication is limited enough that it stimulates an immune response w/out causing disease
What is the most common immunodeficiency dz of domestic animals?FAILURE OF MATERNAL ANTIBODY TRANSFER
List some reasons for failure of maternal antibody xferPremature/weak birth of baby, delay to first suckle, death of dam, low colostrum production, low Ab levels in maternal serum → milk, poor maternal instinct, premature lactation, too many in the litter, domination of weak in little by the strong, poor management
*Know the chart on pg35. Explain it (window of susceptibility)There is a point where the maternal Abs are decreasing (curve going down), & its lower than the level needed for protection BUT there are still enough maternal Abs to neutralize the Vx. The upward curve is the Abs getting developed after vx, but in the window of susceptibility, they might be getting neutralized (so, why we booster etc)
What is the apprx half-life of maternal antibodies in... cattle/horses? cats/dogs? Any variation might be due to what?Cattle/horses= 21 days. Cats/dogs= 10 days. *This will last much longer if the maternal antibodies were very concentrated
What are the 2 types of chronic infections?(1) True latency (2) Persistence
What is "true latency" of a virus?The virus remains completely latent following primary infection. Its genome may be integrated into the cellular genome or exist as episomes(plasmids)
What is "persistence" of a virus?The virus replicates continuously in the body at a very low level
list some mechanisms of viral persistenceAntigenic variation (change surface proteins to avoid host immune response), immune tolerance (causes reduced response to an antigen), restricted gene expression, down-regulation of molecules involved in immune recognition (they hide their MCH1's), they choose to infect immuno-privileged areas of the body so the body cant get to them, direct infection of the immune cells themselves