Virus Infection Cycle
Viruses that must fuse with the cell membrane at some point.
What are enveloped viruses?
The main signaling molecule that activates an antiviral environment (which we focused on in class!)
What is interferon?
Key mechanistic difference between herpes and retroviral latency.
What is integration for retroviruses? Or episome for herpes--either is fine.
The signal for HIV fusion.
What is CD4/CCR4 binding?
You run many different virus proteins on a gel, what determines the placement of the bands on the gel?
What is size and/or charge? (either for 100)
Parts of a virus can you detect inside of a cell if you block attachment during an infection.
None!
Name 3 effector functions of B cells.
What is: Opsonization, Neutralization, and ADCC?
The reason acyclovir works well.
What is better binding affinity to herpes TK than human TK?
Name one of the top three focus methods for HIV cure.
What is "lock & block" / "kick/shock & kill" / "gene editing"
An essential technique in virology used to quantify lytic viruses by counting areas of clearing among a cell monolayer. You are considered a true virologist if you have done this :)
What is a plaque assay?
The Order of viruses that make nested mRNAs.
What is Nidovirales? (I will accept coronaviruses for 200 points)
The reason an inactivated vaccine might induce a better immune response than a protein subunit vaccine.
What is more epitopes? (Whole virus provides more antigens vs just one protein, though it could depend on the virus)
Function of noncoding RNA from IRL region.
Bind and inhibit transcription; inhibits apotosis
Name the current treatment for HIV (100) and 2 (100 ea.) reasons why it works.
Antiretroviral therapy (ART), it works because 1) the protease inhibitor prevents maturation, and 2) the combination therapy lowers selection of resistant mutants.
You have isolated sostressedfromfinals (SSFF) viruses from 2 human patients and one bird. When probing a northern blot for a glycoprotein mRNA, the bird sample does not have a band, but you are sure the RNA was loaded. What could have happened?
Your probe is likely specific to the human variant, and the bird variant has different sequences
The viral enzyme that would be inhibited by a nucleotide analogue antiviral.
What is the polymerase?
Why would someone add aluminum to a vaccine in addition to the antigen?
As an adjuvant--it's in many vaccines including Gardasil 9 (for HPV!)
Delivered when viral tegument enters cells, important for herpesvirus intracellular transport.
What is VP16?
The primate populations HIV-1/2 crossed over from.
What are Chimps/Gorillas/Sooty Mangabeys?
Name 4 experimental techniques (100 pts each) we talked about, either in lecture or on worksheets.
Any 4 of the following (100 each)
A: Radioactive labeling
B: Agarose gels/ gels
C: Molecular probes
D : IFN assays
E: qPCR
F: cloning
G: IF
You want to make an RNA vaccine that elicits a strong response. You think that more RNA is better but it is difficult to make even more RNA with current production costs. What can you add to the RNA such that you are still only injecting the same RNA with the lipid particles, but the patient now has more RNA in their cells?
You can add the gene for RdRp along with the sequences necessary for it to recognize the RNA and make more inside the cells. (This is a real thing!!)
Dengue viruses have a wide cell tropism including immune cells, where the virus enters via endocytosis and fuses in an acidic endosome. Additionally, previous Dengue virus infection could result in antibody-dependent enhancement, where a second Dengue virus infection leads to a worse outcome. Propose a mechanism for why these antibodies would enhance an infection.
Antibodies binding Dengue viruses could attach to Fc receptors on immune cells, where the virus will be taken in by FcR-mediated endocytosis. There, the infection cycle starts anew since the endosome will acidify and allow fusion. This allows more cells to be infected :)
You've discovered a new antiviral against herpesviruses, and you've found it to be a viral nuclease inhibitor. If you isolated just the viral DNA from infected cells, what would you expect to see on a gel when comparing treated vs untreated cells?
You would expect to see a large band in treated cells and a smaller band for untreated cells. If the nuclease is inhibited, then the virus could not cleave the large concatamer.
HIV-1 DNA can no longer integrate. Why might you still see viral mRNAs?
The HIV LTR is still intact, so cellular transcription factors can bind and initiate transcription.
Name all 5 TA's, the professors, and what the professors labs study.
What is Karly, Min Sub, Pablo, Serina, Vivian, Melody, and Oliver. Li lab studies alphaviruses and interferon, Fregoso lab studies HIV and DNA damage response.