Test on Herpes Simplex Virus: Pathogenesis and Therapies
Herpes Simplex Virus: Pathogenesis & Therapies Guide
Test: HSV biology, HSV entry and transmission, HSV latency and reactivation, HSV immunology, Immune evasion, Vaccines, Oncolytic therapy, Gene therapy and vectors, Research
20 questions
Question 1: HSV gC inhibits the complement system by binding to C3b.
A. Ano
B. Ne
Explanation: HSV protein gC inhibits the complement system by binding to C3b.
Question 2: How does the HSV-1 UL41 protein evade the host antiviral response?
A. By degrading cGAS through its RNase activity
B. By deamidating an asparagine residue on cGAS
C. By impairing NF-κB activation through serine protease activity
D. By deubiquitinating TRAF3
Explanation: The study materials state that the HSV-1 UL41 protein degrades cGAS via RNase activity, effectively evading the cGAS/STING-mediated DNA-sensing pathway. Other options describe evasion mechanisms carried out by different HSV proteins.
Question 3: In the trivalent subunit vaccine, gC2 and gE2 were included because they were found to enhance immune evasion.
A. Ano
B. Ne
Explanation: The study materials state that in the trivalent subunit vaccine, gC2 and gE2 suppressed immune evasion, rather than enhancing it.
Question 4: According to the study materials, what was the effect of the HerpV vaccine on HSV-2 shedding following initial vaccination in its Phase 1 trial?
A. It increased HSV-2 shedding by 15%.
B. It reduced HSV-2 shedding by 15%.
C. It reduced HSV-2 shedding by 40%.
D. It had no observed effect on HSV-2 shedding.
Explanation: In a phase 1 trial, HerpV reduced HSV-2 shedding by 15% following initial vaccination, in addition to eliciting HSV-2-specific CD4+ and CD8+ T cells.
Question 5: ONCR-GBM is currently in Phase 1 clinical trials for glioblastoma.
A. Ano
B. Ne
Explanation: Table 3 shows that the status for ONCR-GBM is not disclosed ('—') regarding its clinical trial phase, it does not state that it is in Phase 1 clinical trials.