Antivirals US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Antivirals. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Antivirals US Medical PG Question 1: A 32-year-old man comes to the physician for a follow-up examination 1 week after being admitted to the hospital for oral candidiasis and esophagitis. His CD4+ T lymphocyte count is 180 cells/μL. An HIV antibody test is positive. Genotypic resistance assay shows the virus to be susceptible to all antiretroviral therapy regimens and therapy with dolutegravir, tenofovir, and emtricitabine is initiated. Which of the following sets of laboratory findings would be most likely on follow-up evaluation 3 months later?
$$$ CD4 +/CD8 ratio %%% HIV RNA %%% HIV antibody test $$$
- A. ↓ ↓ negative
- B. ↑ ↑ negative
- C. ↓ ↑ negative
- D. ↑ ↓ positive (Correct Answer)
- E. ↓ ↑ positive
Antivirals Explanation: ***↑ ↓ positive***
- With effective **antiretroviral therapy (ART)**, the **CD4+/CD8 ratio** would increase as **CD4+ T cell counts rise** and **CD8+ T cell counts decrease**.
- **HIV RNA (viral load)** would significantly decrease (ideally to undetectable levels) due to the suppression of viral replication, but HIV antibodies would remain positive indefinitely.
*↓ ↓ negative*
- A decrease in the **CD4+/CD8 ratio** and **HIV RNA** (viral load) along with a negative **HIV antibody test** is inconsistent with successful ART.
- A negative HIV antibody test would mean the patient was never infected, which contradicts the initial positive result and symptoms.
*↑ ↑ negative*
- An increase in the **CD4+/CD8 ratio** is expected with ART, but an increase in **HIV RNA** (viral load) indicates treatment failure.
- A negative **HIV antibody test** is impossible after a confirmed positive result, regardless of treatment success.
*↓ ↑ negative*
- A decrease in the **CD4+/CD8 ratio** would suggest worsening immune function, while an increase in **HIV RNA** indicates treatment failure.
- A negative **HIV antibody test** is not possible once a patient has developed antibodies to HIV.
*↓ ↑ positive*
- A decrease in the **CD4+/CD8 ratio** would indicate immune decline, contrary to the expected improvement with effective ART.
- An increase in **HIV RNA (viral load)** would signify treatment failure, even if HIV antibodies remain positive.
Antivirals US Medical PG Question 2: A 45-year-old man comes to the emergency department with fever, nonproductive cough, and difficulty breathing. Three years ago, he underwent lung transplantation. A CT scan of the chest shows diffuse bilateral ground-glass opacities. Pathologic examination of a transbronchial lung biopsy specimen shows several large cells containing intranuclear inclusions with a clear halo. Treatment with ganciclovir fails to improve his symptoms. He is subsequently treated successfully with another medication. This drug does not require activation by viral kinases and also has known in-vitro activity against HIV and HBV. The patient was most likely treated with which of the following drugs?
- A. Lamivudine
- B. Foscarnet (Correct Answer)
- C. Elvitegravir
- D. Zanamivir
- E. Acyclovir
Antivirals Explanation: ***Foscarnet***
- The patient presents with **cytomegalovirus (CMV) pneumonitis** post-lung transplant, evidenced by **diffuse bilateral ground-glass opacities** and **intranuclear inclusions with a clear halo** on biopsy, and initial treatment with **ganciclovir failed**.
- **Foscarnet** is an alternative antiviral that does not require activation by viral kinases and is effective against viruses that develop **ganciclovir resistance** due to mutations in UL97 phosphotransferase, which activates ganciclovir. It also has known activity against **HIV** and **HBV**, fitting the description.
*Lamivudine*
- **Lamivudine** is a **nucleoside reverse transcriptase inhibitor (NRTI)** primarily used for **HIV** and **HBV** infections.
- It has **no activity against CMV** and would not be used to treat CMV pneumonitis, especially after ganciclovir failure.
*Elvitegravir*
- **Elvitegravir** is an **integrase inhibitor** used in combination therapy for **HIV infection**.
- It has **no activity against CMV** and would not be effective in treating CMV pneumonitis.
*Zanamivir*
- **Zanamivir** is a **neuraminidase inhibitor** used to treat and prevent **influenza A and B viruses**.
- It has **no activity against CMV** and is not indicated for the patient's condition.
*Acyclovir*
- **Acyclovir** is a guanosine analog primarily used to treat **herpes simplex virus (HSV)** and **varicella-zoster virus (VZV)** infections.
- It has **limited to no activity against CMV** at therapeutic doses and would not be effective in this case.
Antivirals US Medical PG Question 3: During an experiment conducted to alter the infectivity of common viruses that affect humans, an investigator successfully increases the host range of human immunodeficiency virus (HIV). The new strain of the virus can infect fibroblast-like cells in addition to the usual target of HIV. Which of the following is the most likely explanation for the increase in the host range of the virus?
- A. Reassortment of genetic material between segments of two viruses
- B. Increased rate of budding out of host cells
- C. Excessive activity of viral RNA polymerase
- D. Point mutations in the hemagglutinin gene
- E. Mutation of the gene coding for viral surface glycoproteins (Correct Answer)
Antivirals Explanation: ***Mutation of the gene coding for viral surface glycoproteins***
- Viral **surface glycoproteins** are crucial for initial host cell recognition and binding, determining **cell tropism** and **host range**. A mutation in these genes can alter the binding specificity, allowing the virus to infect new cell types.
- Changes in these glycoproteins can enable interaction with different host cell receptors, thereby expanding the range of cells the virus can infect.
*Reassortment of genetic material between segments of two viruses*
- **Reassortment** typically occurs in viruses with segmented genomes (e.g., influenza virus), leading to rapid genetic shifts. HIV has a non-segmented RNA genome, so reassortment as described is not applicable.
- While reassortment can increase virulence or transmissibility, it's not the primary mechanism by which non-segmented RNA viruses like HIV would expand their host range to a new cell type through a single event in a controlled experiment.
*Increased rate of budding out of host cells*
- An increased rate of budding affects the **viral load** and potentially the efficiency of spread, but it does not alter the fundamental ability of the virus to infect new cell types by changing its **cellular tropism**.
- This mechanism relates to the release of new virions from infected cells rather than the initial entry or binding to a host cell.
*Excessive activity of viral RNA polymerase*
- **RNA polymerase activity** can impact replication efficiency and mutation rates, but it does not directly determine the host cell specificity or the ability to bind to new cell surface receptors.
- While increased activity might lead to more mutations overall, the specific mechanism for increased host range would still involve a change in a gene coding for a surface protein responsible for cell binding.
*Point mutations in the hemagglutinin gene*
- **Hemagglutinin** is a surface glycoprotein explicitly found in **influenza viruses**, involved in binding to sialic acid receptors. HIV does not possess a hemagglutinin gene.
- Therefore, mutations in this gene cannot explain changes in HIV's host range.
Antivirals US Medical PG Question 4: A 60-year-old man comes to the physician’s office with jaundice. Liver ultrasound reveals a shrunken liver and biopsy reveals cirrhosis. Hepatitis serologies are below:
Anti-HAV: negative
HBsAg: negative
HBsAb: positive
HBeAg: negative
Anti-HBe: negative
Anti-HBc: negative
Anti-HCV: positive
The hepatitis C viral load is 1,000,000 copies/mL. The patient is started on an antiviral regimen including sofosbuvir. What is the mechanism of action of this drug?
- A. Inhibits reverse transcriptase
- B. Inhibits integrase
- C. Inhibits synthesis of DNA-dependent DNA polymerase
- D. Inhibits RNA-dependent RNA polymerase (Correct Answer)
- E. Inhibits hepatitis C protease
Antivirals Explanation: ***Inhibits RNA-dependent RNA polymerase***
- Sofosbuvir is a **nucleotide analog** that targets the **HCV RNA-dependent RNA polymerase (NS5B)**, essential for viral replication.
- By inhibiting NS5B, it acts as a **chain terminator**, preventing the synthesis of new viral RNA strands.
*Inhibits reverse transcriptase*
- This mechanism is characteristic of drugs used to treat **HIV infection**, as reverse transcriptase is an enzyme found in retroviruses.
- Hepatitis C virus (HCV) is an **RNA virus** that replicates via an RNA intermediate, not DNA, and thus does not utilize reverse transcriptase.
*Inhibits integrase*
- Integrase inhibitors are a class of drugs primarily used in the treatment of **HIV infection**, preventing the viral DNA from integrating into the host genome.
- HCV replication does not involve an integration step into the host DNA, making this mechanism irrelevant for HCV treatment.
*Inhibits synthesis of DNA-dependent DNA polymerase*
- Inhibition of DNA-dependent DNA polymerase primarily targets organisms that replicate their DNA, such as **herpesviruses** or host cell processes.
- HCV is an RNA virus and does not synthesize or rely on a DNA-dependent DNA polymerase for its replication cycle.
*Inhibits hepatitis C protease*
- While **protease inhibitors (e.g., -previr drugs)** are an important class of anti-HCV drugs, sofosbuvir specifically targets the viral **RNA polymerase (NS5B)**.
- Protease inhibitors block the **NS3/4A protease**, which is responsible for cleaving the large HCV polyprotein into functional proteins.
Antivirals US Medical PG Question 5: A 40-year-old man presents with problems with his vision. He says he has been experiencing blurred vision and floaters in his left eye for the past few days. He denies any ocular pain, fever, or headaches. Past medical history is significant for HIV infection a few years ago, for which he is noncompliant with his antiretroviral medications and his most recent CD4 count was 100 cells/mm3. His temperature is 36.5°C (97.7°F), the blood pressure is 110/89 mm Hg, the pulse rate is 70/min, and the respiratory rate is 14/min. Ocular exam reveals a decreased vision in the left eye, and a funduscopic examination is shown in the image. The patient is admitted and immediately started on intravenous ganciclovir. A few days after admission he is still complaining of blurry vision and floaters, so he is switched to a different medication. Inhibition of which of the following processes best describes the mechanism of action of the newly added medication?
- A. Protein synthesis
- B. Nucleic acid synthesis (Correct Answer)
- C. Progeny virus release
- D. Viral penetration into host cells
- E. Viral uncoating
Antivirals Explanation: ***Nucleic acid synthesis***
- This patient likely has **cytomegalovirus (CMV) retinitis**, characterized by **blurred vision**, **floaters**, and **necrotizing retinitis** in an HIV-positive individual with a **low CD4 count (100 cells/mm3)**.
- The initial drug, **ganciclovir**, targets nucleic acid synthesis by inhibiting viral DNA polymerase. If ganciclovir fails, a common second-line agent like **foscarnet** or **cidofovir** is used, and both also inhibit viral **nucleic acid (DNA) synthesis** through different mechanisms (foscarnet directly inhibits DNA polymerase, cidofovir is a nucleotide analog).
*Protein synthesis*
- This mechanism is targeted by certain antibacterial and antifungal drugs, but not typically by antiviral medications used for CMV.
- Antiviral drugs generally target specific viral processes, distinct from host protein synthesis, to limit toxicity.
*Progeny virus release*
- This mechanism is primarily targeted by **neuraminidase inhibitors** (e.g., oseltamivir, zanamivir) used to treat influenza, which prevent the release of new viral particles from infected cells.
- It is not a common mechanism for CMV antivirals.
*Viral penetration into host cells*
- Medications that inhibit viral penetration or entry, such as **fusion inhibitors** (e.g., enfuvirtide for HIV) or **CCR5 antagonists** (e.g., maraviroc for HIV), prevent the virus from entering the host cell.
- These mechanisms are not relevant to the treatment of CMV retinitis.
*Viral uncoating*
- **Amantadine** and **rimantadine** are examples of antiviral drugs that inhibit **viral uncoating** by interfering with the M2 ion channel in influenza A.
- This mechanism is specific to influenza viruses and is not involved in the action of CMV antiviral medications.
More Antivirals US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
