Antivirals

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 research group wants to assess the safety and toxicity profile of a new drug. A clinical trial is conducted with 20 volunteers to estimate the maximum tolerated dose and monitor the apparent toxicity of the drug. The study design is best described as which of the following phases of a clinical trial?

• A. Phase 0
• B. Phase III
• C. Phase V
• D. Phase II
• E. Phase I (Correct Answer)

Antivirals Explanation: ***Phase I*** - **Phase I clinical trials** involve a small group of healthy volunteers (typically 20-100) to primarily assess **drug safety**, determine a safe dosage range, and identify side effects. - The main goal is to establish the **maximum tolerated dose (MTD)** and evaluate the drug's pharmacokinetic and pharmacodynamic profiles. *Phase 0* - **Phase 0 trials** are exploratory studies conducted in a very small number of subjects (10-15) to gather preliminary data on a drug's **pharmacodynamics and pharmacokinetics** in humans. - They involve microdoses, not intended to have therapeutic effects, and thus cannot determine toxicity or MTD. *Phase III* - **Phase III trials** are large-scale studies involving hundreds to thousands of patients to confirm the drug's **efficacy**, monitor side effects, compare it to standard treatments, and collect information that will allow the drug to be used safely. - These trials are conducted after safety and initial efficacy have been established in earlier phases. *Phase V* - "Phase V" is not a standard, recognized phase in the traditional clinical trial classification (Phase 0, I, II, III, IV). - This term might be used in some non-standard research contexts or for post-marketing studies that go beyond Phase IV surveillance, but it is not a formal phase for initial drug development. *Phase II* - **Phase II trials** involve several hundred patients with the condition the drug is intended to treat, focusing on **drug efficacy** and further evaluating safety. - While safety is still monitored, the primary objective shifts to determining if the drug works for its intended purpose and at what dose.

Antivirals US Medical PG Question 6: A 49-year-old woman presents to her primary care doctor in late December with malaise. She reports worsening fatigue, myalgias, headache, and malaise that started 1 day ago. She works as a lunch lady at an elementary school. Her past medical history is notable for a distal radius fracture after a fall 2 years ago, but she is otherwise healthy and takes no medications. She does not smoke or drink alcohol. She is married and has 3 adult children who are healthy. Her temperature is 102.9°F (39.4°C), blood pressure is 101/61 mmHg, pulse is 112/min, and respirations are 21/min. On exam, she appears lethargic and uncomfortable but is able to answer questions appropriately. Breath sounds are normal bilaterally. She is started on intravenous fluids and a pharmacologic agent for treatment. Which of the following is the most likely mechanism of action of the drug being used to treat this patient?

• A. Neuraminidase inhibitor (Correct Answer)
• B. Reverse transcriptase inhibitor
• C. RNA-dependent polymerase inhibitor
• D. DNA polymerase inhibitor
• E. Protease inhibitor

Antivirals Explanation: ***Neuraminidase inhibitor*** - The patient's symptoms (malaise, fatigue, myalgias, headache, fever) with rapid onset in **late December**, especially given her exposure to children in an elementary school, are highly suggestive of **influenza**. - **Neuraminidase inhibitors** (e.g., oseltamivir, zanamivir) are the primary antiviral treatment for influenza, preventing the release of new viral particles from infected cells. *Reverse transcriptase inhibitor* - **Reverse transcriptase inhibitors** are primarily used in the treatment of **HIV infection**, which typically presents with a different constellation of symptoms and has a chronic rather than acute course. - This class of drugs targets the enzyme **reverse transcriptase**, which is not central to the influenza virus replication cycle. *RNA-dependent polymerase inhibitor* - While **baloxavir marboxil** (an RNA polymerase inhibitor) is FDA-approved for influenza treatment, **neuraminidase inhibitors** remain the most commonly used first-line agents. - In this clinical scenario without specific contraindications to neuraminidase inhibitors, oseltamivir or zanamivir would be the most likely agents prescribed. *DNA polymerase inhibitor* - **DNA polymerase inhibitors** are primarily used to treat **DNA viral infections** such as herpes viruses (e.g., acyclovir for HSV/VZV) or cytomegalovirus (e.g., ganciclovir). - Influenza is an **RNA virus** and therefore does not have a DNA polymerase for replication. *Protease inhibitor* - **Protease inhibitors** are a class of antiviral drugs predominantly used in the treatment of **HIV** and **Hepatitis C virus** infections. - Influenza viruses do not have a protease target that is typically inhibited by these drugs for therapeutic purposes.

Antivirals US Medical PG Question 7: A 44-year-old man comes to the physician for a follow-up examination. Eight months ago, he was diagnosed with HIV infection and combined antiretroviral treatment was begun. He feels well. He does not smoke or drink alcohol. Current medications include lamivudine, zidovudine, atazanavir, and trimethoprim-sulfamethoxazole. Laboratory studies show: Hemoglobin 11.2 g/dL Mean corpuscular volume 102 μm3 Leukocyte count 2,600/mm3 Segmented neutrophils 38% Lymphocytes 54% Platelet count 150,000/mm3 Serum Folate normal Lactate 6.0 mEq/L (N = 0.5–2.2) Arterial blood gas analysis on room air shows: pH 7.34 pCO2 55 mm Hg pO2 99 mmHg HCO3- 14 mEq/L The drug most likely responsible for this patient's current laboratory findings belongs to which of the following classes of drugs?

• A. Entry inhibitor
• B. Dihydrofolate reductase inhibitor
• C. Nucleoside reverse transcriptase inhibitor (Correct Answer)
• D. Integrase inhibitor
• E. Protease inhibitor

Antivirals Explanation: ***Nucleoside reverse transcriptase inhibitor*** - The patient presents with **macrocytic anemia** (Hgb 11.2, MCV 102), **leukopenia** (2600), **lactic acidosis** (lactate 6.0, pH 7.34, HCO3- 14, pCO2 55), and is on a regimen including **zidovudine** and **lamivudine**. - **Zidovudine** (AZT), a nucleoside reverse transcriptase inhibitor (NRTI), is well-known for causing **myelosuppression** (anemia, leukopenia) and **mitochondrial toxicity**, which can lead to lactic acidosis due to impaired oxidative phosphorylation. *Entry inhibitor* - Entry inhibitors like **enfuvirtide** and **maraviroc** block HIV from entering CD4+ cells; side effects are mainly injection site reactions or hepatotoxicity. - They are not associated with macrocytic anemia, leukopenia, or lactic acidosis. *Dihydrofolate reductase inhibitor* - **Trimethoprim-sulfamethoxazole (TMP-SMX)**, listed as a current medication, is a dihydrofolate reductase inhibitor that can cause **bone marrow suppression** mimicking folate deficiency. - However, the patient's folate levels are normal, and the significant lactic acidosis points away from TMP-SMX as the primary cause of all findings. *Integrase inhibitor* - Integrase inhibitors like **raltegravir** or **dolutegravir** prevent the integration of viral DNA into the host genome. - Their primary side effects are typically gastrointestinal (nausea, diarrhea), headache, or insomnia, and they do not cause macrocytic anemia, leukopenia, or lactic acidosis. *Protease inhibitor* - **Atazanavir**, a protease inhibitor from the patient's regimen, can cause **hyperbilirubinemia** and **lipodystrophy** but is not directly linked to the bone marrow suppression and severe lactic acidosis seen here. - Other protease inhibitors can cause metabolic complications, but not this specific constellation of hematologic and metabolic abnormalities.

Antivirals US Medical PG Question 8: A 26-year-old patient presents to your office with rhinorrhea that you believe to be viral in origin. He respectfully requests treatment with antibiotics, and he demonstrates an understanding of the risks, benefits, and alternatives to treatment. His mental status is intact, and you believe him to have full decision-making capacity. Which of the following is the best course of action?

• A. Refer the patient to an infectious disease specialist
• B. Prescribe ciprofloxacin
• C. Prescribe amoxicillin
• D. Deny the patient's request (Correct Answer)
• E. Prescribe zidovudine

Antivirals Explanation: ***Deny the patient's request*** - As a physician, you have a professional obligation to act in the patient's best interest, which includes avoiding **unnecessary treatments** that could cause harm. - Prescribing antibiotics for a **viral infection** contributes to **antibiotic resistance**, exposes the patient to potential side effects (e.g., *C. difficile* infection), and contradicts evidence-based medical practice. *Refer the patient to an infectious disease specialist* - This is an **unnecessary referral** as the diagnosis is clear (viral rhinorrhea) and does not require specialized infectious disease management. - Referral would incur **additional healthcare costs** and delays for a condition that does not warrant such specialized consultation. *Prescribe ciprofloxacin* - Ciprofloxacin is a **broad-spectrum antibiotic** that is completely ineffective against viral infections and carries a risk of significant side effects, including **tendon rupture** and *C. difficile* infection. - Misuse of powerful antibiotics like ciprofloxacin promotes **antibiotic resistance**, making future bacterial infections harder to treat. *Prescribe amoxicillin* - Amoxicillin is an antibiotic and, like other antibiotics, is **ineffective against viral infections** such as viral rhinorrhea. - Prescribing it would contribute to **antibiotic resistance** and expose the patient to potential drug side effects (e.g., rash, gastrointestinal upset) without any clinical benefit. *Prescribe zidovudine* - Zidovudine is an **antiretroviral medication** specifically used for the treatment of **HIV infection**. - It has absolutely **no role** in treating common viral rhinorrhea and would be an inappropriate and potentially harmful prescription.

Antivirals US Medical PG Question 9: An HIV-positive patient with a CD4+ count of 45 is receiving recommended first-line treatment for a case of cytomegalovirus retinitis. Coadministration with which of the following agents would be most likely to precipitate a deficiency of neutrophils in this patient?

• A. Ritonavir
• B. Raltegravir
• C. Foscarnet
• D. Efavirenz
• E. Zidovudine (Correct Answer)

Antivirals Explanation: ***Zidovudine*** - **Zidovudine (AZT)** is a nucleoside reverse transcriptase inhibitor (NRTI) that is well-known for causing **myelosuppression**, particularly **neutropenia** and **anemia**. - In an HIV-positive patient with a low **CD4+ count** and concurrent treatment for **CMV retinitis** (which often involves drugs like ganciclovir that can also cause myelosuppression), adding zidovudine significantly increases the risk of severe neutropenia. *Ritonavir* - **Ritonavir** is a protease inhibitor primarily known for its role as a **pharmacokinetic booster** in HIV therapy, enhancing the levels of other antiretrovirals. - While it can cause gastrointestinal side effects and hepatotoxicity, **myelosuppression** and specifically neutropenia are not its primary or common adverse effects. *Raltegravir* - **Raltegravir** is an integrase strand transfer inhibitor (INSTI) generally well-tolerated with a favorable side effect profile. - Common side effects include headache, nausea, and fatigue, but it is **not typically associated with significant myelosuppression** or neutropenia. *Foscarnet* - **Foscarnet** is an antiviral agent used for treating CMV retinitis, particularly in cases of ganciclovir resistance. - Its major dose-limiting toxicities include **nephrotoxicity** and **electrolyte disturbances** (e.g., hypocalcemia, hypomagnesemia), not primarily neutropenia. *Efavirenz* - **Efavirenz** is a non-nucleoside reverse transcriptase inhibitor (NNRTI) associated with central nervous system side effects such as dizziness, insomnia, and vivid dreams. - While skin rash and hepatotoxicity can occur, **bone marrow suppression** leading to neutropenia is not a characteristic or frequent adverse effect of efavirenz.

Antivirals US Medical PG Question 10: A 63-year-old man with high blood pressure, dyslipidemia, and diabetes presents to the clinic for routine follow-up. He has no current complaints and has been compliant with his chronic medications. His blood pressure is 132/87 mm Hg and his pulse is 75/min and regular. On physical examination, you notice that he has xanthelasmas on both of his eyelids. He currently uses a statin to lower his LDL but has not reached the LDL goal you have set for him. You would like to add an additional medication for LDL control. Of the following, which statement regarding fibrates is true?

• A. Fibrates inhibit the rate-limiting step in cholesterol synthesis
• B. Fibrates can potentiate the risk of myositis when given with statins (Correct Answer)
• C. Fibrates can cause significant skin flushing and pruritus
• D. Fibrates can increase the risk of cataracts
• E. The primary effect of fibrates is to lower LDL

Antivirals Explanation: ***Fibrates can potentiate the risk of myositis when given with statins*** - **Fibrates** and **statins** can both independently cause muscle toxicity (myopathy, rhabdomyolysis). - When used concomitantly, especially **gemfibrozil** with statins, there is an **increased risk of muscle adverse events** due to pharmacokinetic interactions that raise statin levels. - This combination requires careful monitoring and is often avoided; **fenofibrate** is preferred over gemfibrozil when combination therapy is needed. *Fibrates inhibit the rate-limiting step in cholesterol synthesis* - This statement describes the mechanism of action of **statins**, which inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis. - Fibrates, on the other hand, act primarily by activating **PPAR-alpha receptors**, leading to altered lipid metabolism (increased lipoprotein lipase activity, decreased VLDL synthesis). *Fibrates can cause significant skin flushing and pruritus* - **Niacin (nicotinic acid)** is the lipid-modifying agent most commonly associated with significant **skin flushing and pruritus**, mediated by prostaglandin release. - Fibrates do not cause significant flushing; their side effects include GI disturbances, gallstones, and potential muscle toxicity. *Fibrates can increase the risk of cataracts* - This is **not an established adverse effect** of the fibrate class. - While **clofibrate** (an older, largely discontinued fibrate) showed some association with cataracts in older studies, this is not a recognized risk with modern fibrates like **fenofibrate** and **gemfibrozil**. - Current fibrate therapy does not require routine ophthalmologic monitoring for cataracts. *The primary effect of fibrates is to lower LDL* - The primary effect of **fibrates** is to significantly **lower triglycerides** (by 30-50%) and **increase HDL cholesterol** levels (by 10-20%). - While they can cause a modest decrease in LDL cholesterol (10-15%), this is not their primary or most pronounced lipid-modifying effect. - Fibrates are primarily indicated for **hypertriglyceridemia** and mixed dyslipidemia.

Antivirals Flashcard 1 of 10

Question: Which HAART drugs prevent mature virion formation from large polypeptides?_____

Answer: Protease inhibitors

Antivirals Flashcard 2 of 10

Question: Which HIV protease inhibitor displays the most potent inhibition of CYP450?_____

Answer: Ritonavir

Antivirals Flashcard 3 of 10

Question: Resistance to Cidofovir and Foscarnet occurs with mutations to _____

Answer: viral DNA polymerase

Antivirals Flashcard 4 of 10

Question: Which classes of drugs inhibit HIV RNA to dsDNA formation?_____

Answer: NRTIs and NNRTIs

Antivirals Flashcard 5 of 10

Question: NS3/NS4A protease inhibitors and NS5A inhibitors are under clinical investigation to develop HCV treatment regimens that do not require _____ administration

Answer: interferon/ribavirin

Antivirals Flashcard 6 of 10

Question: amantadine

Answer:

Extra Information: Parkinson's disease, influenza A, rubellaexact mechanism unclear, but leads to increased dopamine releaseataxia

Antivirals Flashcard 7 of 10

Question: _____ insert themselves into the DNA of the reverse transcriptase, halting further elongation

Answer: NRTIs

Extra Information:    https://onlinemeded.org/spa/infectious-disease/hiv/acquire?ref=anki 

Antivirals Flashcard 8 of 10

Question: Enfuvirtide binds _____ of HIV inhibiting viral cell fusion with host cells

Answer: gp41

Extra Information:   Watch Maraviroc, fusion inhibitors, integrase inhibitors [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-antimicrobials/videos/medical-pharmacology-antimicrobials-antivirals-hiv-maraviroc-fusion-inhibitors-integrase-inhibitors?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/microbiology/antivirals/acquire?ref=anki 

Antivirals Flashcard 9 of 10

Question: NRTIs and _____ both are reverse transcriptase inhibitors used in the treatment of HIV

Answer: NNRTIs

Extra Information:    https://onlinemeded.org/spa/infectious-disease/hiv/acquire?ref=anki 

Antivirals Flashcard 10 of 10

Question: Ganciclovir triphosphate then incorporates into viral DNA, inhibiting _____

Answer: viral DNA-dependent DNA polymerase

Extra Information:   Watch Ganciclovir, valganciclovir, foscarnet, cidofovir [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-antimicrobials/videos/medical-pharmacology-antimicrobials-antivirals-other-ganciclovir-valganciclovir-foscarnet-cidofovir?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical] https://onlinemeded.org/spa/microbiology/antivirals/acquire?ref=anki