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pharmacoloy/pain control > antiviral > Flashcards

antiviral Flashcards

1
Q

What class of drug is Acyclovir?

A

A nucleoside analog, specifically a guanosine derivative.

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2
Q

What infections is Acyclovir used to treat?

A

Herpesvirus infections (HSV and VZV).

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3
Q

What enzyme selectively activates Acyclovir?

A

Viral thymidine kinase (TK).

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4
Q

Why does Acyclovir only get activated in infected cells?

A

Because only infected cells have viral thymidine kinase.

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5
Q

What is the first step in Acyclovir’s activation?

A

Phosphorylation by viral TK into acyclovir monophosphate.

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6
Q

What enzymes convert acyclovir monophosphate to its active form?

A

Host cell kinases.

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7
Q

What is the active form of Acyclovir?

A

Acyclovir triphosphate.

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8
Q

What does Acyclovir triphosphate compete with during viral DNA synthesis?

A

Deoxyguanosine triphosphate (dGTP).

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9
Q

What happens when Acyclovir is incorporated into viral DNA?

A

It causes chain termination.

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10
Q

What is the result of chain termination by Acyclovir?

A

It halts viral DNA replication and prevents production of new virions.

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11
Q

Why does Acyclovir specifically target infected cells?

A

Because it depends on viral thymidine kinase (TK) for activation, which is only present in infected cells.

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12
Q

What prevents Acyclovir activation in non-infected cells?

A

The absence of viral thymidine kinase.

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13
Q

How does Acyclovir spare host cells?

A

Non-infected cells cannot activate the drug, preventing toxicity.

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14
Q

What happens if some Acyclovir is phosphorylated in host cells?

A

The active form concentration is too low to affect host DNA polymerase.

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15
Q

What ensures Acyclovir’s selective toxicity?

A

It only reaches effective levels in infected cells and does not significantly inhibit host DNA polymerase.

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16
Q

What do viruses rely on to replicate?

A

Host cell enzymes, ribosomes, and other cellular machinery.

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17
Q

How are viruses different from bacteria in terms of replication?

A

Viruses cannot independently perform protein synthesis or metabolism.

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18
Q

Why is it difficult to design antiviral drugs?

A

Because blocking viral replication can also harm normal host cell processes.

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19
Q

What must selective antiviral drugs target?

A

Viral-specific proteins (like polymerase or protease) or unique steps in the viral life cycle.

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20
Q

What type of virus is HIV?

A

A retrovirus.

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21
Q

Why is HIV classified as a retrovirus?

A

Because it uses reverse transcriptase to convert RNA into DNA.

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22
Q

What receptor does HIV bind to on host cells?

A

CD4 receptor.

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23
Q

What co-receptors help HIV bind and fuse with host cells?

A

CCR5 or CXCR4.

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24
Q

What happens during reverse transcription in HIV replication?

A

Viral RNA is converted into complementary DNA (cDNA) by reverse transcriptase.

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25
What enzyme integrates viral cDNA into the host genome?
Integrase.
26
What does the host cell do after integration of viral DNA?
Produces viral RNA and proteins using transcription and translation.
27
What happens during assembly and budding in HIV?
New viral particles are assembled and bud from the host cell.
28
What do entry inhibitors do in HIV treatment?
Block viral entry into host cells (e.g., maraviroc, enfuvirtide).
29
What do NRTIs do?
Inhibit reverse transcriptase by causing chain termination (e.g., zidovudine, tenofovir).
30
How do NNRTIs work?
Bind allosterically to reverse transcriptase to inhibit it (e.g., efavirenz).
31
What do integrase inhibitors block?
Integration of viral DNA into the host genome (e.g., raltegravir).
32
What do protease inhibitors prevent?
Viral maturation by blocking protease activity (e.g., darunavir).
33
Why is combination therapy used to treat viral infections?
To reduce resistance and enhance efficacy by targeting multiple viral mechanisms.
34
What contributes to drug resistance in viruses?
High mutation rates, especially in RNA viruses like HIV and HCV.
35
How does combination therapy help prevent resistance?
By attacking the virus from multiple angles, reducing the chance of mutations escaping treatment.
36
How does combination therapy improve efficacy?
Drugs with different mechanisms work synergistically to increase effectiveness.
37
What is HAART?
Highly Active Antiretroviral Therapy—a combination of NRTIs, NNRTIs, and protease inhibitors for HIV.
38
What does HAART aim to do?
Combat resistance and suppress viral load in HIV.
39
What combination is used for HCV treatment?
Sofosbuvir (NS5B polymerase inhibitor) + Ledipasvir (NS5A inhibitor).
40
What does the Sofosbuvir + Ledipasvir combo target?
Viral replication and viral assembly in HCV.
40
What class of drug is Sofosbuvir?
A nucleotide prodrug.
41
How is Sofosbuvir activated?
It is converted into its active form (GS-461203) inside the cell.
42
What enzyme does Sofosbuvir inhibit?
NS5B RNA-dependent RNA polymerase.
43
What is the result of NS5B inhibition by Sofosbuvir?
It prevents HCV RNA replication.
44
How does Sofosbuvir differ from traditional nucleoside drugs?
It bypasses the initial phosphorylation step, increasing efficiency.
44
What advantages does Sofosbuvir have in pharmacokinetics?
Greater stability and better tissue penetration.
45
What is the overall effect of Sofosbuvir's improved pharmacokinetics?
Higher efficacy in treating HCV.
46
What do neuraminidase inhibitors do?
Block neuraminidase to prevent the release of new virions from infected cells.
47
What are two examples of neuraminidase inhibitors?
Oseltamivir and Zanamivir.
48
What is the mechanism of Baloxavir marboxil?
Inhibits cap-dependent endonuclease, blocking viral mRNA synthesis.
49
What step does Baloxavir marboxil disrupt in the influenza virus life cycle?
Viral mRNA synthesis.
50
What do Oseltamivir, Zanamivir, and Baloxavir marboxil all have in common?
They all target steps in viral replication.
51
How do the drugs for influenza differ in their targets?
Oseltamivir and Zanamivir block viral release; Baloxavir blocks viral mRNA synthesis.
52
What protein on SARS-CoV-2 allows it to bind to host cells?
The spike (S) protein.
53
What human receptor does the spike protein bind to?
ACE2 (angiotensin-converting enzyme 2) receptor.
54
Where is the ACE2 receptor found in the body?
Lungs, heart, kidneys, and intestines.
55
What happens to the spike protein after it binds to ACE2?
It undergoes a conformational change, exposing the S2 subunit.
56
What does the S2 subunit of the spike protein do?
Facilitates membrane fusion between the virus and host cell.
57
What host enzyme activates the spike protein?
TMPRSS2 (transmembrane serine protease 2).
58
How does TMPRSS2 help the virus enter the cell?
It cleaves and activates the spike protein for membrane fusion.
59
How can SARS-CoV-2 enter the host cell?
Through direct membrane fusion or via endocytosis.
60
What happens after SARS-CoV-2 enters the host cell?
The viral RNA is released into the cytoplasm for replication and translation.
61
What class of drug is Remdesivir?
Nucleotide analog.
62
What enzyme does Remdesivir inhibit?
RNA-dependent RNA polymerase (RdRp).
63
What is the mechanism of action of Remdesivir?
It causes premature chain termination during viral RNA synthesis.
64
What is the result of Remdesivir's action on RNA polymerase?
It prevents viral replication.
65
How is Remdesivir administered?
Intravenously.
66
In what type of patients is Remdesivir typically used?
Hospitalized COVID-19 patients.
67
What clinical benefit does Remdesivir provide?
Reduces recovery time in moderate-to-severe COVID-19 cases.
68
What is Remdesivir’s target in SARS-CoV-2?
The viral RNA polymerase.
69
What class of drug is Paxlovid?
Protease inhibitor.
70
What two drugs make up Paxlovid?
Nirmatrelvir and Ritonavir.
71
What is the function of Nirmatrelvir?
Inhibits the main protease (Mpro) of SARS-CoV-2, blocking viral replication.
72
How does Ritonavir help Nirmatrelvir?
Slows its breakdown, boosting its effectiveness.
73
How is Paxlovid administered?
Orally.
74
What type of COVID-19 cases is Paxlovid used for?
Mild-to-moderate cases in high-risk patients.
75
What is Paxlovid’s target in SARS-CoV-2?
The main protease (Mpro).
76
What class of drug is Molnupiravir?
Nucleoside analog.
77
What does Molnupiravir do during viral replication?
It incorporates into viral RNA and causes mutations.
78
What is the result of the mutations caused by Molnupiravir?
Error catastrophe—rendering the virus non-viable.
79
What type of COVID-19 cases is Molnupiravir used for?
Mild-to-moderate cases.
80
What is Molnupiravir’s target in SARS-CoV-2?
RNA polymerase.
80
How is Molnupiravir administered?
Orally.
81
What class are monoclonal antibodies used for COVID-19?
Neutralizing antibodies.
82
What do monoclonal antibodies bind to on SARS-CoV-2?
The spike protein.
83
How do monoclonal antibodies prevent infection?
They block the spike protein from binding to the ACE2 receptor.
84
What are examples of monoclonal antibodies for COVID-19?
Bamlanivimab, Casirivimab/Imdevimab.
85
How are monoclonal antibodies administered?
Via infusion.
86
When are monoclonal antibodies typically used?
In early COVID-19 cases to reduce severity.
87
What is the target of monoclonal antibody treatments for COVID-19?
SARS-CoV-2 spike protein.
88
What class of treatment are COVID-19 vaccines?
Prophylactic.
89
What is the mechanism of action of COVID-19 vaccines?
They induce an immune response by presenting the SARS-CoV-2 spike protein.
90
What immune responses do vaccines stimulate?
Production of neutralizing antibodies and T-cell responses.
91
What are two mRNA vaccines for COVID-19?
Pfizer-BioNTech (Comirnaty) and Moderna (Spikevax).
92
What is an example of a viral vector COVID-19 vaccine?
Johnson & Johnson (Janssen).
93
What is the purpose of COVID-19 vaccines?
To provide immunity and reduce the severity of infection.
94
What do COVID-19 vaccines target?
The immune system.

pharmacoloy/pain control (34 decks)

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