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POM Y1 Imperial > Antiviral agents > Flashcards

Antiviral agents Flashcards

1
Q

What is a virion?

A

A virus particle outside a cell

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2
Q

What is episomal latency?

A

Viral nucleic acids remain inactive but free in the cytoplasm or nucleus of the infected cell

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3
Q

What is proviral latency?

A

The viral nucleic acid becomes incorporated into the DNA of the infected host cell. It is now termed a provirus, however, with episomal latency, the viral nucleic acid can be reactivated any time

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4
Q

What is prophylaxis?

A

A preventative measure, a prophylactic is a medication or a treatment designed to prevent the occurrence of disease, preventing disease before the aetiological agent is acquired. Example: vaccination or administration of the drug before the infection

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5
Q

What are the vaccines?

A

Prophylactic treatment; attenuated pathogens and (antigenic fragments), involves herd immunity and target group safety > efficacy; provided by the WHO/government

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6
Q

What is therapy in terms of drug treatment?

A

Treating a diagnosed patient upon host infection, antiviral therapy and diagnostics are coupled, diagnostic measures are regulated to identify the specific drug towards treating the particular virus.
Antiviral drugs: Therapeutic random screening for specific effective chemicals or employ hypothesis-driven rational design; prescribed to target group on ad hoc basis

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7
Q

What are nucleosides?

A

Substrate analogs; nucleosides incorporated through viral DNA/RNA synthesis. Nucleosides are chemically modified, altering the affinity in order to selectively target viral enzymes

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8
Q

What is rational drug design?

A

Employed to specifically target viral components, and structure (crystallography), molecules can degrade the structure

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9
Q

What is AZT, which viral enzyme does it inhibit?

A

Resembles a nucleotide and competitively inhibits the enzyme reverse transcriptase

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10
Q

What is acyclovir, which viral enzyme does it inhibit?

A

Cyclic guanosine analog, behaving as a chain terminator of polynucleotide DNA elongation viral DNA polymerase

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11
Q

What is Tamiflu?

A

A competitive inhibitor of the viral enzyme neuraminidase that many viruses, including the influenza virus use to escape from cells

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12
Q

What is ribavirin?

A

It resembles an RNA nucleotide, and inserts into viral RNA, preventing translation from occurring. Therefore, this means that the production of new viral proteins for capsids or viral genomes cannot occur.

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13
Q

What is the mechanism of action for acyclovir?

A

Modified nucleoside incorporated into DNA.Lack of 3-prime OH prevents phosphodiester bond formation.

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14
Q

Which analog is acyclovir?

A

A cyclic analog of 2’deoxyguanosine

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15
Q

Which viral enzymes activates the inactivate acyclovir analog?

A

Thymidine kinase

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16
Q

What function is performed by thymidine kinase?

A

A phosphotransferase responsible for the phosphorylation of nucleosides to nucleotides

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17
Q

Which enzyme phosphorylates Acylo-GMP to GDP?

A

Guanylate kinase

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18
Q

What forms via the phosphorylation of acyclovir?

A

Acylo-GMP

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19
Q

What phosphorylates Acylo-GMP to TP?

A

Phosphotransferase

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20
Q

how does acyclovir selectively target viral DNA?

A

Higher affinity for viral DNA polymerase than host cell DNA Polymerase

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21
Q

How does Acylo-GTP cause chain inhibition?

A

The absence of the 3-hydroxy group means that further phosphodiester bonds cannot form under condensation reactions -ceasing polynucleotide elongation (No further nucleotides can be attached) - chain termination (Vial particles cannot replicate)

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22
Q

Which class of organic molecules is amantadine classified as?

A

Cyclic amines

23
Q

Which transmembrane protein does amantadine inhibit?

A

M2 protein of the virus, M2 inhibitor blocks ion channel by the m2 viral protein

24
Q

How do viruses enter host cells?

A

Through receptor mediator endocytosis, the virus enters the host cell, encapsulated within the endocytic vesicles. Thereafter, acidification of the endocytic vesicle is required for the dissociation of the M1 protein from the ribonucleoprotein complexes. Ribonucleoprotein particles imported into the nucleus by the nuclear pore

25
Q

Which ions are required for the acidification of the endocytic vesicles?

A

Hydrogen ions, pass through the M2 ion channel,

26
Q

How does amantadine block viral nuclear acid entry into the host cell?

A

Blocks the M2 ion channel, preventing the acidification of the endocytic vesicle, thus viral particle cannot uncoat or subsequently replicate

27
Q

How do viruses acquire amantadine resistance?

A

A point mutation can result in alterations, in trinucleotide sequence within the DNA transcript of the structural M2 protein gene, this changes the codon and resulting in another variant of the amino acid being encoded for. Changes in the tertiary structure and bonding of the M2 protein, thereby rending amantadine resistance (specificity is lost)
Position number 31, serine to asparagine. S31n mutation is transmission in the virulent virus developing resistance

28
Q

Which acid is cleaved by neuraminidase?

A

Sialic acid

29
Q

How do viruses leave cells via neuraminidase activity?

A

Neuraminidase enzymatically cleaves sialic acid group from glycoproteins and are required for influenza viral replication, the virus attaches to the interior cell surface through haemagglutinin, a viral surface protein that binds to sialic groups. Inhibition of neuraminidase prevents cleavage thereby release and cell lysis is perturbed

30
Q

What is sialic acid?

A

Sialic acid is a substrate (Consists of hydroxyl groups, carboxylates, and glycerols that stereochemically and structural binds to the active site)

31
Q

Which drug competitively inhibits neuraminidase?

A

Relenza (Zanamivir)

32
Q

How does Relenza inhibit neuraminidase?

A

Competitive inhibition of neuraminidase, consisting of guanidine positive charge - charge adheres to the active site, greater affinity compared to sialic acid; classifies as a “plug drug”. Inhibits enzyme turnover

33
Q

What is the orally available neuraminidase inhibitor?

A

Tamiflu

34
Q

what effect do neuraminidase inhibitors have on the lifespan of illness?

A

Reduces illness to 17 hours and 29 hours in adults and children respectively

35
Q

What is an example of a cap-dependent endonuclease inhibitor?

A

Baloxavir

36
Q

How do Cap dependent endonucleases work?

A

Inhibits Cap dependent endonuclease activity of the influenza polymerase. Influenza endonuclease is a subdomain of viral RNA polymerase. CAP endonucleases process host pre-mRNA to serve as primers for viral MRA, drug blocks transcription of mRNA and inactivates replication

37
Q

How is viral gene transcription primed?

A

Oligonucleotides that are cleaved from the host cell pre-mRNA by endonuclease activity - translation at host ribosomes requires 5’ capping. N-terminal domain of pA subunit has been confirmed to accommodate the endonuclease activity residues

38
Q

How does a point mutation confer resistance to baloxavir?

A

Isoleucine to threnonine

39
Q

Which cells does HIV attack?

A

T helper lymphocytes, macrophages, and dendritic cells

40
Q

What is the structure of HIV?

A

Spherical, enveloped icosahedron, comprises of a viral envelope that is composed of the lipid bilayer taken from the membrane of the human host cell during budding.

41
Q

What type of DNA is enclosed by HIV?

A

Positive sense single-strand RNA

42
Q

What class of virus is HIV?

A

Retrovirus

43
Q

How can HIV produce double-stranded DNA?

A

Reverse transcriptase enzymes

44
Q

How does HIV become AIDS?

A

An environmental trigger causes the viral DNA to be transcribed, producing new RNA genomes, proceeded with translation into viral proteins including capsomere proteins to make new capsids
Thus the viral particle is released by budding from the hosts membrane being enclosed by a lipid envelope derived from the cell membrane

45
Q

Which HIV glycoprotein tail attaches to the cell surface protein?

A

Env glycoprotein

46
Q

Which receptors does HIV bind to?

A

CD4 and co-receptor CCR5

47
Q

What are the four main HIV antiviral classes?

A

1) Fusion inhibitors
2) Reverse-transcriptase inhibitors
3) Integrase strand inhibitors (InSTIs)
4) Protease inhibitors

48
Q

What is the mechanism of action for HIV fusion inhibitors?

A

Inhibition by HIV-1 co-receptor antagonist. The fusion of viral and host cell membranes enables entry of the viral capsid into the cell, whereby the viral RNA can be reversed transcribed to DNA.
This is blocked by the fusion inhibitors - prevents HIV-1 cell entry

49
Q

What are reverse transcriptase inhibitors?

A

Nucleoside analog reverse transcriptase inhibitors (NRTIs)

Non-nucleoside reverse transcriptase inhibitors

50
Q

How do reverse transcriptase inhibitors work?

A

NRTIs competitively inhibit reverse transcriptase, preventing the Viral RNA being reverse transcribed into DNA- cannot subsequently be integrated into the host genome.
HIV-1 cycle terminated.
Enzyme exists only in host cells

51
Q

How do HIV integrase strand inhibitors work?

A

Integrase specific to HIV inhibited and DNA thus cannot be integrated into genome to enter lysogeny

52
Q

How do HIV protease inhibitors work?

A

Virally encoded protease enzymes inhibited by anti-virals: Prevents viral protein translation -HIV protease cleaves polyproteins (GAG, and GAG-pol) for the maturation of protein components of HIV virion.

53
Q

How is antiviral resistance acquired by HIV?

A

HIV is a chronic condition, thereby continuous application of a selection pressure through antiviral exposure stimulates the mechanism of natural selection.
Encourages the proliferation of resistant strains
Amino acid sequence altered, transforming the structure of reverse transcriptase - nucleoside analogs are ineffective and thus no longer complimentary - resistance is developed.

54
Q

What is combination therapy in terms of antivirals?

A

Therapy involves using multiple antiviral drugs alternative target regions and aspects of HIV- reduces the susceptibility of resistance considering the acquisition of gene that concerns for a mutation to overcome specific anti-viral is low.
Multiple specific mutations are required to develop resistance for a combination of drugs – unlikely.

POM Y1 Imperial (34 decks)

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