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BIOM 4090 > unit 09: antivirals > Flashcards

unit 09: antivirals Flashcards

1
Q

wht si a virus

A

sub-microscopic infectious agent that cannot grow or reproduce outside of a host cell.

They are approximately one hundred times smaller than bacteria.

  • simple structure, containing RNA or DNA, protein coat called capsid and some viruses ahve lipid rich envelope
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2
Q

how are viruses classified?

A

baltimore classification system - thier mechanism of mRNA production

  • viruses need to generate mRNA in order to produce proteins and replicate
  • virgal genomes can be ss or ds, RNA or DNA
  • may or may not use Reverse transcriptase

*ssRNA viruses can either be + sense or - antisense

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3
Q

what are the 7 classifications of viruses?

A

I: dsDNA viruses (e.g. adenoviruses, herpesviruses)
II: ssDNA viruses (e.g parvoviruses)
III: dsRNA viruses (e.g reoviruses)
IV: (+)ssRNA viruses (e.g coronaviruses like SARS-CoV-2, flaviviruses like West-Nile)
V: (-)ssRNA viruses (e.g influenzaviruses)
VI: ssRNA-RT viruses (e.g retroviruses like HIV)
VII: dsDNA-RT viruses (e.g hepadnaviruses like hepatitis B)

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4
Q

Viral Life cycle

A
  1. virus attaches to host cell, mediated by proteins on viral surface that bind specifically to particular component
  2. Viron undergoes entry by crossing host cell membrane
  3. virion uncoats losing caspid proteins, nucleic acid becomes available for transcription into mRNAs
  4. mRNAs transcribed and translated (early protein synthesis)
  5. Replication of genome followed by late protein synthesis. Viral proteins are synthesized
  6. Viral proteins assemble with viral genomes within host cell through assembly - many viruses also have mauration after
  7. final release step by lysis or budding

*antivirals taret one of these steps

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5
Q

what drugs target attachment/are entry inhibitors

A

Maraviroc

enfuvirtide (T-20)

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6
Q

what drugs are viral ion channel blockers?

A

amantadine and rimantadine

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7
Q

What drugs are polymerase inhibitors

A

Acylovir, zidovudine and efavirenz

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8
Q

what drug are integrase inhibitors

A

raltegravir

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9
Q

what drugs are protease inhibitors?

A

Saquinavir and ritonavir

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10
Q

what drugs are neuraminidase inhibitors?

A

Zanamirvir and oseltamivir

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11
Q

what are common viral infectiosn, series/chronic ones latent and cancer viral infections?

A

common: colf, flu, chicken pox an now COVID-19

serious/chronic: avian flu, ebola, HIV/AIDS and hepatitis

latent: cold sores and singles

cancer ifnections: HPX and EPstein-barr (monomucleosis)

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12
Q

innate vs adaptive immune system

A

innate: non specific responses to pathogens that activates the adaptive immune response

*invovles macrophages, dendritic cells, neutrophils, eosinophils and basophils/mast cells

adaptive: neutralizing reactiosn that are specific to the offending agent- involve pathogenic recognition

*involves cytotoxic T cells, helper T cells and B cells.

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13
Q

development of cells in immune system

A
  • all hematopoietic cells develop from the pluripotent hematopoietic stem cell -> gives rise to lymphoid stem cell and tri-lineage myeloid stem cell

Lymphoid:

  • mature lymphocytes (B and T cells) mediate adaptive
  • B cells differentiate into antibody-producing plasma cells, and T cells adopt an activated phenotye when exposure to specific antigen

Myeloid

  • megakaryocytes, erythroblasts, and myeloid precursors differentiate itno
    • mature neutrophils, eosinophils, basophils, mast cells, monocytes, platelets, and erythrocytes.
    • in tissues monocytes differentiate tineo macrophages and mast cells precursors diff into mast cells
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14
Q

what is Oseltamivir

A

Aka Tamiflu

For prevention and treatment of early infection of influenza A and B *H1N1 is subtype of influenza A SO IT IS RESPONSIVE TO IT

Neuraminidase inhibitor that blocks viral release from host cell

Influenza virus encodes an envelope-bound enzyme neuraminidase, which permits release of the virus

Without this enzyme, the virus would remain tethered and would be unable to spread.

*administed as pro drug and metabolized in liver and GI, excreted in urine

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15
Q

adverse effects of oseltamivir

A

naesea and GI dsicomfort

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16
Q

reistance to oseltamivir

A

occurs due to mutations in neuraminidase but the mutant strains are usually less virulent

17
Q

what is amantadine

A

also treats influenca

Inhibts viral uncoating by inhibition proton ion channel M2 in the viral envelope of influenza A - inhibits the binding of the virus with endosomes that inhibits uncoating

treatment of early infection by influenza A (not H1N1) and resistance can occur following a mutation in M2

-Distributed throughout body, including CNS and excretedunchanged by kidney

18
Q

adverse effects of amantadine

A

GI disturbances, CNS disturbances (nervousness, insomnia, difficulty concentrating) and renal damage in patients w/ renal insufficiency

19
Q

what causes herpes

A

herpes simplex = viral disease caused by

herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). HSV-1 is responsible for most cold sores while HSV-2 infections cause genital herpes

both are extremely contagious. HSV infections cycle between the active phase and remission.

20
Q

acyclovir

A
  • used to treat herpes by inhibition of viral DNA synthesis
  • activation of drug is 3 step mech:

Acyclovir = guanosine analogue, meaning that when phosphorylated, it competes with dGTP during DNA synthesis

  • when taken up by infected cells the viral thymidine kinase enzyme catalyzes the phosphorylation of the drug
  • phosphorylated acyclovir is then produced only in HSV-infected cells, which interferes with viral DNA synthesis, resulting in DNA chain termination

*oral Iv and topical forms avail

21
Q

adverse effects of acyclovir

A

nausea, vomiting, diarrhea, headache and renal damage (especially following high doses or in dehydrated patients

22
Q

clinicaluse and resistance of acyclovir

A

treatment of active herpes infection, and resistance can occur if thymidine kinase is altered or deficient.

23
Q

what is HIV and AIDS

A

HIV = human immunodeficiency virus -> causes AIDS acquries immune deficiency syndrome

  • HIV can be latent for 2-10 years but once aquire AIDS lifespan of untreated is 1-2 years
24
Q

what type of virus is HIV

A

retro virus that infects CD+ T cells

The virus attaches where interactions between viral proteins (gp41 and gp120) and host cell CD4 and CCR5 receptors occur

  • viral mem fuse w/ host PM allowing HIV genome to enter, uncoat and have genome copied

*DNA is integrated into host cell genome

  • gene transcription produced HIV RNA which is translated into proteins from host ribosomes
  • proteins assumble into immature virons that bud from host cell membrane then maturations to product fully infective virons
25
Q

how many drugs to treat HIV

A

34

26
Q

what is the first line of treatment

A

combo of 3 antiviral agents knows as HAART (highly active antiretroviral therapy)

27
Q

what are the main categoies of antiviral drugs for HIV

A
  1. nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) such as zidovudine or azidothymidine (AZT)
  2. non-nucleoside reverse transcriptase inhibitors (NNRTIs) such as nevirapine
  3. protease inhibitors (PIs) such as ritonavir.

*HAART often involved two NRTis in combo with an NNRT or PI

28
Q

what HIV drugs inhibit viral entry

A

maraviroc

29
Q

what HIV drug inhibts enzyme integrase

A

raltegravir

30
Q

what is zidovudine/AZT

A

thymidine analogue that is activated or phosphorylated by mammalian kinase.

Like with acyclovir- viral reverse transcriptase is not selective, therefore phosphorylated zidovudine/AZT competes with dTTP during DNA synthesis and results in DNA chain termination.

*well distributed even in CNS and metabolized in liver (glucoronidation)

31
Q

adverse efects of Zidovudine/AZT

A

anemia, neutropenia and hepatotoxicity.

Drug interactions exist - esp between those that compete for glucuronidation such as acetaminophen and benzodiazepines

Resistance can develop following a mutation in reverse transcriptase or inefficient kinase activation.

32
Q

resistance to Zidovudine/AZT

A

Resistance can develop following a mutation in reverse transcriptase or inefficient kinase activation.

*approx 1/3 of patients will develop resistance with AZT monotherapy

33
Q

what is nevirapine

A

binds and inhibits reverse transcriptase

  • well abs and dsitributed throughout the body (including CNS) fetus and maternal milk) and metabolized by liver (glucoronidation)
34
Q

adverse effects of nevirapine

A
  • Adverse effects such as rash, psychiatric effects and hepatotoxicity
  • Drug interactions can increase CYP3A4 which increases metabolism of certain drugs including itself, oral contraceptives, azoles, methadone and protease inhibitors.

Similar to zidovudine, resistance can occur if reverse transcriptase is mutated.

35
Q

what is ritonavir

A
  • inhibits HIV aspartyl protease: cleaves viral polyprotein itnp specific proteins
  • drug is unpalatable (not pleasing to the taste) so it is often given with more palatable food (such as chocolate milk or pudding).

It does however have good bioavailability and it is metabolized by CYP3A4

36
Q

adverse effects of ritonavir

A

nausea, vomiting, diarrhea, numbness, elevated liver enzymes and high blood glucose and lipid levels.

Resistance can develop via step-wise mutations in protease enzymes.

37
Q

what is Maraviroc

A

CCR5 receptor antagonist that blocks binding of viral gp120 to CCR5 which prevents viral entry itno host cell

  • approved in 2007 for patients previosuly treated with anti-HIV drugs
  • reported to decrease viral load compared to placebo patients. Long-term effects of CCR5 inhibition is not known at this time, but hepatotoxicity and cardiovascular events have been reported.
38
Q

what is raltegravir

A
  • inhibits viral integrase by decreasing the transfer of viral DNA into the host genome.

It was approved 2007 for patients resistant to HAART drugs and in 2009 for all patients.

Clinical trials have reported a decrease in viral load earlier in patients taking raltegravir combined with HAART drugs compared to those taking HAART drugs alone.

The effect of raltegravir on latent HIV and potential elimination of the virus is currently under investigation.

39
Q

what is the only approved treatment for COVid-19 patietns in hospital

A

remdesivir

  • binds to viral RNA polymerase, inhibitng viral replication through premature termination of RNA transcription
  • trils how that it sig reduced time in recovery in hospitalized COVID-19 pateints with mild to moderate symptoms
  • unclear if it reduced long term morbidity after discharge from hospital or if more beneficial when combined with corticosteroids

*dont give if patient ahs impaired renal funciton

BIOM 4090 (27 decks)

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