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STEP 1 Microbiology > Repro- Viruses and antivirals > Flashcards

Repro- Viruses and antivirals Flashcards

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1
Q

HIV- classification

A

Retrovirus; diploid ssRNA (+); enveloped

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2
Q

HIV- replication

A

ssRNA (+) is converted to DNA intermediate by reverse transcriptase and incorporated into the human genome

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3
Q

HIV- key genes (3)

A

1) GAG => p24, the capsule for RNA strands
2) ENV => makes glycoproteins 160, which is cleaved to gp41 (transmembrane protein) and gp120 (outer glycoprotein)
3) POL => makes reverse transcriptase

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4
Q

HIV- transmission

A

1) sexual
2) vertical (TORCH)
3) bloodborne

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5
Q

HIV- binding

A

Initially targets macrophages (CCR5, early) and helper T cells (CXCR4, late)

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6
Q

HIV- latent period; what happens and for how long?

A

Replication in lymph nodes; lasts up to 10 years

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7
Q

When does HIV become AIDS?

A

CD4+ T cell count of <200 cells/microliter OR presence of AIDS-defining illness

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8
Q

Cancer directly associated with AIDS

A

Diffuse large B cell lymphoma

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9
Q

HIV- treatment ‘name’ and usual combination

A

HAART- highly active antiretroviral therapy; frequently involve 2 NRTIs + another agent

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10
Q

HIV- treatment ‘name’

A

HAART- highly active antiretroviral therapy

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11
Q

Strategies for treating HIV

A

1) nucleotide reverse transcriptase inhibitors (NRTIs)
2) Non-nucleotide reverse transcriptase inhibitors (NNRTIs)
3) protease inhibitors
4) Entry inhibitors
5) Fusion inhibitors
6) Integrase inhibitors

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12
Q

Strategies for treating HIV

A

1) nucleotide reverse transcriptase inhibitors (NRTIs)
2) Non-nucleotide reverse transciptase inhibitors (NNRTIs)
3) protease inhibitors
4) CCR5 inhibition

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13
Q

NRTIs for HIV- mechanism

A

Nucleotide (or nucleoside) reverse transcriptase inhibitors; incorporated into growing viral DNA strands, but lack hydroxyl group for phosphodiester bond formation

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14
Q

Adverse effects common to all NRTIs

A
  • Mitochondrial toxicity

- Lactic acidosis

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15
Q

NRTIs- common suffix and list

A

“-dine”;

  • Zidovudine
  • Lamivudine
  • Stavudine
  • Didanosine
  • Tenofovir
  • Abacavir
  • Emtricitabine
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16
Q

NRTIs- common suffix and list

A

“-dine”;

  • Zidovudine
  • Lamivudine
  • Stavudine
  • Didanosine
  • Tenofovir
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17
Q

Is tenofovir a nucleoside or nucleotide?

A

Nucleotide (no phosphorylation needed for activation)

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18
Q

HIV drugs used for Hepatitis B

A

Lamivudine and tenofovir

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19
Q

Zidovudine- AEs

A
  • Myelosuppression (anemia, neutropenia, granulocytopenia)

- Lipodystrophy/central adiposity

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20
Q

Which NRTI causes a rash, and why?

A

Abacavir causes a type IV hypersensitivity rash in those who carry the HLA-B57:01 allele

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21
Q

Which NRTI causes hyperpigmentation of the palms and soles?

A

Emtricitabine

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22
Q

Which NRTI causes dose-dependent pancreatitis?

A

Didanosine

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23
Q

Adverse events of stavudine

A

Peripheral neuropathy and central adiposity

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24
Q

NNRTIs- suffix and list

A

“-dine”

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25
Q

NNRTIs- adverse effects

A
  • Hepatic failure: jaundice, flulike symptoms

- Skin rash, which may become Stevens-Johnson syndrome

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26
Q

Efavirenz- adverse effects

A
  • CNS symptoms: dizziness, drowsiness, headache, psychosis
27
Q

Why do NNRTIs have many drug-drug interactions?

A

Nevirapine is a moderate inducer of cytochrome P450; efavirenz and delavirdine activate and inhibit the system (and are metabolized by it)

28
Q

Protease inhibitors: suffix and list

A

“-navir”

  • ritonavir
  • atazanavir
  • indinavir
29
Q

Protease inhibitors- MOA

A

Keeps virion immature by preventing cleavage of long HIV polypeptides (protease encoded by POL gene)

30
Q

How does HIV build resistance to protease inhibitors?

A

POL mutations

31
Q

Protease inhibitors- adverse effects

A
  • Hyperglycemia (insulin resistance, potentially leading to DM)
  • Dyslipidemia
  • Lipodystrophy
32
Q

Indinavir- adverse effects

A
  • Nephrolithiasis (within days of starting; maintain hydration)
33
Q

Which protease inhibitor has the strongest P450-inhibitory effect?

A

Ritonavir (interacts with Rifampin, which activates P450!!)

34
Q

What can rifampin be replaced with in patients on protease inhibitors?

A

Rifabutin

35
Q

HIV- spread of virions

A

Virions bud off of infected cells, carrying virion core proteins (p24 and p7) encoded by GAG. ENV codes for envelope proteins crucial for membrane invasion. gp120 must bind to CD4 molecule and a chemokine receptor (CXCR4 or CCR5). gp41 facilitates fusion.

36
Q

Maraviroc- MOA

A

Binds CCR5 receptor to block entry (HIV)

37
Q

Enfuvirtide- MOA

A

Binds gp41 to inhibit fusion (HIV)

38
Q

Raltegravir- MOA

A

Integrase inhibitor disrupts HIV integration into host genome, thus preventing transcription of viral mRNA

39
Q

What can cause HIV resistance to NRTIs, NNRTIs, protease inhibitors, and integrase inhibitors?

A

Mutations in Pol (encodes reverse transcriptase, protease, and integrase)

40
Q

Raltegravir- adverse effects

A

Rhabdomyolysis (rare)

41
Q

HPV- classification

A

Papilloma; dsDNA

42
Q

HPV- presentation (1-4)

A

Verruca vulgaris (cutaneous common wart)

43
Q

HPV- presentation (6 and 11)

A
  • “Low risk” subtypes
  • Laryngeal papillomatosis (recurrent respiratory papillomatosis), typically seen in children and may come from vaginal delivery
  • STI: Anogenital warts/ condyloma accuminata
44
Q

HPV- presentation (16, 18, 31, 33)

A
  • “High risk”

- Anogenital cancers, especially squamous cell carcinomas

45
Q

What type of cells does HPV infect?

A

Squamous cells

46
Q

HPV vaccine (Gardasil) coverage

A

6, 11, 16, and 18

47
Q

What type of vaccine is Gardasil?

A

Inactivated subunit vaccine

48
Q

What is the function of p53 and Rb?

A

Inhibit transition from G1 to S phase

49
Q

Function of HPV E6

A

Promotes proteolysis of p53

50
Q

Function of HPV E7

A

Promotes proteolysis of Rb

51
Q

Detection of cervical cancer? Where, specifically, are cells obtained?

A

Pap smear at the transformation zone

52
Q

What is the transformation zone of the cervix?

A

Squamous epithelium from ectocervix comes in contact with the columnar epithelium of the endocervix

53
Q

What are koilocytes?

A

Squamous cells infected with HPV, which have large, dense nuclei (sometimes binucleate)

54
Q

Name two reasons why HIV+ individuals are at higher risk for cervical carcinoma due to HPV.

A

1) Immunosuppression

2) HIV is thought to increase expression of E6 and E7

55
Q

HSV- morphology

A

Herpesvirus; dsDNA, linear, enveloped

56
Q

HSV-1- presentation

A
  • Initially as gingivostomatitis
  • Cold sores (herpes labialis)
  • Keratoconjunctivitis (serpiginous corneal ulcers)
  • Temporal lobe encephalitis (hemorrhage and necrosis of inferior and medial temporal lobe, causing bizarre behavior and olfactory hallucination
  • Herpetic rash/whitlow
  • Erythema multiforme (1-2 weeks into infection)
  • HSV esophagitis
57
Q

HSV-2- presentation

A
  • Herpes genitalis (painful and vesicular)
  • Painful inguinal lymphadenopathy
  • Herpetic rash/whitlow
  • Aseptic meningitis
58
Q

HSV- diagnosis

A
  • Intranuclear inclusion bodies (Cowdry bodies)
59
Q

HSV- diagnosis

A
  • Intranuclear inclusion bodies (Cowdry bodies)
  • PCR
  • Tzank smear (looking for multinucleated giant cells)
60
Q

HSV- transmission

A
  • Contact
  • Sexual
  • Vertical (TORCH)
61
Q

Where does HSV-1 remain during latency?

A

Trigeminal ganglion

62
Q

Describe the appearance of herpetic rash

A

Vesicles on an erythematous base (“dew drops on a rose petal”)

63
Q

Where does HSV-2 lie dormant?

A

Sacral ganglia

64
Q

HSV treatment

A

Acyclovir or valcyclovir

STEP 1 Microbiology (22 decks)

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