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342 > Current & Advanced Treatments for Sexually Transmitted Viral Infections > Flashcards

Current & Advanced Treatments for Sexually Transmitted Viral Infections Flashcards

1
Q

what do warts most commonly originate from

A

human papilloma virus (HPV)

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2
Q

what does wart treatment focus on

A

removal of wart as opposed to removal of virus

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3
Q

what are the first line treatments of warts

A

imiquimod

podophyllotoxin

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4
Q

how does imiquimod work

A

immunoenhancing drug

cytokines secreted by cells of immune system and have effect on other cells (aka interferons, interleukins, TNF-a)

imiquimod switches on cytokines aka innate immune system to clear wart

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5
Q

imiquimod mechanism of action

A

binds to and activates toll-like receptors (TLR) 7 and 8

activates intracellular signalling pathways through NF-kB

NF-kB translocates to nucleus where it activates gene transcription

causes production of pro-inflammatory cytokines (e.g. TNF-alpha)

pro inflammatory proteins secreted from cell, then switch on immune cells e.g T cells

triggers immune response, wart cells removed

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6
Q

how is podophyllotoxin for warts administered

A

topically

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7
Q

podophyllotoxin mechanism of action

A

internalises into wart cells

binds to microtubules, preventing mitotic division

inhibits topoisomerase 2

cells cannot undergo cell division, triggers apoptosis, wart regresses

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8
Q

other than warts, what does HPV cause

A

cancers

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9
Q

what are the high risk HPVs (2)

A

HPV 16
HPV 18

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10
Q

what are the main types of cancer associated with HPV infection

A

Cervical cancer is the main cancer associated with HPV infection, but can also cause vaginal, vulval, penile, anal, mouth and throat cancers

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11
Q

what % of all cervical cancers are attributed to HPV 16

A

50

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12
Q

what % of all cervical cancers are attributed to HPV 18

A

20

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13
Q

what occurs when the body fails to clear the infection - causing precancerous lesions to develop

A

virus replicates in epithelial cells

can damage DNA

precancerous lesions can develop

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14
Q

what do the precancerous lesions undergo

A

many regress alone

but may undergo further transformation and become a cancerous tumour if infection persists

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15
Q

what vaccine is used by the NHS to protect against HPV 6, 11, 16, 18

A

gardasil

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16
Q

mechanism of action of gardasil

A

contains purified L1 protein ( major capsid protein ) from each HPV strain

L1 proteins self assemble into HPV virus like particles (VLPs) which produce antibodies

reduces risk of viral infection developing into cancers

preventative/ inert vaccination

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17
Q

what is the L1 protein

A

the major capsid protein, come together to form capsomere and then a pentamere

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18
Q

when was the HPV vaccine introduced

A

2008

initially for 16-21 aged females which have seen reduction in HPV by 86%

then in 2019, administering to males and females aged 12 and above

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19
Q

4 examples of the 9 herpes virus types

A

herpes simplex virus 1 - HSV-1

herpes simplex virus 2 - HSV-2

varicella-zoster virus

epstein-barr virus (mononucleosis virus)

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20
Q

what does herpes simplex-1 HSV-1 tend to cause

A

cold sores

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21
Q

what does herpes simplex-1 HSV-1 and HSV-2 tend to cause

A

genital herpes

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22
Q

what are the symptoms of herpes (4)

A

small blisters that burst to leave red open sores around gential, anus, thighs, buttocks

tingling, burning, itching around genitals

pain during urination

vaginal discharge

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23
Q

first like treatment of herpes

A

aciclovir (prodrug)

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24
Q

mechanism of action of aciclovir

A

ACV converted to ACV-monophosphate (ACV-MP)

via HSV-1 thymidine kinase

HSV-1 TK enzyme only expressed in infected cells aka virus cells - rate dependent step, relies on this virus

grants specificity to drug and reduces off-target side effects

ACV-MP undergoes further phosphorylation to ACV-disphosphate (ACV-DP)

via cellular guanylate kinase aka humans take over

ACV-DP converted to ACV-triphosphate (ACV-TP)

via disphosphate kinase

enzymes expressed by cells, not dependent on viral enzymes

ACV-TP misincorporated into viral DNA aka means to target guanine residue but oopsies

ACV-TP misrecognised by DNA polymerase as deoxyguanosine triphosphate (dGTP) - guanine precursor

ACV-TP lacks 3’ hydroxyl group of dGTP so prevents attachment of additional nucleosides into DNA chain

terminates growing viral DNA chain

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25
Q

what does varicella-zoster virus cause

A

(chickenpox/ shingles)

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26
Q

what does epstein-barr virus cause

A

(mononucleosis virus)

27
Q

when is oral aciclovir administered

A

shingles for systemic effect

28
Q

aciclovir mechanisms of resistance (3)

A

reduced or absent HSV-1 thymidine kinase (no monophosphorylation)

altered thymidine kinase activity resulting in decreased aciclovir phosphorylation

altered viral DNA polymerase with dec affinity for aciclovir triphosphate (no more misincorporation)

29
Q

how does the human immunodeficiency virus (HIV) destroy human immune system gradually

A

Attacks a subtype of white blood cell called CD4 cells which protect the body from infection

30
Q

mechanism of HIV

A

uses cell machinery of CD4 to make copies of itself and spread throughout body

31
Q

HIV life cycle - what are the 7 stages

A

1 - binding (HIV attaches to surface of CD4 cell)

2 - fusion (HIV can enter cells)

3 - reverse transcription (virus converts RNA to DNA (dsDNA) and degrades remaining viral RNA)

4 - integration (HIV DNA integrates with cells DNA and is referred to as proviral DNA)

5 -replication (virus uses cell machinery to make copies of HIV proteins and RNA)

6 - assembly (new HIV protein and RNA assemble into immature virus)

7 - budding (immature HIV pushes itself out of cell)

32
Q

what are the two main methods of HIV prevention

A

Pre-exposure prophylaxis (PrEP)

Post-exposure prophylaxis (PEP)

33
Q

what medicines are involved in Pre-exposure prophylaxis (PrEP)

A

Emtricitabine & Tenofovir

34
Q

what medicines are involved in Post-exposure prophylaxis (PEP)

A

Emtricitabine, Tenofovir & Raltegravir

35
Q

what is PrEP (Pre-exposure prophylaxis)

A

commonly given as the combination therapy emtrictabine and tenofovir to HIV-negative patients

36
Q

how often is PrEP (Pre-exposure prophylaxis) administered

A

daily

37
Q

how long for is PEP (Post-exposure prophylaxis) administered

A

28 day course after patient may have come into contact with HIV virus

38
Q

what is Emtricitabine (FTC)

A

Reverse Transcriptase Inhibitor

works in a mechanism similar to aciclovir

does not have an effect on already infected cells

39
Q

what does emitricitabine undergo phosphorylation to form

A

emtricitabine triphosphate (FTC-TP)

40
Q

emtricitabine mechanism of action

A

phosphorylation forming emtricitabine triphosphate (FTC-TP)

FTC-TP misrecognised by reverse transcriptase enzyme (which converts viral RNA to DNA)

misincorporated into DNA instead of cytosine nucleotides

FTC-TP lacks a 3’ hydroxyl group and so this stops the attachment of additional nucleosides into the chain preventing viral replications

terminates chain

41
Q

what is Tenofovir

A

also a reverse transcriptase inhibitor

similar to emticitabine but incorporated instead of adenine

does not have an effect on already infected cells

has a phosphate group so only requires disphosphorylation to become active aka 2 rounds

42
Q

Raltegravir mechanism of action

A

when reverse transcriptase enzymes converts viral RNA to DNA, virus tries to integrate this with host genome

viral integrase enzymes cut host genome

integrase incorporates HIV DNA into host genome, allowing production of new viral proteins

Raltegravir simply acts to inhibit the viral Integrase enzymes

43
Q

current phase 3 trials for HIV treatment

A

into long-acting antiretroviral therapies (LA-ART) with a single-dose every one to three months

One new LA-ART is cabotegravir, a highly potent integrase inhibitor, with a T1/2 of up to 54 days

44
Q

what is cabotegravir

A

long-acting antiretroviral therapy (LA-ART)

highly potent integrase inhibitor

T1/2 of up to 54 days

given as a nanosuspension injection

45
Q

what is a nanosuspension injection

A

A suspension of drugs within the nanoparticle size range which are normally poorly soluble in water

46
Q

what is Cabotegravir being trialled in combination with nanosuspension with

A

rilpivirine, a long-acting reverse transcriptase inhibitor

47
Q

what is rilpivirine

A

a long-acting reverse transcriptase inhibitor

48
Q

what is abacavir

A

used in combination with other antiretroviral therapy for HIV infection

reverse transcriptase inhibitor and so similar to emtricitabine and tenofovir

hypersensitivity reactions have been observed in 5-8% of abacavir-treated patients

49
Q

what are the symptoms of a hypersenstivity reaction (5)

A

Skin rash, fever, malaise, gastrointestinal symptoms and respiratory symptoms

50
Q

in hypersensitivity reactions, what does severe skin rash result in (3)

A

systemic lupus erthematosus
stevens-johnson syndrome
toxic epidermal necrolysis

51
Q

what is Human leukocyte antigen (HLA)-B*5701

A

an allele more common in those who are suspected to have a hypersensitivity reaction to abacavir compared to those who dont

52
Q

what allele is more common in those who are suspected to have a hypersensitivity reaction to abacavir compared to those who dont

A

Human leukocyte antigen (HLA)-B*5701

53
Q

what is HLA 3

A

gene complex encoding major histocompatibility complex (MHC) in humans

cell surface proteins

responsible for regulation of immune system

54
Q

what is the MHC major histocompatibility compex

A

Depending on the specific MHC, it may present antigens to the immune system

allows immune cells e.g. CD4 to hunt for and destroy these antigens

55
Q

how is HLA-B*5701 identified in patients

A

before treatment or if restarting treatment and HLA-B*5701 status not known

by taking a blood or saliva sample, PCR amplifying the gene and sequencing the HLA-B gene

56
Q

what is EBT-101

A

CRISPR-based therapeutic candidate in development as a potential functional cure for chronic HIV

57
Q

what is CRISPR (clustered regularly interspaced short palindromic repeats)

A

is based on a system from bacteria which is used to protect them from viral infection

58
Q

EBT-101 mechanism of action

A

bacteria detects viral DNA

produces two short RNA strands called guide RNA

gRNA contains sequence that matches invading virus

two RNA strands then form complex with Cas9

nuclease, enzyme that cuts DNA

Cas9 cuts invading virus DNA and disables virus from replicating

59
Q

what is Cas9

A

nuclease

60
Q

what is a nuclease

A

enzyme which cuts DNA

61
Q

how is EBT-101 administered

A

a one-time dose using an adeno-associated virus (AAV)

AAV delivers CRISPR-Cas9 and two gRNAs

targets 3 sites in HIV genome

excises large portions of HIV genome

removes HIV proviral DNA

62
Q

how many subtypes of HPV exist

A

over 120

63
Q

when does aciclovir work

A

before forming scab

64
Q

how many worldwide live with HIV/AIDS

A

33 million

342 (9 decks)

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