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Current & Advanced Treatments for Sexually Transmitted Viral Infections Flashcards

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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 (newer gardasil 9 protects against additional 5 HPV strains) - broader scope

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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
what does varicella-zoster virus cause
(chickenpox/ shingles)
26
what does epstein-barr virus cause
(mononucleosis virus)
27
when is oral aciclovir administered
shingles for systemic effect
28
aciclovir mechanisms of resistance (3)
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
how does the human immunodeficiency virus (HIV) destroy human immune system gradually
Attacks a subtype of white blood cell called CD4 cells which protect the body from infection
30
mechanism of HIV
uses cell machinery of CD4 to make copies of itself and spread throughout body
31
HIV life cycle - what are the 7 stages
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
what are the two main methods of HIV prevention
Pre-exposure prophylaxis (PrEP) Post-exposure prophylaxis (PEP)
33
what medicines are involved in Pre-exposure prophylaxis (PrEP)
Emtricitabine & Tenofovir
34
what medicines are involved in Post-exposure prophylaxis (PEP)
Emtricitabine, Tenofovir & Raltegravir
35
what is PrEP (Pre-exposure prophylaxis)
commonly given as the combination therapy emtrictabine and tenofovir to HIV-negative patients
36
how often is PrEP (Pre-exposure prophylaxis) administered
daily
37
how long for is PEP (Post-exposure prophylaxis) administered
28 day course after patient may have come into contact with HIV virus
38
what is Emtricitabine (FTC)
Reverse Transcriptase Inhibitor works in a mechanism similar to aciclovir does not have an effect on already infected cells
39
what does emitricitabine undergo phosphorylation to form
emtricitabine triphosphate (FTC-TP)
40
emtricitabine mechanism of action
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
what is Tenofovir
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
Raltegravir mechanism of action
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
current phase 3 trials for HIV treatment
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
what is cabotegravir
long-acting antiretroviral therapy (LA-ART) highly potent integrase inhibitor T1/2 of up to 54 days given as a nanosuspension injection
45
what is a nanosuspension injection
A suspension of drugs within the nanoparticle size range which are normally poorly soluble in water
46
what is Cabotegravir being trialled in combination with nanosuspension with
rilpivirine, a long-acting reverse transcriptase inhibitor
47
what is rilpivirine
a long-acting reverse transcriptase inhibitor
48
what is abacavir
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
what are the symptoms of a hypersenstivity reaction (5)
Skin rash, fever, malaise, gastrointestinal symptoms and respiratory symptoms
50
in hypersensitivity reactions, what does severe skin rash result in (3)
systemic lupus erthematosus stevens-johnson syndrome toxic epidermal necrolysis
51
what is Human leukocyte antigen (HLA)-B*5701
an allele more common in those who are suspected to have a hypersensitivity reaction to abacavir compared to those who dont
52
what allele is more common in those who are suspected to have a hypersensitivity reaction to abacavir compared to those who dont
Human leukocyte antigen (HLA)-B*5701
53
what is HLA 3
gene complex encoding major histocompatibility complex (MHC) in humans cell surface proteins responsible for regulation of immune system
54
what is the MHC major histocompatibility compex
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
how is HLA-B*5701 identified in patients
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
what is EBT-101
CRISPR-based therapeutic candidate in development as a potential functional cure for chronic HIV
57
what is CRISPR (clustered regularly interspaced short palindromic repeats)
is based on a system from bacteria which is used to protect them from viral infection
58
EBT-101 mechanism of action
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
what is Cas9
nuclease
60
what is a nuclease
enzyme which cuts DNA
61
how is EBT-101 administered
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
how many subtypes of HPV exist
over 120
63
when does aciclovir work
before forming scab
64
how many worldwide live with HIV/AIDS
33 million
65
genital warts are also known as ___ ____
condylomata acuminata (CA)
66
therapy for genital warts
pt specific, no definitive first line
67
imiquimod is available as a cream in ___% and ___%
3.75 5
68
imiquimod cream side effects include
ulceration, muscle aches
69
imiquimod cream wart clearance rate at 5%
56%
70
interferons
last resort therapy as needs local anaesthesia and is expensive systemic wart treatment, interferes with viral replication recent development injected, conflicting studies on effectiveness
71
phodophyllotoxin is administered as a
cream/ gel/ solution
72
phodophyllotoxin works within ____ days
3-5 post admin
73
side effects of phodophyllotoxin
inflammation, erosion, itching
74
gardasil vaccine is admin as
intramuscular injection 3 doses
75
gardasil vaccine is ___% effective
99 no long term evidence of waning immunity over time
76
cervarix vaccine
hpv 16,18 - responsible for 70% of cervical cancers stimulates immune response as contains VLP virus like particles of HPV that mimic outer shell of virus, but do not contain viral DNA body creates antiboidies that protect against VLPs, and if needed, actual HPV as immunity is long term built 3 injection dose high efficacy esp, generally no side effects
77
LA-ART - ___ in HIV-linked mortality rates
sig. reduction
78
rilpivirine is administered at
oral dose of 25mg once daily
79
rilpivirine animal studies
in rats and dogs, 100% bioavailability
80
carbotegravir is a
HIV-1 integrase strand transfer inhibitor
81
carbotegravir is administered at
200 mg/ml PrEP
82
ibalizumab
in development trial phase 2 intravenous infusion every 2-4 weeks
83
atazanivir
in pre clinical rodent/ mammal testing stage protease inhibitor
84
dapivirine PrEP study - antiretroviral therapy
vaginal ring, releases antiretroviral drug dapivirine over time to prevent HIV- long acting microbicide well tolerated with a favourable safety profile and reduced HIV-1 incidence by 31% vs placebo in one study mechanism: dapivirine is an NNRTI non-nucleoside reverse transcriptase inhibitor, inhibits reverse transcriptase stage in HIV cycle local protection via ring designed to be replaced monthly in clinical trials but approved for use in some countries - not UK
85
shit to do with viral that u gots to treat (4)
HPV - wart treatment also HPV can cause cancer Herpes - HSV- 1 , HSV-2 (both cause gential herpes), epstein barr, varicella-zoster we dont care abt treating it but abacavir + HLAB701 allele - hypersensitivity reactions whihc can worsen to systemic lupus erthematosus, stevens-johnson syndrome, toxic epidermal necrolysis HIV
86
all the old/ current meds (9)
HPV: imiquimod, podophyllotoxin (warts) gardasil vaccine Herpes: aciclovir HIV: Pre-exposure prophylaxis (PrEP) - Emtricitabine & Tenofovir Post-exposure prophylaxis (PEP) - Emtricitabine, Tenofovir & Raltegravir
87
new/ developing shit - 6
HPV: cervarix vaccine HIV: atazanivir, LA-ART carbotegravir with aciclovir or raltegravir, dapivirine, new but used EBT-101 Herpes: potentially EBT 101, charcoal drug delivery topical, vaccines not yet successful

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