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2a - microbiology and IDs > HIV (example virus) > Flashcards

HIV (example virus) Flashcards

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Biology 101 flashcards
1
Q

what family of virus is the HIV virus from and why ?

A

retrovirus family

because it uses reverse transcriptase (RT) to make a DNA copy that becomes integrated into the DNA of the infected cell

is a RNA virus

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2
Q

HIV is a small retrovirus

which genus of retroviruses does HIV belong to ? and why ?

A

HIV is a lentivirus

lentiviruses cause chronic diseases and are characterised by long incubation periods (slow viruses)

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3
Q

Replication of HIV mechanism

  1. attachement

how does the HIV attach to the host cell?

A

step 1 = attachment

Glycoproteins on the HIV molecule allow it to dock and fuse onto the CD4 and then CCR5 receptors of host cell

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4
Q

Replication of HIV mechanism

  1. what happens after the HIV attaches to the host cell?
A

step 2 = entry + uncoating

The viral capsid the enters the cell and enzymes and nucleic acid are released

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5
Q

Replication of HIV mechanism

  1. reverse transcription

what happens after the virus has entered the cell and released its DNA ?

A

step 3 = Reverse transcription

Using reverse transcriptase single stranded RNA is converted into double stranded DNA

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6
Q

Replication of HIV mechanism

  1. what happens after the formation of the double stranded viral DNA inside the host cell
A

step 4 = Genome integration

Viral DNA then is integrated into the cell’s own DNA (in nucleus) by integrase enzyme

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7
Q

Replication of HIV mechanism

  1. transcription of viral RNA

what’s involved in this stage

A

step5 = Transcription of viral RNA

When the infected cell divides the viral DNA is read and long chains of viral proteins are made

the mRNA is splices and translated into proteins

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8
Q

Replication of HIV mechanism

  1. what happens after the viral DNA has been translated into proteins within the host cell
A

step 6 = Assembly of new virions

Assembly the viral protein chains are cleaved and reassembled

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9
Q

Replication of HIV mechanism

  1. what is the final step (after the assembling of new virions)
A

step 7 = Budding

immature virus pushes out of the cell taking with it some cell membrane

Immature virus breaks free to undergo more maturation

Maturation protein chains in the new viral particle are cut by the protease enzyme into individual proteins that combine to form a working virus

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10
Q

what is the primary receptor for HIV on host cells?

A

CD4

HIV infects cells that express CD4 a

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11
Q

which glycoprotein on the HIV cell envelope binds to CD4 receptor on host cell, triggering a conformational change ?

A

gp120

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12
Q

Where/when are the targets during the HIV replication cycle for antiretroviral therapy?

A

antiretroviral therapy drugs are mostly integrase inhibitors

they prevent step 4 genome integration

ie. prevent virus from integrating into host DNA,

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13
Q

HIV-1 has the ability to rapidly mutate (evolve)

how does it do this?

A

Has Error-prone replication (the enzyme reverse transcriptase makes at least 1 error in every replication cycle)

Has Rapid viral replication (generation time ~2.5 days)

v Large population sizes (~1010 new virus particles produced each day)

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14
Q

what is AHI ?

A

Acute HIV-1 infection

early stage HIV characterised by high viral load

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15
Q

what symptoms present during AHI?

A

“Glandular fever” like illness (non-specific symptoms)

Fever, lymphadenopathy

Sore throat, oral ulcers

Skin rash (upper trunk)

May include neurological features

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16
Q

HIV infects CD4-expressing cells

give examples of these

A

helper T cells aka. CD4 cells

other T cells

dendritic cells

macrophages

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17
Q

summarise the immune response to HIV

A
  1. initial vigorous immune response but no demonstratable protective immunity
  2. HIV infects CD4+ T helper cells early on, decreasing the immune response and immune exhaustion sets in
  3. Immunological dysfunction
  4. but ongoing viral replication, leading to clinical manifestations of immunodeficiency. virus rises when CD4 levels drop
  5. Takes too long to make antibodies → by the time they are generated, the pathogen has mutated and they are no longer useful

OVEARLL: HIV results in gradual damage to the immune system mainly through depletion of CD4 T-cells

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18
Q

why do we struggle to generate effective antibodies to HIV?

A

HIV-1 virion only has small number of spikes on its envelope which are heavily glycosylated. Makes it hard for human antibodies to bind to them

The envelope proteins can change
Evolves fast to avoid antibody recognition

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19
Q

what are some problems with ART?

(antiretroviral therapy that HIV-infected people live on)

A

Issues of adherence, side-effects, drug resistance

can’t afford to miss tablets due to the big latent HIV reservoir

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20
Q

what is AIDS?

A

acquired immune deficiency syndrome

describes a number of potentially life-threatening infections and illnesses that happen when your immune system has been severely damaged by the HIV virus.

ie. AIDS is a list of conditions caused by HIV

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21
Q

what Two markers are used to monitor HIV infection and make prognosis

A

CD4 cell count – a CD4 count of under 200 is AIDS

HIV viral load – if you can detect a viral load, how high it is

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22
Q

what CD4 count is considered a late diagnosis ?

A

CD4 count of under 350,

when there has been multiple missed opportunities to diagnose

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23
Q

HIV Epidemiology - global

where are majority of new HIV infections?

A

over half of new infections are in sub-Saharan Africa

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24
Q

HIV Epidemiology - global

is the new infection rate of HIV going up or down? why?

A

new infection rate is going down mainly because
- Better access to healthcare
- More effective treatments that prevent infection

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25
Q

HIV Epidemiology - global

is the life expectancy increasing or decreasing for people with HIV?

A

People are now living long lives with HIV

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26
Q

HIV Epidemiology - global

how is the majority of new HIV infections spread?

A

heretosexual transmission

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27
Q

HIV Epidemiology - global

what was the UNAIDS goal (targets for 2020) ?

A

UNAIDS 90/90/90 goals to eliminate pandemic – global target of:

90% of people living with HIV being diagnosed
90% diagnosed on ART (antiretroviral therapy)
90% viral suppression for those on ART by 2020

28
Q

HIV Epidemiology - global

what was the fast track cities initiative?

A

global partnership between a network of over 90 high HIV burden cities,

where political leaders, affected communities, city health officials, clinical and service providers, and other stakeholders
work together to accelerate their local HIV responses

Instead of 90-90-90, want 95-95-95 globally

29
Q

HIV Epidemiology - UK

has the UK achieved the 90-90-90 target?

A

UK achieved 90-90-90 target in 2018
New HIV diagnosis in decline
Ageing population with HIV, new territory

30
Q

what are the 3 transmission routes of HIV?

A

Blood

Sexual

Vertical → ie. mother to child transmission (not called this because implies blame to mum)

31
Q

Prevention of HIV via sexual transmission:

list some methods

A

Voluntary medical male circumcision (HIV like the cells in foreskin)

Treatment of STIs (esp ones that breach epithelium)

condoms

HIV counselling and testing

PEP and PrEP

32
Q

what is the U=U campaign?

A

Undetectable = Untransmittable

signifies that those who receive effective antiretroviral therapy and have achieved and maintained an undetectable viral load cannot transmit the virus to a sexual partner.

What it has done/aims to do:
REMOVING the fear of sexual transmission
Dismantling HIV stigma
Encouraging people living with HIV to start and stay on treatment
Encouraging people to get tested

33
Q

what is PrEP treatment ?

A

Oral pre exposure prophylaxis

highly effective preventative measure GAME CHANGER

take just before sex or daily

eg. used by people who have a partner with HIV

34
Q

what is PEP treatment?

A

Post exposure prophylaxis

28 days Combination Antiretroviral Therapy –must be started within 72 hours

Not as effective as PreP

35
Q

if viral load is undetectable, what does this show?

A

undetectable viral load = there is viral suppression

the viral is not transmittable

36
Q

Benefits of being on treatment for HIV (Prep or pep)

A

Can have healthy baby without HIV

Can have vaginal delivery

Cant spread to partner

Can live normal life span

37
Q

benefits of testing

A

early diagnosis is key –>

get access to appropriate treatment and care

Reduction in morbidity and mortality

Reduction in mother-to-child-transmission (MTCT)

Reduction of sexual transmission

Early diagnosis is cost effective – savings on social care, lost working days, benefits claimed, costs associated with further onward transmission

38
Q

When and why people get tested - what scenarios ?

A

Patient presents to a clinician with indicators of immunosuppressive disease/seroconversion

Routine screening in high prevalence places eg. sub saharan africa

Antenatal screening - to eliminate vertical transmission

Screening in high risk groups

Patient initiated requests for testing

39
Q

issues in the UK - why dont doctors test enough?

A

Underestimate the risk of HIV in their patients eg. in the elderly, in the married

Fear of offending the patient

They don’t think of HIV

40
Q

Patient presentations that might involve HIV

examples

A

Does the patient have an unexplained/severe recurrent medical condition?

acute generalised rash (seen on palms)

glandular fever like symptoms

Unexplained wt loss or diarrhoea, night sweats

41
Q

how do screening tests for HIV work?

A

Venous blood sample

Window period = 7 weeks post exposure

P24 antigen, will detect the vast majority of infections at 4 weeks

High specificity and sensitivity

42
Q

what is the more rapid way of testing HIV?

A

Point of care tests

Finger prick blood
Get Immediate result
But Lower sensitivity and specificity
Can get False positive and negative results
Longer incubation period

however is a way to outreach in to a community and can lead to earlier diagnosis in a non-healthcare seeking individual

43
Q

what happens if you get a negative result from a HIV test

A

repeat the test if within window period (eg. negative at 4 weeks, repeat at 7 weeks)

44
Q

what happens if you get a positive or unclear result from a HIV test

A

Phone Sexual Health for advice and we’ll arrange an appointment within 48 hours, Explain test “reactive” and needs further investigation

45
Q

risk factors for HIV

A

Sexual contact with people from high prevalence groups – MSM, sub-Saharan African/ Thailand

Multiple sexual partners

Rape in high prevalence localities

46
Q

HIV Epidemiology - global

who is most at risk of HIV?

A

Men who have sex with men

Heterosexual women

Injecting drug users

Commercial sex workers

Heterosexual men

Truck drivers

Migrant workers

47
Q

HIV Epidemiology - global

50% of all new infections occurring world-wide are in which age group ?

A

15-24 year olds

48
Q

HIV Epidemiology - global

what region is seeing the most rapid rise in new HIV infections?

A

Eastern europe and central asia

49
Q

what are the 3 routes of transmission of HIV to children ?

A

In utero: transplacental, mostly during the third trimester

intrapartum: exposure to maternal blood and genital secretions during delivery

Breast milk: ingestion of large amounts of contaminated milk

49
Q

what are the 3 routes of transmission of HIV to children ?

A

In utero: transplacental, mostly during the third trimester

intrapartum: exposure to maternal blood and genital secretions during delivery

Breast milk: ingestion of large amounts of contaminated milk

50
Q

In a patient with fever, rash and non-specific symptoms:

A

-Ask about sexual history
-Think of HIV seroconversion

51
Q

Think about doing a HIV test when faced with a common problem that is:

A

in an unexpected patient

Is recussing

Has no clear underlying cause

52
Q

what is the most common opportunistic infection and AIDS defining illness?

A

PCP

pneumocystis pneumonia (fungal)

53
Q

what is meant by Seroconversion?

A

The transition from infection with HIV to the detectable presence of HIV antibodies in the blood.

53
Q

what is meant by Seroconversion?

A

The transition from infection with HIV to the detectable presence of HIV antibodies in the blood.

54
Q

during HIV latency, patient won’t have symptoms

what signs might they have?

A

Might have persistent generalised lymphadenopathy (enlarged lymph nodes)

55
Q

symptoms of PCP

A

Fevers
SOB
Dry cough
Pleuritic chest pain
Extertial drop in oxygen saturations = key feature

56
Q

how to diagnose and treat PCP

A

Diagnose with an induced sputum (send for PCP)

Can treat with co-trimoxazole antibiotic (even though it’s a fungus)

57
Q

aside from PCP, what are other AIDs defining illnesses?

A

Oesophageal candida

Kaposi’s Sarcom

Wastings syndrome

TB

58
Q

TB and HIV

is TB in HIV aids defining ?

A

yes

All patient with TB require a HIV test

TB in HIV at any CD4 count is aids defining

58
Q

TB and HIV

is TB in HIV aids defining ?

A

yes

All patient with TB require a HIV test

TB in HIV at any CD4 count is aids defining

59
Q

what is the formal criteria of AIDS?

A

CD4<200
OR
AIDS defining illness

60
Q

HIV increases the risk of any cancer that is associated with a virus

example: which cancer caused by human herpesvirus 8 is usually associated with HIV?

A

Kaposi’s sarcoma

single or multiple lesions on the skin

Treated with HAART and chemo/radiotherapy

Usually indicates underlying HIV infection

61
Q

HAART (highly active antiretroviral therapy ) uses how many antiretroviral drugs at once?

A

3 or more

Aim to reduce viral load to undetectable levels and increase CD4 count

62
Q

why is using 3 or more different antiretroviral drugs at once effective?

ie. why use triple therapy?

A

They act on different points in the replication cycle to suppress viral replication

reduced risk of resistance forming to the drugs - - the chances of all the mutations for three drugs arising in a single virion simultaneously by chance are effectively zero.
- Thus so long as three drugs are in the system, resistance will not occur.

63
Q

how does HIV resistance to drugs develop?

A
  1. non adherence (missing doses, spontaneous mutations can occur)
  2. drug-drug interactions (other drugs interact with antiretrovirals and decrease their effect eg. steroids or recreational drugs)

2a - microbiology and IDs (13 decks)

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