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Infection > Session 7: Blood Borne Viruses: HIV > Flashcards

Session 7: Blood Borne Viruses: HIV Flashcards

1
Q

4 important viral structures and behaviours to consider concerning viruses.

A

Genome (RNA or DNA + single stranded or double stranded)

Capsid (Protein shell that protects the genome - is it helical or icosahedral)

Lipid envelope (Present or absent)

Replication strategy

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2
Q

Explain HIV with the viral structure and behaviours in mind.

A

HIV is a retrovirus meaning it goes from ssRNA -> DNA -> ssRNA

It infects cells with CD4 surface receptors

It replicates inside the cells and destroys them. They cause inflammation and spread to infect more cells.

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3
Q

HIV infects cells with CD4+ surface receptors. Which cells then?

A

Mainly T helper cells but also monocytes/macrophages.

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4
Q

Explain HIV’s process in a host cell. (Replication)

A

The free virus binds to a CD4 molecule and one coreceptor. The virus will then fuse with the cell expressing the CD4 molecule.

The virus then penetrates the cell and the contents of the virus is emptied into the cell.

Reverse transcription begins where the ssRNA from the HIV is converted into double stranded DNA by reverse transcriptase enzyme.

The viral DNA is now combined with the host cell’s own DNA by integrase enzyme.

When the infected cell divides the viral DNA will also be read and proteins will be made.

Viralproteins (which are cleaved and become functional) come together and via budding the viral proteins are exocytosed within a vesicle. Non-functional proteins which are not cleaved do not come together.

The new virus although immature breaks free from the infected cell and matures. The viral protein chains will make up ssRNA again. This is why it’s called retrovirus.

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5
Q

Transmission of HIV.

A

Sexual contact

Transfusion

Contaminated needles (IV drug users mainly)

Perinatal transmission (infected birth canal, transplacental, ingestion of breast milk carrying virus).

Medical procedures such as skin grafts and organ donation as well.

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6
Q

When is HIV most infectious?

A

After a couple of months of the primary infection. You might not be symptomatic however.

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7
Q

What are the stages of HIV infection.

A 
Primary HIV infection
Stage I
Stage II
Stage III
Stage IV or AIDS
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8
Q

Explain primary HIV infection.

A

Asymptomatic or Seroconversion illness

CD4 count is normal or a temporary drop.

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9
Q

Explain Stage I

A

Asymptomatic

CD4 count >500

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10
Q

Explain Stage II

A

Mild symptoms

CD4 count <500

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11
Q

Explain Stage III

A

Advanced symptoms

CD4 count <350

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12
Q

Explain Stage IV or AIDS.

A

Severe symptoms or AIDS defining symptoms.

CD4 count <200

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13
Q

Main symptoms/signs of acute HIV infection.

A 
Fever
Weight loss
Sores in mouth + candidiasis
Sores in oesophagus
Myalgia
Splenomegaly
Hepatomegaly
Malaise, headache and neuropathy
Lymphadenopathy
Rash
Nausea and vomiting
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14
Q

HIV starts off with the acute symptoms such as lymphadenopathy and thrombocytopenia. As the disease progresses the symptoms will get worse according to CD4 count.

Try to create a timeline of symptoms/signs.

A

At around 500 you will start getting bacterial skin infections.

400 - Kaposi’s Sarcoma

300 - Hairy leukoplakia and tuberculosis

200 - PCP, Cryptococcis and toxoplasmosis

100 - CMV and Lymphoma

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15
Q

Conditions associated with severe HIV.

Give one for each area affected:
Brain
Eyes
Mouth and throat
Blood
Lungs
Bone
Heart
Liver
Stomach
Rep. system
Body
A

Brain:
Meningitis
Toxoplasmosis

Eyes:
CMV

Mouth and throat:
Cold sores and ulcers
Oral candidiasis

Blood:
Hyperglycaemia
Dyslipidaemia

Lungs:
Histoplasmosis
PCP
TB

Bone:
Osteoporosis

Heart:
Heart disease and stroke

Liver:
HCV

Stomach:
MAC

Rep. system:
Genital ulcers
HPV
Cervical cancer
PID
Menstrual problems
Candidiasis

Body:
HIV wasting syndrome

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16
Q

Factors affecting HIV transmission.

A

Type of exposure like what kind of sexual act.
Transfusion vs. needles tick vs mucous membrane.

Viral load in blood. The transmission is unlikely if undetectable viral load.

Condom use

Breaks in skin or mucous during sexual act (sexual assault can be more likely to cause transmission)

17
Q

3 most infectious ways of contracting HIV. (Doesn’t have to be the most common ways)

A

1 - Blood transfusion (90 - 100%)
2 - Receptive anal intercourse (1.11 %)
3 - Sharing needles (0.67%)

18
Q

Life expectancy in UK in general pop vs HIV.

A

Gen pop - 80 yrs

HIV - 78 yrs

19
Q

What makes out a good prognosis of someone who is HIV positive?

A

Early detection with good CD4.
Regular treatment
Adherence
Healthy living

The later you detect it the worse the prognosis.

20
Q

Diagnostic tests of HIV.

A

Blood tests (Serology)

HIV antigen (Ag) - viral protein
HIV antibody (Ab) - immunoglobulin

Current tests carried out today detects both Ag and Ab.
However it can give a false negative result. Result on same day.

PCR (polymerase chain reaction. To detect HIV nucleic acid. This is highly sensitive and can detect very early infection. However it is expensive and the result is slow.

21
Q

There are even more rapid tests to test for HIV that produce a result in less than an hour.
Explain them and why they might be advantageous/disadvantageous.

A

Usually detect HIV antibody
Can be finger-prick or saliva.

If it is negative it is highly accurate.

However you can get a false positive result. If you get a positive result you need to confirm with serology.

22
Q

Who should be tested for HIV?

A 
Bacterial pneumonia / TB
Meningitis/dementia
Sever psoriasis
Chronic diarrhoea
Unexplain blood abnormality
Lymphoma and anal cancer
CIN
Any STI/Hep B or Hep C

This is in a population where the HIV rate is over 2/1000.

23
Q

What is used to treat and reduce prevalence of HIV?

Main group

A

Anti-retroviral drugs (ARVs)

24
Q

What are the aims of HIV treatment?

A

To reduce the HIV viral load to an undetectable level.
To increase the CD4 count to a normal level.
Reduce general inflammation to reduce risk of cancer as well
Reduce risk of transmission
Good quality of life
Normalise life span

25
Q

Referencing back to the HIV replication, where would drugs be suitable to inhibit the replication?

A

The binding to the CD4 receptors and fusing with the cell. (CCR5 inhibitor)

Inhibiting reverse transcriptase to inhibit the ssRNA to become DNA. (Nucleoside reverse transcriptase inhibitors and non-nucleoside reverse transcriptase inhibitors)

Inhibiting integrase enzyme where the viral DNA is combined with the host cell’s DNA. (Integrase inhibitors)

Inhibiting proteases from cleaving the viral proteins to functional proteins to become a new virus. (Protease inhibitors)

26
Q

When should you start treatment?

A

Up until very recently it was when CD4 count got below <350. However now you treat everyone as soon as possible regardless of CD4 count.

27
Q

What kind of ARVs exist? (Main groups)

A

Nucleoside reverse transcriptase inhibitors (NRTI)
Non-nucleoside reverse transcriptase inhibitors (NNRTI)
Integrase inhibitors
CCR5 entry inhibitors
Protease inhibitors

28
Q

Which ARVs would you give in HIV?

A

In almost all cases give two NRTIs and one additional from another group.
So 3 in total.

29
Q

Why do you give 3 ARVs?

A

Because there are millions of rounds of viral replications a day.
The virus also mutates every 2-3 rounds
This means that resistance develops very quickly so if you only have one drug the resistance can develop quickly but with 3 drugs its harder for the virus to develop resistance.

It is important that the patient keeps taking the drugs.

30
Q

What strategies would you use to treat and reduce the prevalence of HIV?

A 
Increase condom usage
Prevention of mother-to-child transmission
ARV treatment as prevention
Medical circumcision
Post-exposure prophylaxis
Pre-exposure prophylaxis
31
Q

Ethical dilemmas in HIV.

A 
Psychological impact of diagnosis
Dealing with stigma from lay people
Patient confidential vs.
Health of mother
Health of unborn child
Health of sexual contact
Health of older child
Risk to patients and staff at workplace

Infection (17 decks)

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