HIV and AIDS symposium

Question 1

HIV =

AIDS =

Answer 1

Human immunodeficiency virus

Acquired immunodeficiency syndrome

Question 2

AIDS caused by

Manifests as

Originated

Answer 2

HIV
Retroviruses

Kaposi’s sarcoma - darkening of skin
In Africa

Question 3

HIV transmission

Answer 3

Sexual contact
Blood - blood contact 
Infected blood products
In utero 
Breast milk

Question 4

HIV types and strains

Answer 4

HIV 1 and 2

1 most common
2 less easily transmitted and less pathogenic

Question 5

HIV is good at

Answer 5

Mutating rapidly because reverse transcriptase does not proofread sequences produced
Hard to produce vaccine

Question 6

3 main groups of HIV1

Answer 6

Main (M-pandemic trains)
New (N)
Outlier (O) - confined to Cameroon
Infected individuals contain a heterogenous viral popn

Question 7

Origins of infection

Answer 7

Chimp co-infection with two SIMEON INFECTIVE VIRUS strains
Viral crossover creates new strain
Transferred to human

Question 8

Origin of HIV-1 in cameroon - spread to congo

Further spread /

Answer 8

Urbanisation, diamonds, rail travel, independence

Question 9

Virus characteristics

Answer 9

Central capsule which protects single stranded RNA genome
Adhesins on exterior which bind to cell receptors
Lipid coat around virion - less resistant to survival outside host
ssRNA genomed virus which is pertinent for its replication

Question 10

Infections

Mechanism

Promoted by

Answer 10

CD4 positive cells - T cells
Initial attachment via gp120 binding to CD4
Loss of cell mediated response

Humoral response

Question 11

Virus binds to receptors

Heterozygous mutation

Homozygous mutation

Answer 11

CCR5/CXCR4 receptors
Co-receptor binding

People with CCR5 mutations are resistant as receptor will no longer bind to virus

Reduced susceptibility

Completely immune

Question 12

Virus mechanism after attachment

When cells are activated

Answer 12

Membrane fusion and internalisation
Virus hides inside host genome
Decorating of virus releases viral mRNA and the reverse transcriptase and integrate enzymes
Converts RNA to DNA in nucleus and then integrates into the chromosome –> RETROVIRUS

Viral proteins produced and thousands of new virus progeny synthesised

Question 13

Virus variation during HIV infection

Answer 13

Isolates from early on in infection - CCR5

• LOW CYTOPATHIC EFFECT
• MORE TRANSMISSABLE

Isolates from late infection - CXCR4
- HIGH CYTOPATHIC ABILITY - LESS TRANSMISSIBLE

Question 14

INFECTION AND DISSEMINATION

Answer 14

Can cross blood-brain barrier

Question 15

Disease progression

Start

End

Answer 15

Associated flu like symptoms, high plasma HIV levels, transient CD4 cell depletion

Ask about graph ??

Question 16

Opportunistic infections are common

Answer 16

Post latency period

**Bacterial-
- Mycobacterium tuberculosis
Salmonella
Haemophilus, Streptococcus, Pneumococcus- Pyogenic infections (pus formers)- recurrent

**Protozoa-
Cryptosporidum (chronic diaarhoea)
Toxoplasma gondii (disseminated, including CNS- from Cats)

Fungal-
Aspergillus - pneumonia
**Candida- oral presentation
**Cryptococcus neoformans- CNS 
**Pneumocystis jiroveci/ carinii- pneumonia

**Viruses-
**HSV- Herpes simplex virus- chronic oral infection
EBV- Hairy leukoplakia, and B- cell lymphomas
HHV-8 – Kaposis Sarcoma

Question 17

Oral manifestations in HIV infection

Answer 17

Thrush
Erythematous candidosis
Gingival erythema
Hairy leukoplakia

Question 18

Progression to AIDS often occurs if

Answer 18

Untreated
10% of HIV infected subjects progress within 2-3 years
5-10% clinically asymptomatic
Remaining subjects progress to AIDS within 10 years
Situation drastically improved by ARVT

Question 19

Graph explained

Answer 19

Steady HIV diagnoses

By 2005 it peaks

Question 20

Most new infections occur

Answer 20

Amongst homosexual communities
Asian and African epidemic more heterosexual
- high STD levels –> ulceration

Question 21

HIV drug targets

Answer 21

Fusion inhibitors

NRTIs - nucleoside reverse transcriptase inhibitor

NNRTIs - non-nucleoside reverse transcriptase inhibitors

Integrase inhibitors

Protease inhibitors

CCR5 entry inhibitors

Question 22

NRTI mechanism

Answer 22

Nucleotide analogues provided

Analogues cause chain termination when RT builds DNA from RNA

Question 23

Treatment is called HAAT

Answer 23

HIGHLY ACTIVE ANTI-RETROVIRAL THERAPY

Question 24

First line reg

Answer 24

2 NRTIs
1 NNRTI - for HIV 2

OR protease inhibitor

Question 25

HIV drug side effects

Resistant is

Answer 25

NRTI - headaches, nausea, neutropenia, lactic acidosis, rashes

NNRTIs - Mucous membrane disorder, teratogenicity

PIs - lipodystrophy- fat loss from legs, fat gain-pot belly

Increasing issue
Drug holidays

Question 26

Alternative first line reg

Answer 26

DTG integrase inhibitor

Question 27

Vaccine prospects

Answer 27

Still some way off
Mutation rates high
Best prospect for eradication

Question 28

Dental transmission control

Normal cross infection control procedures

Answer 28

Very LOW risk - even with risk contact only
1/300

Gloves
Sterilise instruments 
Sharps disposal 
suction 
Blood spillage

Contact occupational health
IF needlestick –> PEP administration - post exposure prophylactic

Question 29

HIV TESTING

Answer 29

ELISA based blood test
Detects HIV antibodies in the blood
Antibody takes 6-12 weeks to develop
Most reliable testing at 3 months