HIV/AIDS

Question 1

HIV

Answer 1

Retrovirus, infects cells of immune system, primarily CD4+ cells
Progressive deterioration of the immune system → immunodeficiency → predisposition to infection

Question 2

Transmission

Answer 2

Unprotected sex - receptive anal 0.04-3%
Unprotected sex - insertive penile-vaginal 0.01% - 0.38%
Mother-child - 25%
Blood transfusion - >90%
Needlestick injuries - 0.3%
Transmission ↑ with co-existing/active STI
Most infective in first 3 weeks following infection, then when have AIDS

Question 3

Pathophysiology

Answer 3

Disrupts CD4+ T-cell function → failure of both cell-mediated and humoral response
Impaired thrombopoeisis (new T cell production)

Question 4

AIDS

Answer 4

Aquired Immuno-deficiency syndrome

Based on signs, symptoms, infections and cancer associated with immune deficiency caused by HIV

Question 5

AIDS-defining conditions

Answer 5

• Candidiasis of oesophagus, airways and lungs
• Cervical cancer
• Histoplasmosis
• Coccidoidomycosis
• Isopsoriasis
• Cryptococcus
• Kaposi’s sarcoma
• CMV
• Burkitt’s lymphoma/primary CNS lymphoma
• HIV encephalopathy
• Mycobacterial infection
• Chronic HSV ulcers
• Chronic bronchitis, pneumonitis or oesophagitis
• PCP
• Recurrent bacterial pneumonia
• Progressive multifocal leucoencephalopathy
• Salmonella septicaemia and cerebral toxoplasmosis
• Wasting syndrome
• CD4 < 200 or < 14%

Question 6

Opportunistic infetions

Answer 6

CD4 >200: TB, candidiasis, HZV, pneumonias
CD4 100-200: pneumocystis, histoplasmosis, PML
CD4 <100: atypical mycobacterial disease, military or extrapulmonary TB, CMV, retinitis, colitis, toxoplasmosis, cryptococcus

Question 7

Prevention of infection

Answer 7

Primary prophylaxis: co-trimazole CD4 <200

Secondary - depends on infection, start after treating infection until immune system has recovered above threshold

Question 8

Malignancy

Answer 8

AIDS defining: non-hodgkins, CNS lymphoma, Kaposi’s sarcoma, Burkitt’s lymphoma
Other: Anal, lung, testicular, head/neck

Question 9

Targets of HIV treatment

Answer 9

1) HIV binds to CD4 cell receptors: ENTRY INHIBITORS or FUSION INHIBITORS
2) Enters cell and inserts genes (RNA)
3) Converts genes to become compatible (DNA): REVERSE TRANSCRIPTASE INHIBITORS, NRTIs, NNRTIs, NtRTIs
4) Inserts its genes into the cell’s genes: INTEGRASE INHIBITORS
5) CD4 cell reads the corrupted gene and produces HIV components
6) HIV components assembled to form new HIV: PROTEASE INHIBITORS
7) New HIV cell destroys CD4 cell as it leaves to infect another cell

Question 10

HAART, efficacy

Answer 10

Highly active antiretroviral therapy
>95% adherence, 80% undetectable viral load
90-95% adherence, 60% undetectable viral load
<10% undetectable viral load

Question 11

Preferred HAART regime

Answer 11

NRTI backbone: Tenofovir and Emtricitabine

3rd agent: atazanavir/ritonavir; darunavir/ritonavir; efevirenz; raltegravir

Question 12

Alternative HAART regime

Answer 12

NRTI backbone: Abacavir and Lamivudine

3rd agent: Lopinavir/ritonavir; fosamprenivir/ritonavir; nevirapine; rilpivirine

Question 13

HAART side effects

Answer 13

Mostly well tolerated
Some NRTIs cause metabolic problems and lactic acidosis
Fat-redistribution and lipoatrophy
Dyslipidaemia
Drug interactions

Question 14

Treatment as prevention of transmission

Answer 14

Treatment ↓ VL in all body compartments → ↓ transmission
Not sexually infective if:
• Antiretroviral therapy taken consistently
• Undetectable viral load for >6 months
• No concurrent STIs
Full immune recovery associated with higher baseline CD4 count