Natural History, classification and testing of HIV

Question 1

ART

Answer 1

Anti-retroviral therapy

Question 2

HAART

Answer 2

Highly active anti-retroviral therapy

Question 3

RTI

Answer 3

Reverse transcriptase inhibitor

Question 4

NRTIs/NNRTIs

Answer 4

Nucleoside/Non-nucleoside reverse transcriptase inhibitors

Question 5

Viral Load

Answer 5

Quantitive measure of HIV infectivity - number of virus particles in blood

Question 6

CD4 count

Answer 6

Measure of disease severity/immunosuppression

>500 is normal, <200 is very low,

Question 7

CDC classification of HIV

Answer 7

Based on CD4 count (1:>500, 2:200-499, 3:<200) and clinical picture (A:asymptomatic/Acute HIV or PGL, B:symptomatic, but not AIDs defining infections, C: AIDs defining illness)

Question 8

WHO classification of HIV

Answer 8

Stage 1–> asymptomatic,persistent generalized LN
Stage 2–> Weight loss, skin conditions, recurrent oral ulcers
Stage 3–> Severe WL, chronic diarrhoea, fever, oral thrush, TB
Stage 4–> AIDs defining illnesses

Question 9

AIDs defining illnesses - opportunistic infections

Answer 9

Pulmonary/esophageal candida, Coccidiodomycosis or Cryptosporidiosis, CMV disease/HSV disease, Histoplasmosis or Isosporiasis, Mycobacterial disease (atypical TB or MAC), Recurrent or pnuemocystis pneumonia

Question 10

AIDs defining illnesses - syndromes

Answer 10

Wasting syndrome due to HIV, Encephalopathy (AIDs dementia or progressive mutlifocal leukoencephalopathy, Kaposi’s sarcoma, Non-hodgkin’s lymphoma and invasive cervical carcinoma

Question 11

Structure and subtypes of HIV

Answer 11

RNA lentivirus

HIV-1 and HIV-2 (less aggressive)

Question 12

Timecourse of HIV infection

Answer 12

Primary infection–> seroconversion (flu-like illness) after 2-6 weeks, rapid CD4 drop and massive VL - Clinical latency–> 6 months to 12 years - Advanced stage–> CD4 50-200 - Late stage–> CD4 <50
AIDs patients will first manifest infections then aggressive cancers

Question 13

Clinical Latency

Answer 13

Clinical latency–> low viral load with CD4 >500 (early) and middle (CD4 200-500).Early–>can be asymptomatic or generalised lymphoadenopathy and skin disorders. Middle–> skin disorders worsen, recurrent infections (herpes, varicella, TB, etc) and constitutional conditions fever, weight loss, night sweats and fatigue

Question 14

Seroconversion

Answer 14

after 2-6 weeks, rapid CD4 drop and massive VL

flu-like illness –> easy to miss and must have low index of suspicion

Question 15

Advanced stage

Answer 15

CD4 50-200 — increasing viral load
Increased manifestation of AIDs –> oppourtunistic infections (PCP, candidasis, multidermal shingles, lymphoma, TB, kaposi’s sarcoma, MAC)

Question 16

Late stage

Answer 16

CD4 <50, CMV retinitis, disseminated MAC, primary brain lymphomas, AIDs dementias, Cryptococcal meningitis

Question 17

HAART

Answer 17

Combination of 3 drugs developed in 1996 which greatly reduced death rates by keeping the VL down allowing for chronic management without progression–> use of prophylatic antibiotics reduces infections (PCP etc)

Question 18

When to start HAART

Answer 18

When CD4 is below 350 (low). When there is any AIDs defining illness
When there is any neurological involvement. Any related STI or cancers requiring treatment. If they have an HIV neg partner

Question 19

Immune reconstruction inflammatory syndrome (IRIS)

Answer 19

After ART is started and the CD4 count returns to a healthier level this syndrome can occur

Question 20

Life expectancy with HIV if on HAART

Answer 20

Normal, if properly treated HIV positive patients will die of non-HIV related problems

Question 21

Direct effects of HIV

Answer 21

Lymphadenitis, encephalopathy/dementia, glomerulopathies, enteropathy, pneumonitis, dermatitides, Histiocytis haemophagocytosis, cardiomyopathy, pulmonary hypertension

Question 22

Indirect effects of HIV

Answer 22

Opportunistic infections

Opportunistic tumours

Question 23

Immune activation syndromes

Answer 23

Gut lymphoid depletion –> primary infection depletes CD4 cells in gut and recovery under HAART is incomplete. Microbial translocation.
Pro-inflammatory state -> increased rate of multiple disease processes

Question 24

Pathogenesis of HIV wasting

Answer 24

Malnutrition–> reduced intake due to poverty or oesohagitis
Malabsorption –> infections
Increased catabolism–> infections and tumours

Question 25

Persistent generalized lymphoadenopathy (PGL)

Answer 25

pretty much what it sounds like
Happens in HIV infection
not good

Question 26

Herpes viruses in HIV

Answer 26

HSV 1+2–> severe local/disseminated blisters/ulcers. Disseminated shingles. EBV can lead to hodgkin’s or non-hodgkin’s lymphoma. CMV can cause retinitis, pneumonitis, encephalitis or be disseminated. HHV-8 causes castleman’s disease, Kaposi’s sarcoma and non-hodgkin’s lymphoma

Question 27

Papilloma viruses in HIV

Answer 27

Genital warts (condylomata accuminata)
squamous cell carcinoma of the cervix, anus, oesophagus or conjunctiva

Question 28

Progressive multifocal leukoencephalopathy (PML)

Answer 28

caused by the JC virus (a papovavirus)

Question 29

Fungal infections in HIV

Answer 29

Candida–>genital, GIT or disseminated
Cryptococcus neoformans & Histoplasma capsulatum–> can effect any organ or be disseminated
Pneumocystis jirovecii/carinii pneumonia (PCP)

Question 30

Protazoan infections in HIV

Answer 30

Cryptosporidium parvum–> small and large bowel
Microsporidia and Isospora belli –>bowel and others
Toxoplasma gondii–> brain, heart and other organs

Question 31

Maligancies in HIV

Answer 31

Hodgkin and Non-hodgkin lymphoma
Primary brain lymphoma
Multiple viral cancers (Kaposi’s, cervical carcinoma)