Clinical features of HIV Baseline investigations Laboratory diagnosis of HIV Algorithm for the use of the diagnosis of HIV-1 or HIV-2 infection. PRINCIPLES OF THERAPY OF HIV INFECTION medications used in treatment Secondary prophylaxis of opportunistic infections Prevention of HIV reference Davidsons Priniciples and Practice of Medicine and Harrisons Manual Of Internal Medicine

3. • CD4 count
• Viral load
• Liver function tests
• Full blood count
• Urinalysis and serum
Creatinine
• Cervical smear in
Women
• Hepatitis B surface antigen
• Hepatitis C antibody
• Syphilis serology
• Tuberculin skin test
• STI screen
• Serum cryptococcal
antigen (if CD4
< 100)

4. CD4 counts
• CD4 lymphocyte counts are usually determined by flow
cytometry.
• The CD4 count is the most clinically useful laboratory
indicator of the degree of immune suppression
 normal CD4 count is > 500 cells/mm3.
 CD4 counts between 200 and 500 cells/mm3 have a low
risk of developing major opportunistic infections.
 count is below 200 cells/mm3- severe immune suppression
and a high risk of major opportunistic diseases

5. Viral load
• The level of viraemia is measured by
quantitative PCR of HIV-RNA, known as the
viral load.
• high viral loads (e.g. > 100 000 copies/mL)
experience more rapid declines in CD4 count,
• Low viral loads (< 1000 copies/mL)have slow or
even no decline in CD4 counts.

6. Virological and immunological progression of
untreated HIV infection.

7. Haematological abnormalities
•Pancytopenia may occur as a consequence of HIV
•Normochromic, normocytic anaemia is very common
•Anaemia is a common adverse effect of zidovudine,which
also causes a macrocytosis.
•Isolated neutropenia is occasionally due to HIV but is
nearly always caused by drug toxicity ( Zidovudine)
•Mild thrombocytopenia

8.  The standard screening test for HIV infection:
• the detection of anti-HIV antibodies using an
enzyme immunoassay (EIA).
EIA kits are available to detect antibodies to both
HIV-1 and -2.

9. • Western blot is - confirmatory test and detects
antibodies to HIV antigens.
Antibodies to HIV begin to appear within 2 weeks
of infection but are not detectable.
• The HIV p24 antigen can be measured using an
EIA-type capture assay.
Plasma p24 antigen levels rise (in first few weeks).
• HIV genetic material can be detected using
reverse transcriptase PCR (RT-PCR)

11. 1. Ongoing HIV replication leads to immune system damage
and progression to AIDS.
2. CD4+ T cell counts indicate the current state of the
immune system.
3. Rates of disease progression differ among individuals, and
treatment decisions should be individualized .
4. Maximal suppression of viral replication is a goal of
therapy.
5. The most effective therapeutic strategies involve the
initiation of combinations of effective anti-HIV drugs .

12. 6. The antiretroviral drugs used in combination regimens
should be used according to optimum schedules and dosages.
7. The number of available drugs is limited. Any decisions on
antiretroviral therapy have a long-term impact on future
options for the patient.
8. Women should receive optimal antiretroviral therapy
regardless of pregnancy status.
9. The same principles apply to children and adults.
10. The simpler the regimen, the easier it is for the patient to
be compliant.

13. Nucleoside reverse transcriptase inhibitors:
These agents act by causing premature DNA-chain
termination during the reverse transcription of viral
RNA to proviral DNA.
Ex. Zidovudine, Abacavir, emtricitabine,
lamivudine, tenofovir
Nonnucleoside Reverse Transcriptase Inhibitors :
interfere with the function of HIV-1 reverse transcriptase
by binding to regions outside the active site and causing
conformational changes in the enzyme that render it
inactive. Ex. nevirapine, delavirdine,efavirenz,
etravirine, and rilpivirine

14. Protease Inhibitors These drugs are potent and selective
inhibitors of the HIV-1 protease enzyme and are active in
the nanomolar range. Ex. Fosamprenavir
HIV Entry Inhibitors:
act by interfering with the binding of HIV to its receptor
or co-receptor or by interfering with the process of fusion.
the fusion inhibitor enfuvirtide and the entry inhibitor
maraviroc.
HIV Integrase Inhibitors These drugs interfere with the
integration of proviral DNA into the host cell genome.
Ex. Raltegravir

15. Recommended initial ART regimens for
all patients:
Non-nucleoside reverse transcriptase inhibitor-
based regimen:
• Efavirenz + Tenofovir + Emtricitabine (or)Lamivudine
Protease inhibitor-based regimens:
• Atazanavir/ritonavir + Tenofovir + Emtricitabine (or)
Lamivudine
lntegrase inhibitor-based regimens:
• Raltegravir + Tenofovir + Emtricitabine (or)Lamivudine

16. Alternative regimens for patients with plasma HIV
RNA <100,000 copies/ml
Non-nucleoside reverse transcriptase inhibitor-based
regimen:
• Rilpivirine + Tenofovir + Emtricitabine (or)Lamivudine
only for patients with CD4 count >200 cells/mm3

17. Secondary prophylaxis of opportunistic infections
Infection Drug regimen
Pneumocystis jirovecii
pneumonia
Co-trimoxazole 960 mg daily
Toxoplasmosis Co-trimoxazole 960 mg daily
Cryptococcosis Fluconazole 200 mg daily
Cytomegalovirus infection Valganciclovir 900 mg daily
Mycobacterium avium complex Clarithromycin 500 mg twice
daily + Ethambutol 800 mg daily
Isospora belli infection Co-trimoxazole 960 mg daily

18. Sexual
• Sex education programmes in schools
• Easily accessible voluntary counselling and testing
centres
• Promotion of safer sex practices (delaying sexual
debut,
condom use, fewer sexual partners)
• Effective ART treatment of HIV-infected individuals
• Pre-exposure prophylaxis for high-risk groups
• Male circumcision

19. Parenteral
• Blood product transmission: donor questionnaire,
routine screening of donated blood
• Injection drug use: education, needle/syringe exchange,
avoidance of ‘shooting galleries’, methadone maintenance
Programmes
Perinatal
• Routine ‘opt-out’ antenatal HIV antibody testing
• Measures to reduce vertical transmission
Occupational
• Education/training: universal precautions, needlestick
injury avoidance
• Post-exposure prophylaxis

20. Post-exposure prophylaxis
• The first dose should be given as soon as
possible,preferably within 6–8 hours.
• dual NRTIs for low-risk exposures, with the
addition of either a PI or efavirenz in high-risk
exposures
• Tenofovir together with emtricitabine is the most
widely used dual NRTI combination,