Dr. VIJAYA MOHAN KALAKOTLA MD (Int.Med) Consultant Physician Divine Touch Hospital Suryapet, Nalgonda, AP NONI Help Line Consultant Founder Trustee - Research Scientist World NONI Research Foundation, Chennai.

Clinical and cellular Improvement with NONI in patients with HIV / AIDS

HIV / AIDS

• • • • Caused by Immunodeficiency virus belongs to Lentivirus subfamily in the retroviral family.

First reported in 1981 -Los Angeles and San Francisco. -In Homosexuals Virus Identified in 1983 - By Luc Montagnier - Robert Gallo.

Origin: In 1999 Scientist found same virus in sub species of Chimpanzees in Africa. Researchers believe HIV1 was introduced into the Human population when hunters were exposed to infected blood.

HIV / AIDS

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EPIDEMIOLOGY

Most serious public health problem all over the world, more with developing countries like India.

Estimated HIV / AIDS patients about 50 millions.

Approximately 20 millions thought to have died of AIDS since 1981.

As of today 15,000 infections are estimated to be taking place every day.

- 95% from the Developing countries S Africa has the largest number of HIV / AIDS patients in the world.

Second largest is India.

China and India share 36% of patients

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HIV / AIDS

High In-come Nations HIV / AIDS due to drug abusers and Homosexuals.

In India – mostly due to - Heterosexuals - Blood Transfusions - MTCT In India – first case recorded – 1984 - Tamil Nadu - Large number of cases - Maharastra - Andhra Pradesh - TamilNadu - Less number of cases - Gujurat and Goa - Pondichery

HIV / AIDS

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PATHOPHYSIOLOGY

HIV essentially causes infection of Immune system.

Categorized HIV-1 and HIV – 2 - with many sub types.

HIV – 1 is more virulent.

Disease Progression (A) Typical - 80 to 90% of infected persons median survival time approx. 10 yrs. (B) Rapid - 5% of infected develop AIDS in 3 to 4 yrs.

(C) Long Term – 5% of infected do not experience the disease progression for an extended period of at least 7 yrs.

HIV / AIDS

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CELL INFECTED BY HIV

Its Polytrophic virus - invade many cells in the body. • Mainly - CD4 cells macrophages, dendrite cells microglial and astrocyts in the brain and mucosa of bowel.

• Major cellular receptor sites for HIV is CD4.

• Resistant to HIV infection.

– Homozygous mutation in CCR-5 gene (Delta 32)

HIV / AIDS

CELL ATTACHMENT AND ENTRY

• HIV attaches – cellular receptors and co-receptors and enter CD4 cells.

- Uncoated – viral RNA is converted to “Complementary DNA (cDNA)” by - Reverse transcriptase.

• cDNA enters CD4 cell nucleus and eventually incorporated into host cell chromosomes - Integrase enzyme

HIV / AIDS

• This integrated DNA is transcribed into messenger RNA, which comes out into cytoplasm, which in synthesize viral proteins (Progeny RNA ) • Progeny RNA and protein together packed and newly formed viral particals comes out from infected CD4 cells by budding process.

- Protease enzyme.

HIV / AIDS

Who is at risk of HIV infection?

1.

2.

3.

4.

5.

6.

7.

8.

Injection drug addicts.

Recipients of blood and its products - Not screened for HIV People with multiple sex partners.

History of STD.

CSW Gay men Health care workers.

Children borned to HIV infected mothers.

* Insets like Mosquitoes and bed bugs which fed on human blood do not spread HIV

HIV / AIDS

CLINICAL STAGES OF INFECTION

• HIV pathogen involves 3 major clinical stages of infections.

1. Early period: - High viraemia - Large number of infected cells in peripheral blood.

- High titers of virus in the plasma and lymph node.

• Natural immunity: - Viral titers decrease dramatically due to viral specific immunity development in the body.

- They include – HIV specific cytotoxin, T-

HIV / AIDS

lymphocyte response - Ab-dependent cellular toxicity - HIV specific CD4 cell response.

These causes – stabilization of viral levels and CD4 cell count for many years. This is called “Set Point”.

This set point is predictor of prognosis of disease.

Higher the set point – worse is the prognosis 2. Persistent Period - Chronic phase of disease - Viral levels are low - CD4 count getting low @ 25 to 60 cells per

HIV / AIDS

Cum per year.

Cellular and humoral immune response to HIV is detected during this phase, which decrease the set point and delay the disease progration.

Citotoxin T-lymphocyte response inhibit viral replication by killing directly or producing chemo kines that inhibit.

Nutralizing anti-bodies help to wipe out the virus.

3. Symptomatic period - Immune exhaustion – lack of adequate T helper self function By this time individual develops symptoms. CD4 cell count usually drop to 300/ mm.

HIV / AIDS

CLINICAL FEATURES OF HIV / AIDS

• Primarily non specific symptoms are manifested-fever, lethergy, sore throat rash and enlargement of LN.

• Occurs during 2 to 6 weeks after acquiring virus.

• Resolve with in 2 to 3 weeks.

• In AIDS – s/s are dependent on the infection in the body.

HIV / AIDS

INVESTIGATIONS

• Spot test – Tridot, slip test.

• Elisa for HIV.

• W. Blot • P24 • PCR-DNA