Dr. VIJAYA MOHAN KALAKOTLA. MD (Int 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 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

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 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 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? 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.

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