Treatment of disease Prevention

As the current viral infection there was no magic treatment, so there is no effective treatment for AIDS means. In addition, HIV viral nucleic acid into host chromosomal DNA integration, the use of host cell replication, to create difficulties for drug treatment. The importance of early treatment of HIV infection. Immune function through the treatment can slow the decline. HIV infected persons suffering from tuberculosis, bacterial pneumonia and Pneumocystis carinii pneumonia, increased risk, the importance of early prevention. 
1, support therapy, AIDS patients as much as possible to improve the sexual consumption. 
Second, the immune modulator therapy: 
(A) interleukin-2 (IL-2): to improve the body of the HIV-infected cells MHC restricted cytotoxicity, but also a non-MHC restricted natural killer cells (NK) and lymphokine-activated killer cells (LAK) of the activity. 
(B) granulocyte colony-stimulating factor (G-CSF) and granulocyte – macrophage colony-stimulating factor (GM-CSF): increase in circulating neutrophils, enhance the body’s anti-infection ability. 
(C) Ling bacilli elements: activating the pituitary – adrenal cortex system, adjust the body’s internal environment and function, enhance the body’s ability to adapt changes in the external environment to stimulate the body to produce humoral antibodies, so that the total number of white blood cells, the phagocytic function of enhanced activation body’s defense system to resist the invasion of pathogenic microorganisms and viruses. 
(D) interferon (IFN): α-interferon (IFN-α), for some patients to be slightly increased CD4 + T cells, 40% Kaposis sarcoma patients have tumor subsided; ② β-interferon (IFN-β):Intravenous administration of IFN-α effect is similar, but subcutaneous injection, anti-Kaposis sarcoma, are less effective; ③ γ-interferon (IFN-γ) increased monocyte – macrophage activity, anti-toxoplasma infections and other conditions might have someeffect. 
3, anti-viral agent: 
(A) inhibit HIV with the host cell binding and penetration of drugs: soluble rsCD4 combination with HIV, accounting for CD4 binding site, so HIVgp120 can not CD4T lymphocytes CD4 binding and can not penetrate infected CD4T lymphocytes. 
Dose: rsCD4 clinical trials 30mg / day, intramuscular or intravenous, 28 consecutive days. 
(B) inhibit HIV reverse transcriptase (RT) of drugs: by inhibiting reverse transcriptase, blocking HIV replication. Better-drugs: AZT, double-deoxycytidine.