Process for the treatment and the prevention of AIDS and other disorders induced by the LAV/HTLV III virus

DETAILED DESCRIPTION We claim: 1.
Process for increasing the T4 cell number in a patient infected with LAV/HTLV III virus, comprising administering an effective amount of cyclosporin A.




Description:
The present invention relates to a process for the treatment and the prevention of AIDS and other disorders induced by the LAV/HTLV III virus.
Only two years after the clinical emergence of the acquired immunodeficiency syndrome (AIDS) and the AIDS related complex (ARC), the discovery of the lentivirus responsible for these syndromes has enabled a decisive breakthrough in the knowledge of the disease, i.
e.
a viral destruction of the pivotal regulatory cell of the immune system, the T helper/inducer (T4) lymphocyte, leading to a progressive and irreversible immunodeficiency.
The AIDS virus (LAV or HTLV III) is an RNA exogeneously transmitted cytopathic non oncogenic lentivirus.
The virus binds selectively to the T4 receptor of T4 cells, but cannot be propagated in vitro into monoctyes, T3, T8 and normal B lymphocytes.
After entering the T4 cell, the viral RNA is retrotranscripted by a specific viral reverse-transcriptase into unintegrated linear DNA.
The major part of the linear DNA is integrated into the cellular genome, each cell containing many copies inserted at random in chromosomal sites, variable from one cell to another (Shaw GM, et al, Molecular characterization of human T-cell leukemia (lymphotropic) virus type III in the acquired immune deficiency syndrome.
Science 1984.
226: 1165-71).
The natural evolution of the disease can be divided into an immunoactive period followed by an immunodepressed period.
1-The first immunoactive period is characterized by a number of clinical, histological and biological manifestations mimicking autoimmune diseases.
This period may be clinically latent or expressed by a PGL, which is initially isolated or associated with systemic symptoms occurring generally after 1 to 3 years.
During this period, many features are suggestive of an intensive immune response: (a) the outbreak of the disease, 2 to 4 weeks after the contamination by an influenza-like syndrome with fever, sore throat, macular rash, arthralgies and lymphadenopathy occuring simultaneously with the seroconversion and lasting a few weeks