Abstract
Drugs which inhibit different stages of the HIV infection process, such as cell entry through CD4 and chemokine receptors, production of double stranded DNA from the HIV genome and maturation of newly produced viruses, are now proposed for AIDS therapy. None of these treatments, however, solve the problem of complete HIV eradication and the frequent appearance of mutants displaying drug resistance. We have recently detailed a strategy describing how HIV protects itself from the human complement and propose that interference of this resistance could be a possible target for therapy.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
AIDS Vaccines / pharmacology*
-
AIDS Vaccines / therapeutic use
-
Animals
-
Anti-HIV Agents / pharmacology*
-
Anti-HIV Agents / therapeutic use
-
Antibodies, Monoclonal
-
Complement C3b
-
Complement Factor H / physiology
-
Complement System Proteins / drug effects*
-
Complement System Proteins / physiology*
-
HIV / drug effects
-
HIV / physiology
-
HIV Envelope Protein gp120
-
HIV Envelope Protein gp41
-
HIV Infections / drug therapy*
-
HIV Infections / immunology*
-
Humans
-
Peptide Fragments
Substances
-
AIDS Vaccines
-
Anti-HIV Agents
-
Antibodies, Monoclonal
-
CFH protein, human
-
HIV Envelope Protein gp120
-
HIV Envelope Protein gp41
-
HIV envelope glycoprotein gp41 (593-603)
-
Peptide Fragments
-
Complement C3b
-
Complement Factor H
-
Complement System Proteins