title: Inactivation of HIV infectivity by the chlorite-oxygen reaction product tetrachlorodecaoxygen.
abstract: OBJECTIVE
  Since the chlorite-oxygen reaction product tetrachlorodecaoxygen (TCDO) anion complex promotes efficaciously tissue repair and has antibacterial activity, our aim was to determine the effects of TCDO on the replication of HIV and on the infectivity of free HIV particles.
  
  
  METHODS
  The effects of TCDO on cellular HIV replication machinery and the consequences of TCDO for infectivity of HIV virions were evaluated.
  
  
  METHODS
  Virus yields in supernatants of TCDO-supplemented cultures of HIV-infected cells or virus infectivity in TCDO-treated virus stocks were quantified by titration assays and then calculating the 50% tissue culture infectious dose.
  
  
  RESULTS
  First, TCDO did not affect the replication of HIV in persistently infected lymphocytic and monocytic cell lines or in peripheral blood mononuclear cells. Second, supplementation of HIV stocks with TCDO markedly decreased the infectivity of HIV particles in a concentration dependent manner. Third, the binding of gp120 envelope glycoprotein of HIV-1 to cells is blocked by pre-incubation with TCDO. Fourth, the inhibition of HIV replication by the reverse transcriptase inhibitor 3'-azido-3'-deoxythymidine (zidovudine) in de novo infected cell cultures was not affected by the simultaneous addition of TCDO. However, the delayed virus spread of HIV in cultures in the presence of suboptimal concentrations of zidovudine could significantly be blocked by the simultaneous addition of TCDO. Fifth, TCDO failed to induce the chromosomally integrated HIV-1 provirus in the T-lymphoma cell line ACH2.
  
  
  CONCLUSIONS
  TCDO appears to inactivate HIV particles directly, but has no influence on the intracellular replicative machinery of HIV. Our results suggest that a clinical evaluation of the TCDO complex as chemotherapy for HIV infection and full-blown AIDS should be considered, particularly in patients concomitantly receiving zidovudine.
authors.affiliation: Paul-Ehrlich Institute, Langen, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Ennen
authors.forename: K
authors.initials: K
authors.lastname: Werner
authors.forename: F W
authors.initials: FW
authors.lastname: Kühne
authors.forename: R
authors.initials: R
authors.lastname: Kurth
mesh_terms: D000998:Antiviral Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D002713:Chlorine / Q000494:pharmacology*; D016049:Didanosine / Q000494:pharmacology; D004347:Drug Interactions; D015699:HIV Envelope Protein gp120 / Q000378:metabolism; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics / Q000472:pathogenicity; D015498:HIV-2 / Q000187:drug effects* / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology; D006801:Humans; D010087:Oxides / Q000494:pharmacology*; D014407:Tumor Cells, Cultured; D014779:Virus Replication / Q000187:drug effects; D015215:Zidovudine / Q000494:pharmacology
chemical_list: D000998:Antiviral Agents; D015699:HIV Envelope Protein gp120; D010087:Oxides; D015215:Zidovudine; D002713:Chlorine; C041955:tetrachlorodecaoxide; D016049:Didanosine