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We report the history of an 8-year-old girl who was treated for suspected lung lesions of respiratory papillomatosis with Indole-3-Carbinol, local and intravenous injections of Cidofovir for 27 months. This is the first report where a complete cure of the lung lesions occurred in a child, and was sustained for at least 24 months.
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Virtually all the compounds that are currently used or are subject of advanced clinical trials for the treatment of HIV infections, belong to one of the following classes: (i) nucleoside reverse transcriptase inhibitors (NRTIs): i.e., zidovudine, didanosine, zalcitabine, stavudine, lamivudine, abacavir, emtricitabine and nucleotide reverse transcriptase inhibitors (NtRTIs) (i.e., tenofovir disoproxil fumarate); (ii) non-nucleoside reverse transcriptase inhibitors (NNRTIs): i.e., nevirapine, delavirdine, efavirenz, emivirine; and (iii) protease inhibitors (PIs): i.e., saquinavir, ritonavir, indinavir, nelfinavir, amprenavir, and lopinavir. In addition to the reverse transcriptase and protease reaction, various other events in the HIV replicative cycle can be considered as potential targets for chemotherapeutic intervention: (i) viral adsorption, through binding to the viral envelope glycoprotein gp120 (polysulfates, polysulfonates, polycarboxylates, polyoxometalates, polynucleotides, and negatively charged albumins); (ii) viral entry, through blockade of the viral coreceptors CXCR4 (i.e., bicyclam (AMD3100) derivatives) and CCR5 (i.e., TAK-779 derivatives); (iii) virus-cell fusion, through binding to the viral envelope glycoprotein gp41 (T-20, T-1249); (iv) viral assembly and disassembly, through NCp7 zinc finger-targeted agents [2,2'-dithiobisbenzamides (DIBAs), azadicarbonamide (ADA)]; (v) proviral DNA integration, through integrase inhibitors such as 4-aryl-2,4-dioxobutanoic acid derivatives; (vi) viral mRNA transcription, through inhibitors of the transcription (transactivation) process (flavopiridol, fluoroquinolones). Also, various new NRTIs, NNRTIs, and PIs have been developed that possess, respectively: (i) improved metabolic characteristics (i.e., phosphoramidate and cyclosaligenyl pronucleotides by-passing the first phosphorylation step of the NRTIs), (ii) increased activity ["second" or "third" generation NNRTIs ( i.e., TMC-125, DPC-083)] against those HIV strains that are resistant to the "first" generation NNRTIs, or (iii), as in the case of PIs, a different, modified peptidic (i.e., azapeptidic (atazanavir)) or non-peptidic scaffold (i.e., cyclic urea (mozenavir), 4-hydroxy-2-pyrone (tipranavir)). Non-peptidic PIs may be expected to inhibit HIV mutant strains that have become resistant to peptidomimetic PIs.
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Summary Tumor growth in NMRI mice infected neonatally with the Moloney murine sarcoma virus was effectively inhibited by an aqueous eluate from the silica gel “Kieselgel PF 254.” This inhibitory effect was observed whether the silica gel eluate was injected 12 hr before virus inoculation or mixed directly with the virus inoculum. Upon mixing with the Moloney murine sarcoma virus, the silica gel eluate was barely effective if the virus-eluate mixture was incubated for only 1 min (at 25°) but significantly more effective if the mixture was incubated for 5 min (or more) (at 25°), suggesting that the antitumor activity of the eluate was due to a direct inactivating effect on the virus. This virus-inactivating effect was equally well expressed in immunocompetent (NMRI) as in immunoincompetent (genetically thymusless nude) mice. The postulated virucidal effect of silica gel eluate appeared to be limited to oncogenic RNA viruses; the eluate did not alter the infectivity of other viruses such as vaccinia, herpes simplex, Newcastle disease, vesicular stomatitis, and polio. The Moloney murine sarcoma virus-inhibiting effect of the silica gel eluate might have been related to a stimulatory effect on the RNA-dependent DNA polymerase activity of oncogenic RNA viruses, as a markedly increased DNA synthesis was noted in an in vitro DNA polymerase assay with the Moloney murine leukemia virus. However, the silica gel eluate did not affect the integrity of the Moloney murine leukemia virus, as assayed by isopycnic centrifugation of treated and untreated virus particles in a sucrose density gradient.
