Daisy Sun

Inhibition of HIV replication by liposomal encapsulated amphotericin B

This report shows the potential of using a liposomal encapsulated preparation of amphotericin B (a polyene macrolide antibiotic) for the in vitro inhibition of HIV. There was no significant difference between the effective doses of the free form of drug when compared to the liposomal encapsulated preparation in inhibiting the growth of HIV. Virus expression was suppressed at a concentration of 5-10 micrograms/ml of the drugs. The liposomal preparation showed greatly reduced cytotoxicity in experiments using cultures of murine leukocytes. These results show the potential usefulness of liposomal encapsulated drugs in the treatment of patients with AIDS or AIDS related complex.

Dual biological activity of apurinic acid on human lymphocytes: induction of interferon-γ and protection from human immunodeficiency virus infection in vitro

The chemically modified DNA, apurinic acid (APA), is cytotoxic for human lymphocytes at concentrations above 100 micrograms/ml. At low concentrations (0.05-1 micrograms/ml) APA acts as an inducer interferon gamma (IFN-gamma) in lymphocytes in vitro; the maximum interferon titer of 50 units/ml was reached at 0.4 micrograms/ml. When added to the cells in combination with phytohemagglutinin A (PHA), APA displays a significant synergistic interferon-inducing ability; the maximum titer of 940 units/ml was obtained with 10 micrograms/ml of APA and 6.25 micrograms/ml of PHA. APA also proved to be an effective inhibitor of human immunodeficiency virus (HIV-1) replication in H9 cells. At a concentration of 10 micrograms/ml, APA causes a 49% inhibition of virus growth, while 20 micrograms/ml of APA are required to inhibit expression of HIV-1 p17 and p24 gag proteins by 60%. The mechanism of anti HIV-1 activity of APA likely occurs at the level of viral reverse transcriptase. This enzyme is inhibited by APA in a noncompetitive way with a Ki of 0.39 microM, while the cellular DNA polymerases alpha, beta and gamma are 140- to 300-fold less sensitive to APA.

Inactivation of Human Immunodeficiency Virus (HIV) by Ionizing Radiation in Body Fluids and Serological Evidence

A method to use ionizing radiation to inactivate HIV (Human Immunodeficiency Virus) in human body fluids was studied in an effort to reduce the risk of accidental infection to forensic science laboratory workers. Experiments conducted indicate that an X-ray absorbed dose of 25 krad was required to completely inactivate HIV. This does not alter forensically important constituents such as enzymes and proteins in body fluids. This method of inactivation of HIV cannot be used on body fluids which will be subjected to deoxyribonucleic acid (DNA) typing.

Inhibition of HTLV-III Replication in Cell Cultures

A human T-lymphotropic retrovirus (HTLV-III) has been identified as the etiological agent for acquired immune deficieny syndrome (AIDS) and AIDS related complex (ARC) (1–4). Various therapeutic approaches are currently being investigated to control the disease either with inhibitors of reverse transcriptase and virus replication or with a vaccine. HTLV-III is a cytopathic retrovirus which selectively infects T-helper cells and kills OKT4+ T helper cells resulting in immune suppression (1–5). HTLV-III contains an RNA directed DNA polymerase (reverse transcriptase) and buds from the cell membrane like other animal retroviruses (6,7). The replication of virus in the infected cells and further infection of uninfected cells with the newly produced virus can be interfered by chemotherapeutic agents that can attack the various steps in the replication cycle (Fig. 1) including virus attachment, reverse transcription, and DNA integration.

Terminal Transferase and Adenosine Deaminase Activities in Human Neoplasia: Their Role in Modulating Cancer Treatment

Terminal deoxynucleotidyl transferase (TdT) and adenosine deaminase (ADA) are two enzyme markers that have been exstensively utilized to define the stage of the disease and the cell types involved in human leukemia B cell proliferation and severe combined immune deficiency syndrome (SCID). The use of these biological markers has been very useful in selecting treatment protocols for patients with leukemia/lymphoma and SCID.