Tadafumi S. Tochikura

Inhibition (in vitro) of replication and of the cytopathic effect of human immunodeficiency virus by an extract of the culture medium of Lentinus edodes mycelia

An extract of culture medium of Lentinus edodes mycelia (LEM) was prepared. This was further fractionated by 50% ethanol precipitation and both the resulting product, E-P-LEM, and LEM were studied to evaluate their effect on the activity of human immunodeficiency virus (HIV) in vitro. The experiments were performed using either a cell-free infection system with MT-4 cells, or a cell-to-cell infection system with MOLT-4 cells, which induces multinucleated giant cells very efficiently. E-P-LEM almost completely blocked both the cytopathic effect of giant cell formation and specific antigen expression due to HIV, whereas LEM before ethanol precipitation blocked the expression of HIV antigen in MT-4 cells only at a high concentration. Pretreatment of the virus with E-P-LEM before infection blocked HIV infection in the target cells. Thus, the inhibitory effect of LEM and E-P-LEM on HIV could be due to a blocking of the initial stages of HIV infection. Moreover, reverse transcriptase activity of avian myeloblastosis virus was inhibited.

INACTIVATION AND ELIMINATION OF VIRUSES DURING THE FRACTIONATION OF AN INTRAVENOUS IMMUNOGLOBULIN PREPARATION: LIQUID HEAT TREATMENT AND POLYETHYLENE GLYCOL FRACTIONATION

Abstract. A method for the heat treatment of human IgG solution at 60 °C for 10 h was established. Human immunodeficiency, mumps, vaccinia and 4 other viruses were added to the IgG solution in 33% sorbitol and heated at 60 °C. Those viruses were inactivated within 1 h. Heat‐treated intravenous IgG (IVIG‐H) was prepared by heat treatment and polyethylene glycol (PEG) fractionation. Conventional nonheated intravenous IgG (IVIG‐C) was prepared from the same source paste by the fractionation method. No physicochemical or biological difference was observed between the heated and control IVIG preparations.

Pradimicin A inhibition of human immunodeficiency virus: Attenuation by mannan

The mechanism of action of a novel anti-HIV antibiotic, pradimicin A, has been studied using cell-free (MT-4 cells) and cell to cell (MOLT-4 and MOLT-4/HIVHTLV-3B cells) HIV infection systems. The data indicate that (1) preincubation of the cells with HIV at 0 degrees for 1 hr, followed by the addition of pradimicin A and further incubation at 37 degrees, resulted in a complete inhibition of infection while preincubation at 37 degrees did not. Similar data were obtained with the coculture between MOLT-4 and MOLT-4/HIV cells. (2) Virus treated with pradimicin A followed by washing did not show any inhibition on subsequent HIV binding to cells. (3) The inhibitory effect of pradimicin A on HIV infection was prevented by mannan but not by other sugars tested. Mannan, however, did not interfere with the anti-HIV activity of other known inhibitors. (4) Use of EGTA suggested that pradimicin A required Ca ions to exert its anti-HIV activity. These data imply that pradimicin A inhibits an early step in HIV infection, probably through its binding to mannose residues of HIV glycoprotein.

A biological response modifier, PSK, inhibits human immunodeficiency virus infection in vitro

PSK, a biological response modifier (BRM), was studied to determine its anti-viral activity on human immunodeficiency virus (HIV) in vitro. Either a novel infection system using human T-cell lymphotropic virus type I (HTLV-I)-carrying MT-4 cells or a coculture system using MOLT-4 cells and its virus-producing cells MOLT-4/HIVHTLV-IIIB which induces multinucleated giant cells very efficiently was used. PSK almost completely blocked the cytopathic effect such as giant cell formation and HIV-specific antigen expression both in MT-4 cells and MOLT-4 cells at a concentration of 0.4 and 0.8 mg/ml, respectively. Pretreatment of the virus with PSK may specifically interfere with early stages of HIV infection by modifying the viral receptor.

A biological response modifier, PSK, inhibits reverse transcriptase in vitro

We found that PSK has an antiviral effect on human immunodeficiency virus (HIV) in vitro. One of the mechanisms of this effect is attributable to the inhibition of binding of HIV with lymphocytes. Here, we found that PSK inhibits reverse transcriptase in a non-competitive way in vitro. Such inhibition may be important in its anti-HIV effect as well as its inhibitory effect on the binding of HIV with lymphocytes.

Efficacy of an Immunoglobulin Preparation from HIV Carriers in Preventing HIV Replication in vitro

Abstract. Immunoglobulin samples (HIV‐Ig) were prepared by cold ethanol fractionation of human plasma containing antibody against human immunodeficiency virus (HIV). The ability to prevent viral spreading was studied using either human T‐cell leukemia virus type I (HTLV‐I)‐carrying MT‐4 cells or in a coculture system using MOLT‐4 cells and virus‐producing MOLT‐4/HIVHTLV‐IIIB cells. Treatment of HIV‐infected MT‐4 cells with HIV‐Ig effectively blocked the appearance of antigens of HIV and the virus‐induced cytopathic effect. HIV‐Ig blocked multinucleated giant cell formation in the MOLT‐4 and MOLT‐4/HIVHTLV‐IIB coculture system.