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Biomedical subjects

K Banerjee

Publications and source records attributed to K Banerjee.

At least 199 records · Page 11Linked to original sources
PubMed1983

Human leukocyte interferon subtypes have different antiproliferative and antiviral activities on human cells.

The antigrowth effects of 5 different cloned human leukocyte IFN subtypes (IFN-alpha A, B, C, D, F) and 2 molecular hybrids between them (IFN-alpha AD(Bg1II) and IFN-alpha DA(Bg1II)) were examined on 6 different human cell lines. The results indicate that the interferons sort into two distinct groups: IFN-alpha B, C and F showed comparable antiproliferative activity which was greater than that of IFN-alpha A, D, AD(Bg1II) and DA(Bg1II). The interferons could also be assigned to one of two groups on the basis of their antiviral activity. IFN-alpha A, D and AD(Bg1II) were observed to be more protective than IFN-alpha B, C and F against HSV-2 and EMCV infections, i.e. the relative antiviral efficacies of the cloned IFN subtypes were the reverse of their antiproliferative activities.

Antiviral Agents↗
PubMed1983

Antiviral activities of cloned human leukocyte interferons against herpes simplex virus type 2 infections of mice.

Human alpha-interferons (IFN-alpha s) made in bacteria were examined for antiviral activity against herpes simplex virus type 2 (HSV-2) infections of mouse L-cells in vitro, and acute cervicovaginal and lethal systemic HSV-2 infections of BALB/c mice. The recombinant DNA-derived hybrid interferon IFN-alpha AD(Bgl) showed pronounced antiviral activity in vitro, exceeding the activity of either of the parental subtypes IFN-alpha A and IFN-alpha D and that of the other hybrids IFN-alpha AD(Pvu) and IFN-alpha DA(Bgl). A combination of topical and systemic treatments with IFN-alpha A and IFN-alpha AD(Bgl) failed to protect mice from subsequent challenge with an acute cervicovaginal infection of HSV-2. Protection from lethal systemic HSV-2 infection in mice was observed when IFN-alpha AD(Bgl) and IFN-alpha AD(Pvu) were administered systemically, whereas IFN-alpha A failed to confer protection. These results suggest that for protection against infection with HSV-2, the routes of introduction of the virus and of the interferon influence the host response to interferon therapy.

Animals↗