Comparative Therapeutic Efficacy of Recombinant Interferons-α, -β, and -γ Against Alphatogavirus, Bunyavirus, Flavivirus, and Herpesvirus Infections

Abstract

Recombinant (r) preparations of interferons (IFN)-alpha, -beta, and -gamma were shown to protect mice against experimental virus infections with herpes simplex virus type 2 (HSV-2), and with three RNA-containing viruses from different families: Banzi, a flavivirus; Semliki Forest virus (SFV), an alphatogavirus; and Caraparu, a bunyavirus. The antiviral effects of the three different types of IFN were different with each virus. HSV-2 was the most sensitive virus, followed by SFV. Against Banzi virus, IFN-gamma was only effective when given both before and after infection. Against Caraparu virus, only IFN-gamma had a significant effect. These results suggest that IFN therapy might be valuable in human infections with these viruses, but that the correct choice of IFN and dose regimen is likely to be important.

Correlation between breakdown of the blood–brain barrier and disease outcome of viral encephalitis in mice

“…The interferon-inducing compound Ampligen (poly I: poly C 12 U) is a mismatched doublestranded (ds) RNA molecule with proven efficacy against both alphavirus-and flavivirusassociated encephalitis in experimental animal models (Pinto et al 1990;). The compound, (courtesy of David Strayer, Hemispherx Biopharma, Philadelphia, PA) was provided as a viscous 2.4 mg/mL solution (stored at -20°) and was diluted in diethylprocarbonate (DEPC) treated sterile water to the appropriate concentrations.…”

The BglII-N fragment of herpes simplex virus type 2 contains a region responsible for resistance to antiviral effects of interferon.

“…Exogenous IFNs reduce the progression of HSV-induced diseases (Pinto et al, 1990 ;Sanitato et al, 1984) and endogenously produced IFNs play an important role in host defences against HSV infection (Hendricks et al, 1991 ;Lausch et al, 1991 ;Stanton et al, 1987 ;Su et al, 1990). However, the therapeutic effectiveness of IFNs against HSV-induced diseases is considered not as high as expected (Jones et al, 1976 ;Kaufman et al, 1972 ;Sugar et al, 1973).…”

Modulation of Dengue Virus Infection in Human Cells by Alpha, Beta, and Gamma Interferons

“…Induction and activation of specific host molecules by IFN block virus infection at several levels, including transcription, translation, and RNA degradation (8). Although several studies suggest that IFN-␣, -␤, and -␥ modulate infection of members of the family Flaviviridae in vitro and in vivo (16,20,21,41,49), only one study has identified a specific inhibitory mechanism (37). Moreover, the role of IFN-␥ in DV infection is still controversial.…”