To investigate the transmission of influenza viruses via hands and environmental surfaces, the survival of laboratory-grown influenza A and influenza B viruses on various surfaces was studied. Both influenza A and B viruses survived for 24-48 hr on hard, nonporous surfaces such as stainless steel and plastic but survived for less than 8-12 hr on cloth, paper, and tissues. Measurable quantities of influenza A virus were transferred from stainless steel surfaces to hands for 24 hr and from tissues to hands for up to 15 min. Virus survived on hands for up to 5 min after transfer from the environmental surfaces. These observations suggest that the transmission of virus from donors who are shedding large amounts could occur for 2-8 hr via stainless steel surfaces and for a few minutes via paper tissues. Thus, under conditions of heavy environmental contamination, the transmission of influenza virus via fomites may be possible.
We conducted a placebo-controlled, double-blind study of acyclovir therapy for acute herpes zoster in immunocompromised patients. Of the 94 patients enrolled in the study, 52 had localized skin lesions at entry, and 42 had disseminated cutaneous zoster. A one-week course of intravenous acyclovir (1500 mg per square meter of body-surface area per day) halted progression of zoster in both groups, as determined by development or progression of cutaneous dissemination, development of visceral zoster, or proportion of cases deemed treatment failures. Significantly fewer patients treated with acyclovir within the first three days after the onset of exanthem had complications of zoster, as compared with patients treated with placebo (P = 0.02 by Fisher's exact test), but acyclovir also stopped progression of zoster in patients treated after three days of rash (P = 0.05 by Fisher's exact test). Acyclovir recipients with disseminated cutaneous zoster had a significantly accelerated rate of clearance of virus from vesicles, as compared with placebo recipients (P = 0.05 by the Breslow test).
Acyclovir is a specific antiviral agent. The triphosphate form inhibits viral DNA replication by competing for incorporation into the replicating DNA chain or by inhibiting viral DNA polymerase. Cells not infected with herpesvirus are generally unaffected. Oral acyclovir inhibits most herpes simplex virus types 1 and 2, and varicella-zoster virus at concentrations used clinically. Oral acyclovir has an average plasma half-life of three hours and is eliminated primarily by renal mechanisms. Peak plasma concentrations occur 1.5 to 2.5 hours after administration and the oral bioavailability is 15 to 30 percent. Acyclovir distributes into most body tissues, including vesicular fluid and the central nervous system. Oral acyclovir is effective treatment of initial and recurrent genital herpes and can suppress frequently recurring genital herpes in both immunocompetent and immunocompromised patients. It is also effective for acute herpes zoster in the immunocompetent and possibly immunocompromised patient. No role is established in either Epstein-Barr virus or cytomegalovirus infections. Oral acyclovir appears to be effective and relatively safe, nontoxic therapy when administered in doses of 1-4 g/d. Oral acyclovir represents a major therapeutic advance in the treatment of herpesvirus infections.
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