Passive immunoneutralization of human immunodeficiency virus in patients with advanced AIDS.

Infusions of 55-500 ml plasma from one of two donors selected for high anti-p24 antibody titre and neutralising capacity were given to six patients with advanced AIDS. Human immunodeficiency virus (HIV) antigenaemia cleared immediately and the recipients' serum acquired the HIV antibody profile of the donor together with HIV neutralising activity. The passive antibody effects persisted for up to eleven weeks depending upon the volume of plasma given, which had a half-life of about 12 days. The infusions were followed by fewer symptoms, a transient increase in T lymphocytes, a reduction in the frequency of opportunistic infections, and a decline in the rate at which HIV could be cultured from plasma or lymphocytes.

Human immunodeficiency virus (HIV) antigenemia (p24) in the acquired immunodeficiency syndrome (AIDS) and the effect of treatment with zidovudine (AZT).

Infection with human immunodeficiency virus (HIV) may cause viral antigenemia, detected primarily as p24 viral core protein. Among 16 patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex studied serially, 12 had or developed antigenemia ranging from 16 to 3006 pg/mL in plasma. The level could be categorized as high (greater than 100 pg/mL) or low (15 to 65 pg/mL). Three patients with anti-p24 antibody had no antigenemia. Zidovudine (AZT), 200 or 250 mg every 4 hours, reduced antigenemia by about 90%; other regimens were less effective. Leukocyte cultures were positive for HIV from patients with antigenemia, and in one third of samples in the absence of antigenemia. High levels of antigenemia correlated with symptoms, CD4 cell count, and prognosis. Drug toxicity requiring a lower dose was followed by increased antigenemia, recurrent symptoms, and decreased CD4 cells, suggesting lymphocyte toxicity. Monitoring antigenemia can be useful in evaluating patients with HIV infection and in evaluating the effect of antiviral chemotherapy.

Topical enviroxime against rhinovirus infection.

Enviroxime, an inhibitor of rhinovirus replication, was studied in a double-blind, placebo-controlled trial with 99 volunteers. The efficacy of a nasal-spray formulation of enviroxime was tested as pretreatment or as postchallenge treatment for rhinovirus type 4 infection. In the regimens used, drug administration neither prevented infection nor reduced the frequency of specific colds. The mean concentration of enviroxime in nasal washes (12 h after a dose) differentiated two groups of responders. Those in whom the drug concentration exceeded 100 ng/ml had some benefits, although these were statistically insignificant.

Nosocomial conjunctivitis caused by adenovirus type 4.

An outbreak of conjunctivitis caused by adenovirus type 4 (AV 4) occurred in hospital personnel who had contact with a patient with AV 4 pneumonia. Nine ill individuals were identified. AV 4 infection was demonstrated in all by isolation of AV 4 and/or a fourfold or greater rise in serum titer of specific neutralizing antibody. The incubation period was seven to 10 days, and the illness lasted five to seven days. Infectious virus was regularly present in the affected eyes for one week but not usually for more than 10 days after the onset of symptoms. Visual disturbance persisted for at least five months in one patient, who developed subepithelial deposits. The outbreak occurred after isolation procedures were abandoned in the care of the patient. No secondary case appeared. Isolation of patients with adenovirus pneumonia and barrier nursing are recommended as practical means of preventing nosocomial adenoviral infection and its consequences.

Search for latent cytomegalovirus in renal allografts.

Cytomegalovirus (CMV) infection is common after renal transplantation, and cytomegaloviruria occurs in about two-thirds of the recipients. These observations suggest that the allografts may be a site of latent infection with CMV and its reactivation may be the source of viruria. To investigate this possibility, 130 kidney specimens from 85 persons were cultured, and simultaneous explants were made of 63 of them from 50 people. No CMV was received from 33 normal kidney or cadaver donors or from 19 allograft recipients who had no evidence of posttransplantation infection with CMV. The experiment included 37 primary organ explants that yielded no evidence of latent virus. Among 33 allograft recipients with posttransplantation CMV infection, overt infectious virus was isolated from 6 of 57 allograft biopsies. All six positive specimens were from four patients, all of whom had viruria simultaneously. Organ explants from 20 of the recipients with demonstrated postoperative CMV infection, including 13 viruric patients, failed to unmask any latent CMV. Thus, allograft kidneys were infrequently infected with CMV (6%), even in patients with viruria (24%). The kidney parenchyma appears to be an uncommon site of latent CMV infection and may not be the usual source of virus in patients with viruria.

Effect of a topical interferon inducer on rhinovirus infections in volunteers.

Six controlled trials of a topical interferon inducer, N',N'-diotadecyl-N',N'-bis-(2-hydroxyethyl) propanediamine (CP 20961), against rhinovirus infection in volunteers were reviewed. Controls were the drug vehicle (which consisted of a mixture of polysorbate-80 in gylcerol and saline), saline only, and oral lactose. Multiple doses of the inducer given before challenge in any of three regimens reduced the symptomatic response to viral infection. Treatment with three doses of drug the day before challenge enhanced the interferon response to virus; four days of treatment with either the drug or its vehicle before challenge produced a refractoriness to further interferon induction. Both the drug and its vehicle were capable of inducing nasal interferon. When interferon was present at the time of viral inoculation, symptoms were reduced with or without an increase in the interferon response to infection. The rates of infection and illness were increased after a single dose of drug and decreased after a single dose of the vehicle alone.

Increased virus shedding with aspirin treatment of rhinovirus infection.

In two double-blind trials, volunteers challenged with rhinovirus were treated with aspirin or placebo. Aspirin treatment did not alter the rates of infection or illness but was associated with a moderate reduction in the frequency or severity of some symptoms. The overall benefit in rhinovirus infection was not statistically significant. Aspirin treatment appeared to cause a highly significant increase in the rate of virus shedding in treated subjects. The increase in virus shedding must be considered an adverse event that could influence the course of the disease in the individual and increase the likelihood of the spread of the infection to contacts.