Epidemic gastroenteritis was transmitted to human volunteers by the oral administration of fecal filtrates. The original inocula were obtained from patients in a natural outbreak which occurred at Marcy State Hospital in the winter of 1946–47. The experimental disease closely resembled that of the donors. The incubation period ranged from I to 5 days, with a mean of 3 days. The disease was carried through three generations, in the last two by means of fecal filtrates. Oral administration of unfiltered throat washings from experimental cases of the disease likewise induced gastroenteritis but subjects who inhaled a portion of the same throat washings remained asymptomatic. Volunteers who inhaled throat washings taken from patients in the epidemic at Marcy State Hospital also failed to develop the disease. Five volunteers who had previously been inoculated with fecal filtrates were reinoculated with the same material. Gastroenteritis followed in one of the two subjects who had failed to contract the disease the first time. The others remained well. Embryonated hens' eggs were inoculated with one of the two unfiltered stool suspensions used in the pool which had induced gastroenteritis in each of the three volunteers to whom it was fed. Three sets of eggs were inoculated: one on the chorioallantoic membrane, another into the yolk sac, and a third into the amniotic sac. Three serial passages were carried out by each method at varying time intervals. Penicillin and streptomycin were employed as antibacterial agents. Tissue and extraembryonic fluids from the third passage were non-infective for volunteers.
The e determinant of hepatitis B surface antigen (HBS Ag) was found in 23 of 42 patients with chronic hepatitis B virus (HBV) infection. Presence of e antigen was associated with increases in DNA polymerase activity and in the number of circulating Dane particles. In the group with detectable e antigen, the average DNA polymerase activity was 367+/-78 counts per minute (cpm; mean+/-standard error [SE]), and the average number of Dane particles counted in electron micrographs was 4.4% of the total HBS Ag. In contrast, e antigen-negative patients had an average DNA polymerase activity of 40+/-6.9 cpm (P less than 0.1) and an average Dane particle count equal to 0.6% of the HBS Ag. The e antigen was detected in 68% of patients who were HBS Ag carriers or had persistent viral hepatitis and 40% of those with chronic active type B hepatitis. Thus, the presence of e antigen correlated with both the chronicity and presence of infectious HBV. However, it did not correlate with the type or severity of liver disease after HBV infection, since e antigen was present in both chronic benign and chronic aggressive hepatitis B infections.
and Summary.-The purpose of this report is to call attention to the probable biological utility of a physical constant, the temperature of compensation (Tj) We suggest that determination of T, in biological systems might be of value in (1) establishment of whether an observed phenomenon results from the same process or mechanism as another observed phenomenon; (2) prediction of rates-or other behavior under relevant conditions; and (3) classification.The compensation effect' is simply defined as that which occurs when a series of Arrhenius plots, related by variation of a single parameter, pass through a common point. The temperature for this point has been termed the temperature of compensation. Systems exhibiting the compensation (or isokinetic) effect show linear variation of change in enthalpy with change in entropy, and the slope IjH/iS is T,, which is the temperature of compensation (or isokinetic temperature). 2 Although the compensation effect has been extensively studied by physicists and chemists, relatively little attention has been paid to it by biologists. We have investigated the effect of salt concentration on the kinetics of thermal inactivation of Sindbis virus at different temperatures as a biological example of the compensation effect. We propose that the temperature of compensation is a physical constant of biological interest since we found that, by determining the rate of thermal inactivation of the virus in different concentrations of two different salts, both families of Arrhenius plots generated from these data indicate the same temperature of compensation within fairly close limits.
3-Methyleneoxindole (MO), an oxidation product of the plant auxin indole-3-acetic acid, can selectively inhibit the repfication of herpes-, mengo-, polioviruses, and Sindbis virus. The antiviral action of MO, a sulfhydryl binding compound, is neutralized by 2-mercaptoethanol if the latter is added soon after exposure of infected cells to MO. If addition of 2-mercaptoethanol is delayed, the antiviral action of MO appears to be irreversible. Data Virus assays. The inhibitory effects of MO on virus replication were tested during a single cycle of multiplication. Monolayers of CEF and HeLa cells growing in 60-mm plastic petri dishes in a 5% CO.atmosphere were rinsed with 0.14 M NaCl and infected with the indicated viruses at a multiplicity of infection of 10. Generally, virus was allowed to adsorb to the cells for 1 h at 37 C, but the adsorption period of herpesvirus to HeLa cells was extended to 2 h. After adsorption, infected cells were rinsed three times with 0.14 M NaCl and incubated with 5 ml of growth medium containing the indicated concentration of MO. The growth of Sindbis virus and herpesvirus on CEF was estimated extracellularly by removing and pooling 1 ml of the growth medium from duplicate dishes at various times postinfection. Separate dishes were used for each time interval. The samples were stored at 70 C before measuring infectivity. To examine the effects of MO on the replication of poliovirus grown on HeLa cells, total virus was estimated by freezing the infected cells and medium at -70 C at the indicated times. The cells were frozen and thawed three times before measuring infectivity.
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