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An epidemic of coxsackievirus B2 infections occured at a boys summer camp. The resulting illness was characterized by malaise, headache, muscle pain, and high fever that persisted for four to six days. The boy in the index case arrived at the camp the first day of the season. The attack rate was 89% among campers and 47% among counselors. The spread of infections appeared to be on a person-to-person basis and in a disorderly fashion. Unusual features of the epidemic included the high attack rate, restriction of infection to the camp residents, and evidence of prolonged pharyngeal viral shedding. Conditions at camps are ripe for similar epidemic and the potential problem is greater than is generally realized.

Two outer capsid rotavirus proteins, VP3 and VP7, have been found to elicit neutralizing-antibody production, but the immunogenicity of these proteins during human rotavirus infection has not been determined. The relative amounts of serum neutralizing antibody against the VP3 and VP7 proteins of the CJN strain of human rotavirus were, therefore, determined in adult subjects before and after infection with this virus. Reassortant strains of rotavirus that contained the CJN gene segment for only one of these two neutralization proteins were isolated and used for this study. The geometric mean titer of serum neutralizing antibody to a reassortant virus (CJN-M) that contained VP7 of CJN and VP3 of another human rotavirus was 12.7 times less than that of antibody to CJN before infection and 20.3 times less after infection. This indicated that most neutralizing antibody was against the VP3 rather than the VP7 protein of CJN. This result was confirmed with other reassortants between CJN and animal rotavirus strains (EDIM and rhesus rotavirus). These findings suggest that VP3 is the primary immunogen that stimulates neutralizing antibody during at least some rotavirus infections of humans.

The efficacy and safety of prophylactic low dose amantadine hydrochloride was assessed in two double-blind, placebo-controlled, randomized studies. In a study of 476 subjects aged 18 to 55 years, adverse reactions were not significantly different between the group receiving 100 mg/day amantadine and the placebo group but significantly greater in the group given 200 mg/day (P less than 0.009). The influenza attack rate in this study was too low to assess efficacy. In an experimental challenge study of influenza A/Beth/1/85 in 78 subjects of similar age the prophylactic administration of 50 mg, 100 mg or 200 mg/day doses of amantadine were more effective than placebo in preventing influenza illness (P less than 0.02, 66, 74 and 82% protection, respectively), and in suppressing viral replication (P = 0.02). There was no significant difference between amantadine groups in influenza illness or viral shedding. Compared with the placebo group the 100 and 200 mg amantadine groups showed a significant decrease in infection rate (100 mg: 40% protection: P = 0.012; 200 mg: 32% protection: P = 0.045) whereas the 50 mg group did not (20% protection: P = 0.187). These results suggest that 100 mg/day of amantadine will reduce toxicity but maintain the prophylactic efficacy seen with 200 mg/day.

Cytomegaloviurs (CMV) infections are a recognized problem in the first six months after renal transplantation. Studies have suggested that primary infections produce symptomatic disease, whereas reactivation infections are usually asymptomatic. Two patients are described who developed fatal CMV infections in the second year after transplantation. Both patients had typical CMV disease with fever, pneumonitis, and hepatitis. Results of serologic studies in one patient were characteristic of primary infection, with seroconversion at the time of disease and appearance of specific IgM antibodies. The other patient had a similar antibody response at the time of his illness, but serial antibody tests showed that he had had a transient seroconversion earlier, in the second month after transplanation, that was not associated with clinical symptoms. These patients indicate that CMV infection must be considered in the differential diagnosis of serious febrile illnesses even in the late posttransplantation period and may occur either as the result of primary or reactivation infection. Serologic studies at the time of illness may not allow distinction between the types of infection.

A method for isolation of mouse nasal lymphocytes is described. Lymphocyte-enriched suspensions are examined for their morphologic, surface immune staining and mitogenic characteristics. This method will allow testing of immune function in the upper respiratory tract of the mouse.

Phytohemagglutinin-induced lymphocyte deoxyribonucleic acid synthesis, dermal hypersensitivity, and peripheral blood thymus-derived lymphocyte numbers were assessed in nine men with experimentally induced rubella infection. Five of these men and two additional volunteers received treatment with tilorone dihydrochloride, an antiviral drug. Response to phytohemagglutinin was not changed during rubella; T lymphocyte numbers in peripheral blood were not influenced by the viral illness. However, dermal hypersensitivity was markedly impaired in all volunteers during the height of the illness. Tilorone alone, or with rubella, had no effect on any of the parameters studied.

Rabbits were inoculated intravenously with "wild" rubella virus, RA 27/3 rubella vaccine virus, or rubella virus isolated from recipients of RA 27/3 vaccine. Rabbits receiving "wild" virus developed rubella hemagglutination inhibition antibody, and those receiving vaccine virus did not. One of the five reisolates tested produced a low transient antibody response in two of the five rabbits inoculated with this strain. The study indicates that the rabbit immunogenic marker after intravenous injection can be used to determine if a rubella virus isolated from a patient is of "wild" or vaccine origin. There was no significant change in the reduced immunogenicity characteristics of the RA 27/3 vaccine virus after human passage.

A serologic survey for rubella and measles immunity was conducted to determine the immunity levels among a nonurban, relatively isolated pediatric population. Among 1,273 students in grades kindergarten through 9, the overall susceptibility rate was 24.3% for rubella and 16.3% for measles. There was significant variation in susceptibility rates among the various grades and schools involved. The susceptibility rates were similar to those found for urban populations. The results indicated that vaccination efforts for the population have been partially successful, but additional effort was needed.

A loading dose and short-term administration of oral ribavirin significantly improved symptoms and signs of influenza type A or B infection in 25 patients. The antiviral effect was not significant. No adverse clinical effects or significant laboratory values were observed. Oral treatment of patients with influenza A or B infection might be possible with ribavirin.

The induction and persistence of local rotavirus antibodies, including stool IgA, jejunal IgA, and jejunal neutralizing antibody, were evaluated in 14 adult volunteers infected with the CJN strain of human rotavirus. In addition, the relationships between local rotavirus IgA and serum rotavirus IgA, IgG, and neutralizing antibody were determined. Both stool and serum rotavirus IgA appeared to have similar kinetics. Both antibodies peaked by days 14-17 after inoculation in all subjects, then decreased rapidly. By days 26-28, titers had fallen to 13% and 30% of their respective peaks. Serum rotavirus IgG peaked somewhat later, occurring in five subjects on days 26-28. Serum neutralizing antibody peaked on days 26-28 in all but three subjects. Both serum IgG and neutralizing antibodies also declined more slowly than rotavirus IgA. Although all antibody concentrations had decreased to only a fraction of their peak responses by days 270-365 after rotavirus inoculation they remained higher than baseline levels. For example, stool rotavirus IgA concentrations were 13.5-fold higher than baseline, while jejunal rotavirus IgA and neutralizing antibody were 8.9- and 4.3-fold above baseline, respectively. Similarly, serum antibodies remained 3.7- to 11.2-fold higher than baseline at 270-365 days after rotavirus inoculation. These studies imply that serum rotavirus IgA is a good indicator of local antibody responses. Furthermore, although both serum and local antibody titers peaked within 2-4 weeks after infection, these antibodies persisted at above baseline concentrations for at least 9-12 months after infection.

A survey of adult patients admitted to a general hospital showed that 1.5% had hepatitis B surface antigen in the blood and 22% had hepatitis antibody. The majority of patients with hepatitis B did not have clinical hepatitis and would not have been recognized without screening all hospital admissions for hepatitis B antigen. The question of routine screening is discussed in relation to the risk of acquiring hepatitis.

A two-part study of echovirus-12 was done in volunteers. In the first part the human infectious dose of the virus was determined in 149 healthy adults with undetectable serum antibody, each of whom drank 0-330,000 plaque-forming units (pfu) of virus in 100 ml of nonchlorinated water. Infection was defined as fecal shedding of virus or significant (fourfold or greater) increases in serum antibody titer. The HID50 (i.e., the dose required for infection of 50% of the volunteers) was 919 pfu. Through statistical analysis of the data by probit transformation, a 1% human-infectious dose of 17 pfu was predicted. These results were used in the second portion of the study to determine the effect of previous infection on the infectious dose. Previously infected volunteers (those with neutralizing serum antibody) were given a dose of echovirus-12 (1,500 pfu) that had been found to infect 60% of persons with undetectable serum antibody. The presence of serum antibody caused no significant change in the percentage of volunteers infected by this dose. Furthermore, the concentration of serum antibody did not affect the rate of infection or the duration of viral shedding. These results indicate that previous infection with echovirus-12 does not provide lasting protection against reinfection.

Increased rubella antibody titres have been reported in patients with juvenile rheumatoid arthritis (JRA) and it has been suggested that rubella virus may be of importance in the aetiology or pathogenesis of the disease. In the present study, rubella and rubeola antibody titres in 85 patients with JRA were compared to age- and sex-matched controls. 41% of the patients did not have rubella antibody, but the geometric mean titre of those with JRA who had antibody was slightly higher than that of the controls with antibody (58-9 against 42-7; P less than 0-05). The level of rubella antibody titre correlated with serum IgG levels. There was no difference in rubeola antibody titres between patients and controls, and rubeola antibody did not correlate with serum IgG. Fifteen JRA patients developed rubella antibody after rubella vaccine or natural disease. This did not result in unusually high antibody titres and was associated with a mild exacerbation of symptoms in only two patients. This study suggests that the slight increase in rubella antibody in JRA is a nonspecific manifestation of increased immunoglobulins.

Complement-fixing antigens specific for rubella were made in tissue cultures of RK-13 rabbit kidney cells and primary cultures of kidney from the African green monkey. The antigens were prepared with the infected cell monolayer diluted to 30 percent with supernatant fluid and frozen and thawed three times. Complement-fixing antibody appeared in patients with rubella soon after the termination of rash and persisted for at least 8 months. In 8 out of 12 individuals who had the disease 10 to 20 years before they were tested, no complement-fixing antibody was found, but neutralizing antibody was present.

Twenty-three infants less than six weeks of age with fever of 100.4 degrees F, or higher and no evidence of bacterial infection were seen at the Cincinnati General Hospital from July to December, 1971. Seventeen of these were admitted to the hospital; 15 were treated with penicillin and kanamycin for possible sepsis. Viral isolation was attempted on 21 of these infants, and ECHO viruses were isolated from 14 (66.7 per cent), compared to three (14.3 per cent) of 21 controls. Eleven of the 14 ECHO viruses isolated were type 4, and the other 3 were types 6, 11, and 25 respectively. Acute and convalescent serum was obtained from 11 of the 21 infants; seven had a fourfold rise in antibody to ECHO virus type 4. Most of the children had fever with irritability, six of the 23 had a fine maculopapular rash, and three had aseptic meningitis. This study suggests that ECHO viruses may be a significant cause of febrile illness in young infants during the summer and fall and may account for illnesses which lead to hospitalization as possible sepsis.

In 19 lots of standard commercial gamma globulin from humans, the titers of antibody neutralizing rubella virus varied from, 256 to 2048. The titers could not be correlated with geographic location of the donors, method of extraction, or tissue source. Samples of gamma globulin from rubella convalescents had titers of 4096. These titers were approximately 20 times higher than those in serum specimens from patients ill with natural or experimental infection. Serum antibody appears to persist for a number of years at nearly the original titers.