The EH 24/70 virus, now identified as an antigenic variant of coxsackievirus type A24 in tube neutralization and immunodiffusion tests, was found to be the etiological agent of the 1970 outbreak of acute conjunctivitis in Singapore. The following year, strains identical to EH 24/70 virus were isolated in Hong Kong from a number of patients with acute conjunctivitis. Thus EH 24/70 virus seems to be the first human enterovirus incriminated in a large outbreak with acute conjunctivitis as the dominant clinical feature. Serologic responses substantiated the causative role of EH 24/70 virus in human disease. Human conjunctiva was not the sole habitat of the EH 24/70 virus, as it was also readily isolated from throat washings of patients in the acute phase of illness.

In 1975 in Bulgaria a severe epidemic of central nervous system (CNS) disease occurred. Clinically, histopathologically, and epidemiologically the cases resembled poliomyelitis, aseptic meningitis, meningoencephalitis, and, in some cases, encephalomyocarditis. About 21% of the 700 reported cases developed paralysis, 44 with fatal outcome [ref. 1]. In 65 cases, 92 strains of enterovirus of the same serologic type were isolated: 38 strains from the CNS, 10 from mesenteric lymph nodes and tonsils, and 44 from feces [ref. 1 2]. A typical representative strain, No. 258, isolated from the spinal cord of a 3-month-old baby who died on the 5th day of disease with signs of focal polioencephalitis, was selected for intensive study. Cross-neutralization tests established the antigenic identity of the Bulgarian 258 strain (Stanchev) with American strains of enterovirus type 71 (BrCr and JaFr strains) and Swedish strains of the same type (Nos. 52343, 52500, and 6041). From its biological [ref. 1,2], physicochemical [ref. 3], and antigenic properties, the etiological agent of this large epidemic can be classified as a member of enterovirus type 71, one of the most highly pathogenic of the recently recognized entero-viruses.

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During a 15-month period, cytomegalovirus (CMV) isolations were attempted from leukocytes derived from 290 healthy blood-bank donors. The major proportion of the specimens were tested 2 to 5 hr after donation. However, CMV was not recovered from any of the specimens examined. At the time of donation, 75% of donors had CMV complement-fixing antibodies demonstrable in titers of 10 to > 320. The age of the study group ranged from 17 to 57 years. During the same time period and with the use of identical isolation techniques, postnatal cytomegaloviremia was demonstrated in four infants with cytomegalic inclusion disease. Failure to detect cytomegaloviremia in 290 normal blood donors questions its occurrence outside pathological conditions. These results do not support the concept that CMV infection, concurrent with post-transfusion mononucleosis syndrome, is transmitted through the blood donor's leukocytes.

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The polypeptides synthesized in HEp-2 cells infected with 7 type 1 and 8 type 2 strains of herpes simplex virus were examined by PAGE. The polypeptides produced were consistent for each type and clearly different from those produced by infection with the other type.

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