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We isolated 872 strains of mumps virus from naso-pharyngeal secretions in seven different districts of Japan from January 2000 to July 2001. Among them, 57 strains were geno-typed by nucleotide sequencing in part of the hemagglutinin-neuraminidase (HN) and small hydrophobic (SH) protein regions. Four different genotypes (B, G, K, and L) of mumps virus were co-circulating in Japan and the distribution of genotypes varied in geographically different districts. Two new clusters designated as genotypes K and L had more than 7% nucleotide variation in the SH gene. Among the 57 strains, 11 were classified as B, 35 as G, three as K, and eight as L, which was mainly isolated in Tokyo. We also examined 104 stains isolated in a clinic in Mie prefecture from 1993 to 2003. Genotype B was the indigenous strain and genotype K was introduced in 1994. Genotypes B and K co-circulated in the 1990s and were replaced by genotype G in 2000. There was no significant change in neutralizing test antibody titers against genotypes B, G, K, and L using seven post-vaccination sera with Hoshino strain (genotype B) and these four genotypes had a different antigenicity from genotype A. We should continue to watch on mumps virus molecular epidemiology.

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Clinically apparent mumps reinfection is considered extremely rare, but several cases have been suspected of reinfection in an out-patient clinic. In this study, virological examination, virus isolation, the reverse transcription loop-mediated isothermal amplification (RT-LAMP), and IgG and IgM EIA antibodies, were examined in order to identify mumps reinfection. Patients were divided into three categories; the reinfection group comprised 29 patients with a history of natural infection, the vaccine-failure group consisted of 37 patients with an immunization history, and two patients had histories of both immunization and mumps infection. Another 25 patients were enrolled as a primary infection group. Mumps virus was isolated in 5 (17%) and the genome was detected in 12 (41%) of 29 in the reinfection group. Reinfection was confirmed in 21/28, demonstrating high avidity of IgG EIA. Mumps virus was isolated in 15 (41%) and there was a higher positivity of genome amplification in 25 (68%) of 37 patients in the vaccine-failure group. Among these, 23 were confirmed as secondary vaccine failure by high avidity IgG EIA serology. In the primary infection group, the isolation rate and genome detection rate was higher in 16 (64%) and in 18 (72%) of 25 patients, respectively. There was no significant difference in virus load among the three groups but high mumps virus load was suspected in the IgM EIA-positive group based on the shorter amplification time on RT-LAMP. Mumps virus reinfection was confirmed by RT-LAMP and an IgG avidity test and was not a rare event.

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ABSTRACT. Objective. To elucidate clinical features of patients with primary human herpesvirus 7 (HHV-7) infection and serologic and virologic findings between HHV-7 and human herpesvirus 6 (HHV-6).Materials and Methods. During a 19-month observation period, 71 infants and children (35 boys and 36 girls with a mean age of 14.5 months [range, 1 month to 48 months]) who had acute febrile respiratory illness with or without skin rash were examined clinically and virologically. Heparinized blood samples were used for isolation of HHV-6 and HHV-7 and detection of both virus DNA sequences by a nested polymerase chain reaction amplification. Both virus antibody activities were measured by an indirect immunofluorescent assay.Results. HHV-7 infection was observed in 15 (6 boys and 9 girls with a mean age of 12.9 months [range, 7 months to 27 months]), 1 of 10 with upper respiratory infection and 14 (28%) of 50 with febrile exanthem, whereas HHV-6 infection was in 22 (44%) of the 50. Fever (37.5°C) was observed in all 15, with an average maximum body temperature of 38.7°C (range, 37.6°C to 39.8°C), which persisted for 2.9 days (range, 1 to 5 days). Papular, macular, or maculopapular rash was observed in 14 (93%) of the 15, which appeared on day 2.9 of fever (range, days 2 to 5) on the face, trunk, and extremities and persisted for 2.7 days (range, 1 to 5 days). A convulsive seizure that persisted for a few minutes developed in 1 patient on the first day of elevation of fever. HHV-6 antibody was demonstrated in 13 (87%), and a simultaneous significant increase to HHV-6 antibody titers was observed in 8 (53%) of the 15 during primary HHV-7 infection. HHV-7 and HHV-6 DNAs were almost always detected in mononuclear cells (MNCs) during acute and convalescent phases, whereas HHV-7 DNA was positive in some plasma samples obtained during the acute phase of the disease.Conclusions. Primary HHV-7 infection occurred somewhat later than HHV-6, which was confirmed by the isolation of HHV-7 from blood and/or seroconversion to the virus. Clinical features of a virologically confirmed patient with primary HHV-7 infection were comparable with those of primary HHV-6 infection. Preexisting HHV-6 antibody increased significantly in the half of patients with primary HHV-7 infection. HHV-7 DNA was detected in peripheral blood MNCs and plasma in the acute phase and persisted in MNCs thereafter. Pediatrics 1997;99(3). URL: http://www.pediatrics.org/cgi/ content/full/99/3/e4; human herpesvirus 7, human herpesvirus 6, exanthem subitum, roseola infantum, polymerase chain reaction.

SUMMARYNewborn rats were inoculated intraperitoneally with haemorrhagic fever with renal syndrome (HFRS)-related virus (B-1 strain), and virus isolation from their various organs was attempted between 1 and 25 weeks after inoculation. Virus could be isolated repeatedly from lung, brain, spleen and kidney and also from peripheral blood. When virus isolation was carried out on fractionated peripheral blood cells, virus was associated mainly with the macrophage fraction and to a lesser extent with granulocytes. Virus replicated well in peritoneal exudate cells of normal rats and it grew in the adherent mononuclear cells from normal human peripheral blood. These data suggest that macrophages, permissive for HFRS-related virus replication, might contribute to the spread of viral infection in vivo.