Jpn. J. Infect. Dig., 53, 2000

Laboratory and Epidemiology Communications
Duration of EchoviruS 30 Excretion in Stools from Patientswith Aseptic Menlngitis●Shinichi Takao*, Yoshitaka Komazawal, Shinji Fukuda, Yhkie Shimazu,
Masahiro Noda and Shizuyo TbhlmOtO
Division of Microbiology II, Hiroshima Prefectural Institute ofHea/th and EnviflOnment,
Minami‑machi I‑6‑29, Minami‑ku, Hiy10Shimq 734‑0007 andJDeparlment of Pediatrics, Shoubara Red Cross Hospital,
Nishihon‑machi 2‑ 7‑I 0, Shoubara, Hiroshima 72 7‑0013
Communicated by Hiroo lnouye(Accepted July 5, 2000)

Asepticヮeningitis (AM) is chiefly a childhood disease

times in and out of the hospital, and we investlgated the du‑caused by vlruSeS. Most serotypes of enteroviruses have been
isolatedfrom patients with AM ( 1 ). EchoviruS 30 (E30), which
was first isolated in New York State from a patient with AM
in 1958 (2), was the most predominant serotype (3)･ Feca1‑

ration orvirus excretion. Most (82.2%; 1 89/230) or仇e stool

samples showed E30 for up to 10 days (Table). In one case,
E30 was recovered from the stool continuously for 23 days

(Figure). These results suggested that a patient with AM due

0ral contamination is well‑known as the most Important routeto E30 infection may excrete the virus over days or even few

by which many enterovirus infections are spread (4)･ This

weeks, after recovery from the illness.

route of transmission is especially common in families with

An enterovirus infection such as E30 is highly communi‑
cable withina community. The viruses generally spread hori‑young children or in nursery school. Therefわre, it is impor‑zontally through preschool children and thus to their fami‑lies. nLerefore, good hygienlC Practices such as handwashingtant to understand the duration of virus excretion in order toprevent the secondary transmission of viruses. We describe
here the duration of E30 excretion in the stools of AM pa‑

are necessary for several weeks to prevent secondary trans‑

tients.

mission of the virus, especially in homesand nursery schools.

From May to September in 1998, an ouぬreak of AM oc‑

curred in Shoubara City, the northem area of Hiroshima Pre‑REFERENCES

fecture. E30 was isolated from the stool and/or cerebrosplnal
nuid ofa total of 162 patients wi血AM. Most (96.9%; 157/

1. Grist, N. 良., Bell, E. ∫. andAssaad, F. (1978): Entero‑162) patient.s ranged from 3 months to 14 years of age, withthe highest Incidence in 5‑year‑old children. After the onset

viruses in humandiseases. Prog. Med. Viro1., 24, 1 14‑I 57.
2. Plager, H. and Decher, W. (1963): A newly‑recognizedof illness, 230 stools were collected from the patients several

enterovirus isolated from case of aseptic menlngitis.Am.

Table. Duration of E30 excretion in stools舟om patients with AM

Numberofpatients

Numberofstools

E30Daysisolationol

Positive

162

23456339

38

16137148498after

109ll

23

onset

1222

ofillness

13814

3

15

16

17

2

126

18

19

120

21

1

1

1

5

12

2

2

1

1Days after
0

123

4

5678

91011‥‥‥‥‥‥23

onsot of川noss

Hospitalization

Fovor

H eadac ho

戯盛.

Fn3:ti.S.?l'ation++Figure･ Clinicaland virologiCalObservation on one AM patient with E30 (8‑year‑old, female).

*Corresponding author: Fax +8 1 ‑82‑254‑ 1 908, E‑mail: takao@urban.neJP

132231230
Negative22Jpn. J. Infect. Dis., 53, 2000

4･ Grandien, M･･ Forsgr.en･ M･ and Ehmest･ A･ (1989):

J. Hyg., 77, 26.

3. Yamashita, K., Miyamura, K., Yamadera, S., Kato, N.,
Akatsuka, M., Hashido, M., Inoue, S. and Yamazaki, S.

Enterovirusesand reovlruSeS. P.5 1 3‑578. In Schmidt, N.J.

and Emmons, R.W. (ed.), Diagnostic Procedures for( 1 994): Epidemics of aseptic meningids due to echoviruSViral, Rickettsial and Chlamydial Infections. 6th ed.Am.

30 in J叩an. Jpn. ∫. Med. S°i. Bio1., 47, 221‑239.

Public Heal血Assoc., Washington, D.C., USA.

Laboratory and Epidemiology Communications
Possible Enhancement of GB Virus C Infection in Cultured Cells

by Addition ofAnti‑E 1 Antibodies
Minako Hijikata*, Yohko K. Shimizu, Tomoko Kiyoharal,
Shunj i Mishiro2 and Hiroshi Yoshikura
Department ofRespiratoyy Diseases, ReseaflCh Institute, International Medical Center ofJapan,
Toyama 1‑21‑I, Shinjuku‑ku, Too,0 162‑8655,
lDepartment of Viral Disease and Vaccine Conty10l, National Institute ofInfectious Diseases,
Musashimurayama‑shi, Tob70 208‑0011 andZDepartment of Medical Sciences, Toshiba General Hospital,
Shinagawa‑ku, To砂0 140‑8522

Communicated by Hiroshi Yoshikura(Accepted July 10, 2000)

Recently, a novel member of the virus family FJaviviridae
was identified as a causative agent for human non‑A‑E
hepatitis, called GB vims C (GBV‑C) or hepatitis G vimS

E 1 peptide (amino acid number 6ト80) in Freund's a句uvant,(HGV). GBV‑C is distantly related to hepadtis C virus (HCV).
HCV virions are bound to anti‑HCV antibodies as immunethat the immune serum was reactive with the homologous

and a serum sample was obtained 6 weeks a鮎r the last injec‑

tion. Enzyme‑linked immunosorbent assay (ELISA) revealed
peptide. Double irrmunoprecIPitation using GBV‑C and HCV
positive plasma #53 (3) revealed that the majority ofGBV‑C

complexesinthe circulation of chronically infected hosts,andthis phenomenon is related to the antibody‑escapemutations
inthe hypervariable reglOn OfE2 protein. However, GBV‑C hasvirions were brought by the immune serum to the pellet.

no hypervariable reglOn Within envelope proteins. Therefore,
the mechanism for GBV‑C to establish persistent infection
may be different from that for HCV.

56oC for 30 minand diluted 10‑fold. One hundred microliters
ofdiluted sera were mixed with an equal volume of 1:100

We obtained serial sera &om a Japanese patient with acutewere inoculated into 1 ml ofH‑903 cell (3) suspension (5 ×The immune and control pre‑immune sera were heated atdilution of #53 serum and incubated at 4oC ovemight. They

repeated blood transfusions. The patient was found to be105/cells) and incubated for 2 h at 37oC. After being washedonce,the cells were cultured further in the continuous presence

infected with GBV‑C. Immunoprecipitation of the sera withof immune or pre‑immune serum at a final concentration oflymphatic leukemia who had developed hepatitis afteranti‑human lgG fわllowed by detection of GBV‑C RNA by

10‑2. presence of the viral sequence in the cells and in theRTIPCR (1) revealed that, in the first sample, GBV‑C RNA

supernatants was monitored for 32 days by the RT‑PCR

was present only in the supematant, while from the second

method as described in a previous report (3).Asshown in thesample on, GBV‑C RNA was present in the pellet as well;i.e., from the second polnt On, the antibody was present. Insplte Of the presence orthe antibody, however, GBV‑C RNA

Table. Detection ofGBV‑C RNA by RTIPCR in cell culture

continued toincrease; i.e.,the抑tibody did not suppress GBV‑C

Pre‑immune serum Immune serum

replication (Figure). TYlis observation led us to the hypothesisCellSupCel1Sup

that the antibody was enhanclng even the infection, as371 31 72 2732

reported for otherflaviviruses (2).

+++++++In order to test this possibility, we examined the effect ofEl antibody on GBV‑Cinfection in cultured cells. A rabbit
was injected intradermally twice (at a I‑month interval)

with500 LLg keyhole limpet hemocyanin‑conjugated synthetic
十*Corresponding author: Fax: + 8 I 13‑3207‑1 038, E‑mail: minakoh

PI: post inoculation, Sup: supematant@ri. imcj.go.jp
133

十 十 + + + 一+++++++一