• No results found

Past and Present Hepatitis G Virus Infections in Areas Where Hepatitis C is Highly Endemic and Those Where It Is Not Endemic

N/A
N/A
Protected

Academic year: 2020

Share "Past and Present Hepatitis G Virus Infections in Areas Where Hepatitis C is Highly Endemic and Those Where It Is Not Endemic"

Copied!
5
0
0

Loading.... (view fulltext now)

Full text

(1)

Copyright © 1998, American Society for Microbiology

Past and Present Hepatitis G Virus Infections in Areas Where

Hepatitis C is Highly Endemic and Those Where It Is

Not Endemic

EIJI TANAKA,

1

* MICHAEL TACKE,

2

MASAKAZU KOBAYASHI,

1

YOSHIYUKI NAKATSUJI,

1

KENDO KIYOSAWA,

1

SUSANNE SCHMOLKE,

2

ALFRED M. ENGEL,

2

GEORG HESS,

2

AND

HARVEY J. ALTER

3

Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto 390, Japan

1

; Boehringer

Mannheim GmbH, 82377 Penzberg, Germany

2

; and Department of Transfusion Medicine, National Institutes of

Health, Bethesda, Maryland 20892

3

Received 14 July 1997/Returned for modification 22 September 1997/Accepted 8 October 1997

We reported previously on an area in Japan where over 30% of the inhabitants were positive for hepatitis C

virus (HCV) antibody. In the present study, clinical features of hepatitis G virus (HGV) infection in this area

of high endemicity were compared to those in an area where HCV is not endemic. A total of 400 individuals were

selected randomly from those who were medically screened for liver disease in 1993; 200 were from the

high-endemicity area, and the other 200 were from the no-endemicity area. HGV RNA was measured by reverse

transcription and PCR with primers in the 5

*

noncoding region. Antibody to HGV envelope protein E2 was

measured by an enzyme-linked immunosorbent assay. Prevalence of any HGV marker in the high-endemicity

area (32%) was significantly (P < 0.0001) higher than that in the no-endemicity area (6%); similar differences,

32% versus 3% (P < 0.0001), had been observed for HCV markers (HCV RNA and HCV antibody). In areas

of both high and no endemicity, HCV markers were significantly more prevalent in individuals with any HGV

marker than in those without HGV markers, and age-specific prevalence of HGV markers was distributed

similarly to that of any HCV marker. Among possible routes of HGV transmission that were analyzed, folk

medicine was significant in the high-endemicity area, but blood transfusion was the major route in the

no-endemicity area. The rate of accompanying viremia in HGV infection (15%) was significantly lower than

that in HCV infection (78%) (P < 0.0001). In conclusion, HGV infection was highly prevalent in the area of high

HCV endemicity and was closely associated with HCV infection. HGV seemed to be transmitted via the practice

of folk medicine as well as blood transfusion. HGV resulted in a chronic carrier state less frequently than did

HCV.

The GB virus C and the hepatitis G virus (HGV) were

identified recently as possible causative agents of human viral

hepatitis (12, 17). Molecular characterization of these two

agents has shown them to be closely related strains of the same

virus, and they are supposed to represent a new genus in the

family Flaviviridae (3). As the nomenclature of the new virus

has not been settled, the term HGV is used in this paper.

HGV, like hepatitis C virus (HCV), is transmissible through

blood transfusion and is associated with acute and chronic

infections (4, 5, 15, 22, 24). Studies on HGV have depended on

the measurement of HGV RNA in serum, which reflects active

HGV infection. Recently, an assay for antibody to HGV

en-velope protein E2 (HGV-E2 antibody), which indicates

recov-ery from HGV infection, has been developed (6, 16, 18, 19).

The combined use of these assays has allowed for more

com-prehensive epidemiological studies of both past and present

HGV infection.

We previously reported on an area in which HCV is highly

endemic, where over 30% of the inhabitants were infected with

HCV (10). In that study, analyses of risk factors for HCV

infection elucidated inapparent modes of parenteral

transmis-sion, particularly folk medicine procedures. In the present

study, we determined the prevalence and patterns of HGV

infection in areas of high and low HCV endemicity to compare

the transmission patterns of these two common Flaviviridae

infections.

MATERIALS AND METHODS

Patients.A total of 420 individuals over 18 years old (62% of total inhabitants with corresponding ages) in an area in which HCV infection was endemic were medically screened for liver diseases in July 1993. Of those, the first 200 indi-viduals who prepared for screening were selected randomly for evaluation in this study. Those subjects included 79 males and 121 females aged 18 to 84 years (mean6standard deviation [SD], 56.3617.7 years). Medical screening was also conducted in an area in which HCV was not endemic and which is located near the high-endemicity area. Of 482 individuals (65% of total inhabitants with corresponding ages) who underwent medical screening in the no-endemicity area, 200 individuals were selected randomly for evaluation in the same manner as in the high-endemicity area. These control subjects included 48 males and 152 females aged 20 to 89 years (mean6SD, 56.8613.4 years).

Data from the HCV high-endemicity area (Arahiro) were reported previously (10), but the no-endemicity area (Sakaue) was not involved in the previous study. In both areas the main source of income is forestry, most people are middle class, Buddhism is the predominant religion, and the lifestyle does not seem to differ from that in other parts of Japan. Folk remedies in the areas of high and no endemicity include acupuncture with needles and so-called “Suidama” therapy, in which the skin is cut with knives (10). Nonsterilized knives and needles had been used in the high-endemicity area, but the use of sterilized instruments began after 1986 under direction of the public health center. Use of nonsterilized tools had not been noted in the no-endemicity area. Health screening and blood sample collections were done in the same manner as reported previously (10). Informed consent was obtained from each subject. Serum samples were stored at 270°C until assayed.

Laboratory tests.Second-generation HCV antibody, hepatitis B surface (HBs) antigen, HBs antibody, and hepatitis B core (HBc) antibody were detected with

* Corresponding author. Mailing address: Second Department of

Internal Medicine, Shinshu University School of Medicine, 3-1-1

Asahi, Matsumoto 390, Japan. Phone: 81-263-37-2634. Fax:

81-263-32-9412. E-mail: etanaka@gipac.shinshu-u.ac.jp.

110

on May 15, 2020 by guest

http://jcm.asm.org/

(2)

commercially available enzyme-linked immunosorbent assay kits (International Reagents Co., Kobe, Japan).

Alanine aminotransferase (ALT) (normal range, 7 to 45 IU/liter) was mea-sured on a multichannel autoanalyzer.

Measurement of HCV RNA in serum.RNA extraction and reverse transcrip-tion (RT) were carried out in 100ml of serum. The serum HCV RNA was measured by a nested RT-PCR with primers targeting the 59noncoding region (14). Procedures to avoid contamination of samples were implemented through-out the study (11). In each PCR assay, two negative controls and one positive control of 10 copies/ml were tested in addition to the samples of interest.

Measurement of HGV RNA in serum.HGV RNA in serum was detected by nested RT-PCR using primers in the 59noncoding region as described previously (21). Briefly, total RNA was extracted from 100-ml serum samples. After RT with Moloney murine leukemia virus reverse transcriptase, the first 30 cycles and then the second 30 cycles of PCR were performed (94°C for 1 min, 55°C for 1 min, and 72°C for 1 min). PCR products were analyzed by gel electrophoresis with 3% agarose. In each PCR assay, two negative controls and one positive control of 10 copies/ml (15) were tested in addition to the samples of interest.

In the RT-PCR assays for HCV and HGV RNAs, all negative controls were negative and all positive controls were positive.

Measurement of HGV-E2 antibody in serum.HGV-E2 antibody was measured by an enzyme-linked immunosorbent assay described previously (18, 19) in which recombinant E2 protein was bound to a microtiter plate. After addition of diluted serum samples, specifically bound antibodies against E2 protein were detected with an anti-human immunoglobulin G conjugated with peroxidase. Positive or negative results were judged as reported previously (18, 19).

Statistical analysis.Statistical analyses were performed with Student’s t test, the chi-square test, and Fisher’s exact test. A significance level was set at a P value of 0.05.

RESULTS

Backgrounds and viral markers in areas of endemicity

ver-sus areas of no endemicity.

Clinical and virological features of

the 200 individuals in the high-endemicity area were compared

to those of the 200 individuals in the no-endemicity area

(Ta-ble 1). A history of folk remedies was significantly more

prev-alent in the high-endemicity area than in the no-endemicity

area, while histories of surgery and blood transfusion were

similar in the two areas. Prevalence of HGV-related markers

was significantly higher in the area of endemicity than in the

no-endemicity area, as was observed for HCV-related markers.

Prevalence of HBs antigen did not differ between the two

areas, but that of any hepatitis B virus (HBV) marker was

significantly higher in the area of endemicity. Of the 400

sub-jects, 75 (19%) were positive for HGV RNA and/or HGV-E2

antibody, 7 (9%) were positive for HGV RNA only, 4 (5%)

were positive for both HGV RNA and HGV-E2 antibody, and

64 (86%) were positive for HGV-E2 antibody only.

Age-specific prevalence.

Age-specific prevalences of

hepati-tis viruses in the high-endemicity and no-endemicity areas are

shown in Fig. 1. Individuals who had a marker indicating the

existence of viremia were defined as having ongoing infection,

the presence of HBs antigen was defined as indicating HBV

infection, the presence of HCV RNA was defined as indicating

HCV infection, and the presence of HGV RNA was defined as

indicating HGV infection. On the other hand, individuals who

had antibody in the absence of viremia were considered to

have resolved or past infection. Age-specific prevalences of

total infection (viremia plus antibody) were similar for HBV,

HCV, and HGV in the high-endemicity area. The prevalence

was around 10% in groups under 50 years old and around 40%

in groups over 50 years old. This difference in distribution

between groups under and over 50 was statistically significant

(chi-square test) for each hepatitis virus: 10% versus 42% for

HBV (P

,

0.0001), 8% versus 42% for HCV (P

,

0.0001), and

10% versus 41% for HGV (P

,

0.0001). In the no-endemicity

area, the prevalence did not differ between the two age groups

for either HBV, HCV, or HGV.

Current versus past infection.

To analyze the proportion of

present HGV infections to total HGV infections, cases in the

high- and no-endemicity areas were combined, because the

proportions were similar in each area for each hepatitis virus

(6% versus 5% for HBV, 79% versus 60% for HCV, and 14%

versus 17% for HGV, respectively). The overall percentage of

current (to total) infections (15%, 11/75) was significantly

higher for HGV than for HBV (6%, 6/106 [P

5

0.04 by the

chi-square test]) but significantly lower than for HCV (78%,

53/68 [P

,

0.0001]).

HGV-infected versus noninfected groups.

Clinical and

viro-logical features were compared between groups with and

with-out HGV infection (including past and present infections) in

the high- and low-endemicity areas (Table 2). A history of

exposure to folk remedies was more frequent in HGV-positive

subjects than in HGV-negative subjects in the high-endemicity

area but not in the no-endemicity area. In contrast, a history of

blood transfusion was significantly more common among

HGV-positive subjects than among HGV-negative subjects in

the no-endemicity area. The prevalence of HBV-related

mark-ers did not differ between the two groups, while that of

HCV-related markers was significantly higher in the HGV-positive

group.

In the high-endemicity area, HGV infection (past and

present) was significantly more common (P

5

0.0233 by

Fish-er’s exact test) in individuals exposed to folk remedies before

1986 (44%, 37/82) than in those exposed after 1986 (11%, 1/9).

Similarly, HCV infection was significantly more common (P

5

0.0160 by Fisher’s exact test) in individuals exposed before

1986 (48%, 39/82) than in those exposed after 1986 (11%, 1/9).

Thus, HGV or HCV infection was less common in individuals

who were exposed to folk remedies after the use of sterilized

tools was adopted in 1986.

[image:2.612.49.290.90.287.2]

Mean levels of ALT in serum were compared according to

the status of HCV and HGV RNAs (Table 3). The mean level

was significantly higher in those with HCV and HGV RNAs

and those with HCV RNA alone than in those without HCV or

HGV RNA. Other comparisons among the four groups were

not statistically significant, including the comparison between

those with HGV RNA alone and those without HCV or HGV

RNA.

TABLE 1. Comparison of clinical and virological characteristics

between individuals in high- and no-endemicity areas

Characteristic

No. (%) of patients in area of:

P

High endemicity

(n5200) No endemicity(n5200)

History of:

Surgical operation

50 (25.0)

45 (22.5)

.

0.2

Blood transfusion

14 (7.0)

20 (10.0)

.

0.2

Folk remedy

91 (45.5)

54 (27.0)

0.0001

HBs antigen

4 (2.0)

2 (1.0)

.

0.2

a

HBs antibody

50 (25.0)

36 (18.0)

0.0884

HBc antibody

54 (27.0)

38 (19.0)

0.0573

Any HBV marker

64 (32.0)

42 (21.0)

0.0127

HCV RNA

50 (25.0)

3 (1.5)

,

0.0001

HCV antibody

64 (32.0)

5 (2.5)

,

0.0001

Any HCV marker

64 (32.0)

5 (2.5)

,

0.0001

HGV RNA

9 (4.5)

2 (1.0)

0.0323

HGV-E2 antibody

58 (29.0)

10 (5.0)

,

0.0001

Any HGV marker

63 (31.5)

12 (6.0)

,

0.0001

aObtained by Fisher’s exact test; all other P values were obtained by the

chi-square test.

on May 15, 2020 by guest

http://jcm.asm.org/

(3)

DISCUSSION

We previously reported that there was a small outbreak of

community-acquired, non-A, non-B acute hepatitis among

adults in the Arahiro area between 1981 and 1982. Subsequent

study (10) showed that the outbreak was due to HCV infection

spread mainly via folk remedies in which nonsterilized needles

and knives were used. Age-specific prevalence of HCV

anti-body showed that inhabitants who were infected were

predom-inantly over 40 years old when screened in 1986. By 1993

(present study), a high prevalence was found only in those over

50 years old, suggesting a cohort effect and indicating that the

outbreak of HCV infection had already ceased in the Arahiro

area following the adoption of sterilized tools in the practice of

folk remedies.

HGV-E2 antibody has been reported as a marker of

recov-ery from HGV infection, based on observations that HGV

RNA and HGV-E2 antibody are generally mutually exclusive

and that clearance of HGV RNA generally coincides with the

appearance of HGV-E2 antibody (6, 16, 18). Our results

show-ing that only 5% of individuals with any HGV marker were

positive for both HGV RNA and HGV-E2 antibody further

support the previous observations.

Tacke et al. (18) reported that 2.5% of healthy blood donors

were positive for HGV RNA and that 9% were positive for

HGV-E2 antibody. Similarly, Dille et al. (6) reported that 1%

of donors were positive for HGV RNA and that 3% were

positive for HGV-E2 antibody. Our data in the no-endemicity

area were similar, showing a 1% prevalence of HGV RNA and

a 5% prevalence of HGV-E2 antibody. Thus, in an area of low

HCV endemicity in Japan, the rates of HGV infection are

similar to those in Western nations.

When we previously compared HCV and HGV infections in

the high-endemicity area by testing HCV and HGV RNAs

(23), the prevalence of HGV infection (5%) appeared much

lower than that of HCV infection (34%). However, with the

advent of the HGV-E2 antibody assay, it became obvious that

prevalence of both past and present HGV infection (32%) was

as high as that of HCV (32%) or HBV (32%) infection in the

high-endemicity area. The prevalence of total infection (past

and present infections) for each virus was significantly higher

in the high-endemicity area than in the no-endemicity area.

However, the proportions of the infections that were active

(viremic) were similar in the low- and high-endemicity areas

for each virus. The overall proportions of subjects who were

antigenic or viremic were 6% for HBV, 15% for HGV, and

78% for HCV. Seventy to 85% of patients with acute HCV

infection become chronic HCV carriers (1, 2, 20) and usually

maintain the carrier state for long periods afterwards (7, 9, 20).

Although several reports have shown that HGV can cause a

chronic carrier state (4, 5, 13, 15), the frequency with which it

occurs and the rate by which it is maintained has not been

clarified sufficiently. Our data suggest that the rate of

persis-FIG. 1. Age-specific prevalences of HBV, HCV, and HGV infections in high-endemicity and no-endemicity areas. Prevalence of exposure is indicated by both filled and open bars and reflects a positive test for at least one viral marker (HBs antigen, HBs antibody, and/or HBc antibody for HBV; HCV RNA and/or HCV antibody for HCV; and HGV RNA and/or HGV-E2 antibody for HGV). Filled bars indicate a positive test for a marker of viremia (HBs antigen for HBV, HCV RNA for HCV, and HGV RNA for HGV).

on May 15, 2020 by guest

http://jcm.asm.org/

[image:3.612.98.502.68.401.2]
(4)

tence does not differ between areas with different prevalences

of HGV infection, and it is higher than that of HBV but

markedly lower than that of HCV.

HGV infection was closely associated with HCV infection

both in areas of endemicity and in areas of no endemicity;

individuals with total (past plus present) HGV infections had

high prevalences of HCV markers and similar patterns of

age-specific prevalence. Among possible routes of HGV

transmis-sion, folk remedies were significant in the area of endemicity,

but blood transfusion was most significant in the no-endemicity

area; similar trends were observed in our previous study of

HCV transmission (10). Thus, our results indicate that HGV is

transmissible not only by blood transfusion but also by folk

remedies such as acupuncture and cutting of the skin with

nonsterilized knives and that HGV infection had spread in

parallel with HCV in the area of high HCV endemicity.

ALT levels of individuals with active HCV infection did not

differ among those with and without concurrent HGV

infec-tion. Further, individuals with active HGV infection alone

tended to exhibit normal or very-low-level elevations of ALT.

These results are consistent with the findings of previous

stud-ies (4, 5, 8, 13, 21) that suggested a minimum-pathogenic-effect

HGV.

ACKNOWLEDGMENTS

This research was supported in part by a grant-in-aid from the

Ministry of Health and Welfare in Japan and in part by a grant-in-aid

from the Ministry of Education, Science, Sports and Culture (no.

09670529).

We thank members of the South Kiso hepatitis study group for

assistance at the medical screenings performed in the Arahiro and

Sakaue areas. We also thank Kafumi Todoriki for technical assistance.

REFERENCES

1. Aach, R. D., C. E. Stevens, F. B. Hollinger, J. W. Mosley, D. A. Peterson, P. E. Taylor, R. G. Johnson, L. H. Barbosa, and G. J. Nemo.1991. Hepatitis C virus infection in post-transfusion hepatitis: an analysis with first- and sec-ond-generation assays. N. Engl. J. Med. 325:1325–1329.

2. Alter, H. J., R. H. Purcell, J. W. Shih, J. C. Melpolder, M. Houghton, Q. L. Choo, and G. Kuo. 1989. Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis. N. Engl. J. Med. 321:1494–1500.

3. Alter, H. J. 1996. The cloning and clinical implications of HGV and HGBV-C. N. Engl. J. Med. 334:1536–1537.

4. Alter, H. J., Y. Nakatsuji, J. Melpolder, J. Wages, R. Wesley, J. W. K. Shih, and J. P. Kim.1997. The incidence of transfusion-associated hepatitis G virus infection and its relation to liver disease. N. Engl. J. Med. 336:747–754. 5. Alter, M. J., M. Gallagher, T. T. Morris, L. A. Moyer, E. L. Meeks, K. Krawczynski, J. P. Kim, and H. S. Margolis.1997. Acute non-A–E hepatitis in the United States and the role of hepatitis G virus infection. N. Engl. J. Med. 336:741–746.

6. Dille, B. J., T. K. Surowy, R. A. Gutierrez, P. F. Coleman, M. F. Knigge, R. J. Carrick, R. D. Aach, F. B. Hollinger, C. E. Stevens, L. H. Barbosa, G. J. Nemo, J. W. Mosley, G. J. Dawson, and I. K. Mushahwar.1996. An ELISA for detection of antibodies to the E2 protein of GB virus C. J. Infect. Dis. 225:293–299.

7. Farci, P., H. J. Alter, D. Wong, R. H. Miller, J. W. Shih, B. Jett, and R. H. Purcell.1991. A long term study of hepatitis C virus replication in non-A, non-B hepatitis. N. Engl. J. Med. 325:98–104.

8. Kao, J. H., P. J. Chen, M. Y. Lai, W. Chen, D. P. Liu, J. T. Wang, M. C. Shen, and D. S. Chen.1997. GB virus-C/hepatitis G virus infection in an area endemic for viral hepatitis, chronic liver disease, and liver cancer. Gastro-enterology 112:1265–1270.

9. Kiyosawa, K., T. Sodeyama, E. Tanaka, Y. Gibo, K. Yoshizawa, Y. Nakano, S. Furuta, Y. Akahane, K. Nishioka, R. H. Purcell, and H. J. Alter.1990. Interrelationship of blood transfusion, non-A, non-B hepatitis and hepato-cellular carcinoma: analysis by detection of antibody to hepatitis C virus. Hepatology 12:671–675.

10. Kiyosawa, K., E. Tanaka, T. Sodeyama, K. Yoshizawa, K. Yabu, K. Furuta, H. Imai, Y. Nakano, S. Usuda, K. Uemura, S. Furuta, Y. Watanabe, J. Watanabe, Y. Fukuda, T. Takayama, and the South Kiso Hepatitis Study Group. 1994. Transmission of hepatitis C in an isolated area in Japan: community-acquired infection. Gastroenterology 106:1596–1602. 11. Kwok, S., and R. Higuchi. 1989. Avoiding false positives with PCR. Nature

339:237–238.

12. Linnen, J., Jr., J. Wages, Z. Y. Zhang-Keck, K. E. Fry, K. Z. Krawczynski, H. Alter, E. Koonin, M. Gallagher, M. Alter, S. Hadziyannis, P. Karayiannis, K. Fung, Y. Nakatsuji, J. W. K. Shih, L. Young, Jr., M. Piatak, C. Hoover, J. Fernandez, S. Chen, J. C. Zou, T. Morris, K. C. Hyams, S. Ismay, J. D. Lifson, G. Hess, S. K. H. Foung, H. Thomas, D. Bradley, H. Margolis, and J. P. Kim.1996. Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent. Science 271:505–508.

13. Masuko, K., T. Mitsui, K. Iwano, C. Yamazaki, K. Okuda, T. Meguro, N. Murayama, T. Inoue, F. Tsuda, H. Okamoto, Y. Miyakawa, and M. Mayumi. 1996. Infection with hepatitis GB virus C in patients on maintenance hemo-dialysis. N. Engl. J. Med. 334:1485–1490.

14. Matsumoto, A., E. Tanaka, T. Suzuki, H. Ogata, and K. Kiyosawa. 1994. Viral and host factors that contribute to efficacy of interferon-a2a therapy in patients with chronic hepatitis C. Dig. Dis. Sci. 39:1273–1280.

15. Nakatsuji, Y., J. W. K. Shih, E. Tanaka, K. Kiyosawa, Jr., J. Wages, J. P. Kim, and H. J. Alter.1996. Prevalence and disease association of hepatitis G virus infection in Japan. J. Viral Hepatitis 3:307–316.

16. Pilot-Matias, T. J., R. J. Carrick, P. F. Coleman, T. P. Leary, T. K. Surowy, J. N. Simons, A. S. Muerhoff, S. L. Buijk, M. L. Chalmers, G. J. Dawson, S. M. Desai, and I. K. Mushahwar.1996. Expression of the GB virus C E2 glycoprotein using the Semliki Forest virus vector system and its utility as a serologic marker. Virology 225:282–292.

[image:4.612.49.290.98.296.2]

17. Simons, J. N., T. P. Leary, G. J. Dawson, T. J. Pilot-Matias, A. S. Muerhoff, G. G. Schlauder, S. M. Desai, and I. K. Mushahwar.1995. Isolation of novel

TABLE 2. Comparison of clinical and virological characteristics

between individuals with and without any HGV marker in high- and

no-endemicity areas

Characteristica

No. (%) of patients with any HGV markerb

P

Positive Negative

High-endemicity area

c

History of surgical operation

17 (27.0)

33 (24.1)

.

0.2

History of blood transfusion

5 (7.9)

9 (6.6)

.

0.2

History of folk remedies

38 (60.3)

53 (38.7)

0.0043

HBs antigen

0 (0.0)

4 (2.9)

.

0.2

d

Any HBV marker

23 (36.5)

41 (29.9)

.

0.2

HCV RNA

34 (54.0)

16 (11.7)

,

0.0001

Any HCV marker

41 (65.1)

22 (16.1)

,

0.0001

No-endemicity area

e

History of surgical operation

3 (25.0)

42 (22.3)

.

0.2

History of blood transfusion

4 (33.3)

16 (8.5)

0.0055

History of folk remedies

3 (25.0)

51 (27.1)

.

0.2

HBs antigen

0 (0.0)

3 (1.6)

.

0.2

d

Any HBV marker

5 (41.7)

37 (19.7)

0.0698

HCV RNA

2 (16.7)

1 (0.5)

0.0096

d

Any HCV marker

3 (25.0)

2 (1.1)

0.0016

d

aAny HBV marker, positive for HBs antigen, HBs antibody, and/or HBc

antibody; any HCV marker, positive for HCV RNA and/or HCV antibody.

bAny HGV marker, positive for HGV RNA and/or HGV-E2 antibody. cTotal positive, 63; total negative, 137.

dObtained by Fisher’s exact test; all other P values were obtained by the

chi-square test.

eTotal positive, 12; total negative, 188.

TABLE 3. Comparison of mean ALT levels in serum according to

the status of HGV and HCV RNAs

Viral marker statusa No.

positive Mean ALT levelSD (IU/liter)6

HGV RNA alone

4

20.5

6

8.3

HCV RNA alone

46

33.4

6

29.0

Both HGV and HCV RNAs

7

52.7

6

63.9

Neither HGV nor HCV RNA

343

16.8

6

10.9

aStatistical analyses by Student’s t test: HCV RNA alone versus neither HGV

nor HCV RNA, P,0.0001; both HGV and HCV RNAs versus neither HGV nor HCV RNA, P,0.0001. Other comparisons among the four groups were not significant.

on May 15, 2020 by guest

http://jcm.asm.org/

[image:4.612.49.289.626.692.2]
(5)

virus-like sequences associated with human hepatitis virus. Nat. Med. 1:564– 569.

18. Tacke, M., K. Kiyosawa, K. Stark, V. Schluter, B. Ofenloch-Haehnle, G. Hess, and A. M. Engel.1997. Detection of antibodies to a putative hepatitis G virus envelope protein. Lancet 349:318–320.

19. Tacke, M., S. Schmolke, V. Schlueter, S. Sauleda, J. I. Esteban, E. Tanaka, K. Kiyosawa, H. J. Alter, U. Schmitt, G. Hess, B. Ofenloch-Haehnle, and A. M. Engel.Humoral immune response to the E2 protein of hepatitis G virus is associated with long-term recovery from infection and reveals a high frequency of HGV exposure among healthy blood donors. Hepatology, in press.

20. Tanaka, E., K. Kiyosawa, Y. Nakatsuji, Y. Inoue, T. Miyamura, J. Chiba, and S. Furuta.1993. Clinical significance of antibodies to nonstructural and core proteins of hepatitis C virus in posttransfusion hepatitis patients during long-term follow-up. J. Med. Virol. 39:318–324.

21. Tanaka, E., H. J. Alter, Y. Nakatsuji, J. W. K. Shih, J. P. Kim, A. Matsumoto, M. Kobayashi, and K. Kiyosawa.1996. Effect of hepatitis G virus co-infec-tion on patients with chronic hepatitis C. Ann. Intern. Med. 125:740–743. 22. Tanaka, E., K. Yamaguchi, K. Uemura, M. Kobayashi, A. Iijima, K.

Kiyo-sawa, S. Yagi, and A. Hasegawa.1997. Hepatitis G virus/GB virus C infection in patients with chronic non-B, non-C hepatitis. Int. Hepatol. Commun. 6:137–143.

23. Tanaka, E., Y. Nakatsuji, M. Kobayashi, A. Iijima, T. Ichijo, H. Imai, K. Yoshizawa, T. Sodeyama, and K. Kiyosawa.1997. Hepatitis G virus/GB virus C infection in an area of high endemic hepatitis C virus infection. Hepatol. Res. 7:130–135.

24. Wang, J. T., F. C. Tsai, C. Z. Lee, P. J. Chen, J. C. Sheu, T. H. Wang, and D. S. Chen.1996. A prospective study of transfusion-transmitted GB virus C infection: similar frequency but different clinical presentation compared with hepatitis C. Blood 88:1881–1886.

on May 15, 2020 by guest

http://jcm.asm.org/

Figure

TABLE 1. Comparison of clinical and virological characteristicsbetween individuals in high- and no-endemicity areas
FIG. 1. Age-specific prevalences of HBV, HCV, and HGV infections in high-endemicity and no-endemicity areas
TABLE 2. Comparison of clinical and virological characteristicsbetween individuals with and without any HGV marker in high- and

References

Related documents

Comparison of gene expressions of invasive cancer with those of normal oral tissue (from controls) and dysplasia combined using ~21,000 filtered probe sets, followed by elimination of

The developed system ensures that solely licensed drivers will drive the vehicle and misuse of vehicles by others will be prevented.The system makes sure that vehicles access

This study shows that although prolonged totally con- trolled mechanical ventilation in normocapnia alters dia- phragm contractility in vivo , maintaining a moderate

The results obtained from this research show the following trends – 1) Tamoxifen decreases cell viability and growth in a dose-dependent manner (figures 1a

Note that for a large sample size it is enough to estimate the probability distribution, see for the meshgrid consideration in the figure 3, where all the peaks are showing

Baseline characteristics of HIV-Infected adults at the time of ART initiation in public health facilities of Arba- Minch town, Southern Ethiopia, 2013 ( n = 411). In a

There was no major difference in the attitude of women of both areas regarding whether they should stop feeding the child when they are sick and whether

In In Quest of the Ordinary, Cavell describes a significant challenge to the skeptical threat as the resettling of the everyday, a domestication of skepticism that makes life