ライフサイエンスコーパス: acute hepatitis

1 more abundant and sustained in children with acute hepatitis.

2 virus (HEV) is a human pathogen that causes acute hepatitis.

3 te institution, months prior for undiagnosed acute hepatitis.

4 tective effects of BV in models of shock and acute hepatitis.

5 her asymptomatic or present with symptomatic acute hepatitis.

6 g telithromycin, the patients presented with acute hepatitis.

7 ent in the mouse liver within the context of acute hepatitis.

8 that clinically and pathologically resembles acute hepatitis.

9 wild-type-like acute infection and developed acute hepatitis.

10 s C virus (HCV), infects tamarins and causes acute hepatitis.

11 s of laboratory tests were characteristic of acute hepatitis.

12 sappeared concordant with the development of acute hepatitis.

13 cificity to patients who have recovered from acute hepatitis.

14 er CD8(+) T cells that cause liver injury in acute hepatitis.

15 on by HEV ranges from asymptomatic to severe acute hepatitis.

16 counts for approximately 10% of all cases of acute hepatitis.

17 ms underlying the expression of IL-33 during acute hepatitis.

18 les of these processes in the development of acute hepatitis.

19 through the Sentinel County Surveillance for Acute Hepatitis (1998 to 2006).

20 most common type of toxic liver disease was acute hepatitis (33.5 %).

21 A total of 15 children were identified with acute hepatitis - 6 (40%) who had hepatitis with an iden

22 ) accounts for approximately 20% of cases of acute hepatitis, 70% of chronic hepatitis, and 30% of en

23 serum samples from patients with acute Hepatitis A (12/ 75 in Tel-Aviv and 31 patients ho

24 The incidence of acute hepatitis A and B infection has declined significa

25 Given the public health implications of acute hepatitis A and hepatitis B in patients with CLD,

26 HAV vaccination during a recent outbreak of acute hepatitis A between 2015 and 2017, a 1:4 case-cont

27 because a large proportion of patients with acute hepatitis A do not have any identifiable risk fact

28 ges in virus control following resolution of acute hepatitis A in Ifnar1(-/-) mice and may have relev

29 Acute hepatitis A is a major public health problem in de

30 Acute hepatitis A superimposed on chronic liver disease

31 culture or present in sera from humans with acute hepatitis A.

32 gnificant impact on the overall incidence of acute hepatitis A.

33 c inflammatory cell infiltrates in mice with acute hepatitis A.

34 f paracrine signaling in the pathogenesis of acute hepatitis A.

35 transferase (ALT) elevations associated with acute hepatitis A.

36 In a murine model of acute hepatitis, administration of a PD-1H agonist mAb s

37 The virus caused acute hepatitis after intravenous inoculation into Afric

38 on was investigated as the possible cause of acute hepatitis among 88 military patients stationed at

39 cytokine family, positively correlates with acute hepatitis and chronic liver failure in mice and hu

40 Although uncommon, the onset of severe acute hepatitis and even of life-threatening liver failu

41 ratios for P falciparum malaria and also for acute hepatitis and HIV/AIDS.

42 iously healthy children were identified with acute hepatitis and human adenovirus viremia.

43 the liver is critical for viral clearance in acute hepatitis and in the pathogenesis of chronic infla

44 RVFVmiR-122-infected C57BL/6 mice survived acute hepatitis and instead developed late-onset encepha

45 1d-dependent, nonclassical NKT cell-mediated acute hepatitis and liver injury.

46 Hepatitis E virus (HEV) is a major cause of acute hepatitis and mainly transmitted faecal-orally.

47 tion is usually self-limited but may lead to acute hepatitis and rarely to fulminant hepatic failure.

48 requently fails to occur after recovery from acute hepatitis and that traces of virus can maintain th

49 atitis E virus (HEV) is a causative agent of acute hepatitis, and it is the sole member of the genus

50 of outcomes, including mild illness, severe acute hepatitis, and, of particular concern, chronic pro

51 tion prolongs survival times of patient with acute hepatitis associated with alcoholic liver disease

52 her NHPs after her initial presentation for acute hepatitis at the first institution and continued t

53 ths after OLT) and the other patient died of acute hepatitis B (7 months after OLT).

54 ded us to identify the changing incidence of acute hepatitis B (AHB) in children and young adults.

55 As a control, 38 patients with acute hepatitis B (AHB) without liver failure were inclu

56 t patients infected during adulthood develop acute hepatitis B (AHB), which usually results in viral

57 ly 1992, a 47-year-old woman became ill with acute hepatitis B after undergoing a thymectomy in which

58 from 134 individuals including patients with acute hepatitis B and C as well as chronic hepatitis B,

59 Reported cases of symptomatic acute hepatitis B and hepatitis C occurring in persons>/

60 t in two (11%) of 19 Caucasian patients with acute hepatitis B and nine (27%) of 33 Caucasian patient

61 ibe the results of enhanced surveillance for acute hepatitis B at 7 federally funded sites over a 6-y

62 using whole-genome sequences (n = 179) from acute hepatitis B cases (n = 1,206) identified through t

63 lness, suggesting that more than half of the acute hepatitis B cases might have been prevented throug

64 In the 6-year period, 2220 acute hepatitis B cases were reported from the 7 sites.

65 to factors potentiating hepatic damage with acute hepatitis B contributed to the outbreak's high mor

66 uring this period, the reported incidence of acute hepatitis B declined by 76.1% from 13.8 cases per

67 analysis of HBV whole genomes from cases of acute hepatitis B identified from 1998 to 2006 in the Un

68 irectly proportional to tissue injury during acute hepatitis B in humans.

69 n encouraging trend is that the incidence of acute hepatitis B in the United States declined as much

70 riod of decline in the reported incidence of acute hepatitis B in the United States.

71 scribes an uncommon original diagnosis of an acute hepatitis B infection occurring in a vaccinated bu

72 ca. 2002, coinciding with transient rises in acute hepatitis B notification rates among adults; D3 un

73 Death related to acute hepatitis B occurs in approximately 1% of patients

74 hich a thoracic-surgery resident who had had acute hepatitis B six months earlier assisted.

75 increased level of arginase in patients with acute hepatitis B suppresses the functions of activated

76 earlier was in favor of an evolution from an acute hepatitis B toward a chronic hepatitis B.

77 f T-bet in virus-specific CD8 T cells during acute hepatitis B virus (HBV) and hepatitis C virus (HCV

78 Some patients with acute hepatitis B virus (HBV) infection develop chronic

79 Clearance of acute hepatitis B virus (HBV) infection is associated wi

80 Recovery from acute hepatitis B virus (HBV) infection occurs in 95% of

81 Acute hepatitis B virus (HBV) infection remains a freque

82 Recovery from acute hepatitis B virus (HBV) infection requires a broad

83 During acute hepatitis B virus (HBV) infection viral loads reac

84 Following an acute hepatitis B virus (HBV) infection, clearance or pe

85 ogical profile suggesting a previous cleared acute hepatitis B virus (HBV) infection, including high

86 Acute hepatitis B virus (HBV) infections either resolve

87 rted a substantial increase in the number of acute hepatitis B virus (HBV) infections in the United S

88 cratic drug-induced liver injury DILI (22%), acute hepatitis B virus infection (12%), autoimmune hepa

89 iral antigens in a transgenic mouse model of acute hepatitis B virus infection.

90 982-1998, enhanced sentinel surveillance for acute hepatitis B was conducted in 4 counties in the Uni

91 A total of 362 of 11 311 (3.2%) cases with acute hepatitis B were vaccinated.

92 lood mononuclear cells from 67 patients with acute hepatitis B, and 12 patients convalescent from acu

93 In liver biopsy specimens from patients with acute hepatitis B, but not chronic hepatitis B or contro

94 nvasive Haemophilus influenzae type b (Hib), acute hepatitis B, hepatitis A, varicella, Streptococcus

95 s targeted since 1980 including hepatitis A, acute hepatitis B, Hib, and varicella.

96 ompensated cirrhosis, organ transplantation, acute hepatitis B, pregnancy, coinfection with hepatitis

97 In patients with acute hepatitis B, the expansion of activated and prolif

98 ully vaccinated individuals among cases with acute hepatitis B, the proportion of preventable cases i

99 patitis B, and 12 patients convalescent from acute hepatitis B, were stimulated with three panels of

100 plays a central role in the pathogenesis of acute hepatitis B.

101 medicine clinic in the UK was diagnosed with acute hepatitis B.

102 s) using blood samples from 18 patients with acute hepatitis B.

103 quence changes were easily detectable in the acute, hepatitis B e antigen-positive phase of infection

104 atitis A virus (HAV), the causative agent of acute hepatitis, barely grows in cell culture and in the

105 te that JUNB/AP-1 promotes cell death during acute hepatitis by regulating IFN-gamma production in NK

106 We identified 20 participants with acute hepatitis C (10 with hepatitis C virus [HCV] monoi

107 to develop chronic hepatitis than those with acute hepatitis C (23% vs. 68%; P < .05).

108 Therapy of acute hepatitis C (AHC) has not yet been standardized an

109 Treatment of patients with acute hepatitis C (AHC) is more effective, with sustaine

110 ortion of HIV(+) patients manage to overcome acute hepatitis C (AHC) spontaneously.

111 ease resolution in a cohort of patients with acute hepatitis C (AHC), analyzing epidemiological, clin

112 els of IP-10, with outcomes of patients with acute hepatitis C (AHC).

113 The Australian Trial in Acute Hepatitis C (ATAHC) was a prospective study of the

114 ubjects, enrolled in the Australian Trial in Acute Hepatitis C (ATAHC), using HCV peptide enzyme-link

115 Approximately three quarters of acute hepatitis C (HCV) infections evolve to a chronic s

116 We examined trends in incidence of acute hepatitis C among young persons reported to the Ce

117 Hepatitis C virus (HCV) causes acute hepatitis C and can lead to life-threatening compl

118 e epidemiologically distinct from those with acute hepatitis C and have a significantly more severe a

119 are essential for spontaneous resolution of acute hepatitis C and long-term protection from persiste

120 emed essential for spontaneous resolution of acute hepatitis C and long-term protection.

121 Patients with acute hepatitis C and schistosomiasis coinfection cannot

122 Acute hepatitis C and spontaneous clearance was also ass

123 Acute hepatitis C and spontaneous clearance was associat

124 ants identified from the Australian Trial in Acute Hepatitis C and the Networks study were followed l

125 cal correlates of clearance in patients with acute hepatitis C and their sexual contacts.

126 Further, PBMC from patients with acute hepatitis C as well as HCV-infected Huh7.5 cells h

127 markedly prolonged the incubation period of acute hepatitis C but did not prevent or delay HCV infec

128 covery occurs in a minority of patients with acute hepatitis C but is associated with vigorous and lo

129 Clinically, acute hepatitis C can increase concentrations of alanine

130 ceptor (TLR) expression and signaling during acute hepatitis C correlates with clinical outcomes.

131 Approximately 85% of persons with acute hepatitis C develop chronic hepatitis as determine

132 nclude that approximately 85% of people with acute hepatitis C develop persistent viremia.

133 Acute hepatitis C developed in both the IGIV-treated and

134 ells from healthy controls and patients with acute hepatitis C efficiently recognized both HCV-infect

135 Although the incidence of acute hepatitis C has declined, there is a large reservo

136 virin and also with spontaneous clearance of acute hepatitis C in a heterogeneous population.

137 d the efficacy of PEG IFN-alpha treatment in acute hepatitis C in relation to the kinetics of hepatit

138 mately 10% of persons with reported cases of acute hepatitis C in the United States report a history

139 Reports of acute hepatitis C in young persons in the United States

140 From 2006 to 2012, reported incidence of acute hepatitis C increased significantly in young perso

141 Peginterferon alfa-2b monotherapy in acute hepatitis C induces high sustained virologic respo

142 s with FPAs were compared with patients with acute hepatitis C infection without FPAs.

143 In acute hepatitis C infection, close monitoring of hepatit

144 There is a paucity of information on core in acute hepatitis C infection.

145 od samples from participants in the Montreal Acute Hepatitis C Injection Drug User Cohort Study who w

146 Our results show that the outcome of acute hepatitis C is associated with a functional hierar

147 The outcome of acute hepatitis C is associated with efficient virus-spe

148 Acute hepatitis C is marked by appearance of HCV RNA in

149 Acute hepatitis C is most often diagnosed in the setting

150 chronic hepatitis C, but neither its role in acute hepatitis C nor the biologic basis for its action

151 Mechanisms by which spontaneous clearance of acute hepatitis C occurs are unclear.

152 Symptomatic acute hepatitis C occurs in only about 15% of patients w

153 A patient developed acute hepatitis C shortly after tissue transplantation.

154 ve used this resource to study parameters of acute hepatitis C virus (HCV) infection among 94 donor-r

155 r (NK) cells likely contribute to outcome of acute hepatitis C virus (HCV) infection and interferon (

156 e a patient with hypogammaglobulinemia whose acute hepatitis C virus (HCV) infection appeared to reso

157 Outbreaks of acute hepatitis C virus (HCV) infection are occurring in

158 Acute hepatitis C virus (HCV) infection becomes chronic

159 Acute hepatitis C virus (HCV) infection culminates in vi

160 Although 20%-40% of persons with acute hepatitis C virus (HCV) infection demonstrate spon

161 Since 2002, a global epidemic of acute hepatitis C virus (HCV) infection has been noted i

162 sequelae during the first two decades after acute hepatitis C virus (HCV) infection have been well s

163 tween IL28B and the clinical presentation of acute hepatitis C virus (HCV) infection in a homogeneous

164 ness and cost-effectiveness of screening for acute hepatitis C virus (HCV) infection in human immunod

165 Fibrosis progression after acute hepatitis C virus (HCV) infection in human immunod

166 appearance of neutralizing antibodies during acute hepatitis C virus (HCV) infection is associated wi

167 Spontaneous clearance of acute hepatitis C virus (HCV) infection is associated wi

168 Acute hepatitis C virus (HCV) infection is often asympto

169 Acute hepatitis C virus (HCV) infection is rarely studie

170 Acute hepatitis C virus (HCV) infection is underdiagnose

171 Treatment of acute hepatitis C virus (HCV) infection leads to a susta

172 une responses during the first few months of acute hepatitis C virus (HCV) infection seem crucial for

173 guidelines now recommend that patients with acute hepatitis C virus (HCV) infection should be treate

174 Acute hepatitis C virus (HCV) infection was the final di

175 Historically, acute hepatitis C virus (HCV) infection was treated with

176 over, these cells were highly permissive for acute hepatitis C virus (HCV) infection, and persistent

177 e thought to be important for the control of acute hepatitis C virus (HCV) infection, but to date lit

178 In acute hepatitis C virus (HCV) infection, programmed deat

179 In the setting of acute hepatitis C virus (HCV) infection, robust HCV-spec

180 In studies of acute hepatitis C virus (HCV) infection, the early host

181 c liver disease may develop many years after acute hepatitis C virus (HCV) infection, the past incide

182 e early events that determine the outcome of acute hepatitis C virus (HCV) infection, we compared the

183 are the hallmark of spontaneous clearance of acute hepatitis C virus (HCV) infection, whereas compara

184 therapy has not been adequately evaluated in acute hepatitis C virus (HCV) infection.

185 ics and evolution predict outcome of primary acute hepatitis C virus (HCV) infection.

186 variation is a determinant of recovery from acute hepatitis C virus (HCV) infection; however, to dat

187 Sexually transmitted acute hepatitis C virus (HCV) infections (AHIs) have bee

188 estigation was to prospectively characterize acute hepatitis C virus (HCV) infections and to evaluate

189 States, the annual number of newly acquired acute hepatitis C virus (HCV) infections has declined fr

190 Acute hepatitis C virus (HCV) is typically defined as ne

191 we hypothesized that early DAA treatment of acute hepatitis C virus (HCV) with DAAs may normalize mo

192 ered for 8, 12, or 24 weeks in patients with acute hepatitis C virus infection a total of 161 patient

193 Spontaneous resolution of acute hepatitis C virus infection cannot be predicted, a

194 These findings indicate that, during acute hepatitis C virus infection in vivo, virus-specifi

195 ed virologic response rates in patients with acute hepatitis C virus infection, thus preventing devel

196 a total of 161 patients were identified with acute hepatitis C virus infection.

197 Acute hepatitis C was associated with marked changes in

198 ks in addition to 14 untreated subjects with acute hepatitis C were prospectively followed.

199 and immunological studies on 7 patients with acute hepatitis C who received antiviral therapy and wer

200 Forty subjects with proven acute hepatitis C who received either PEG IFN-alpha plus

201 Of 45 patients with acute hepatitis C, 40.0% were simultaneously infected wi

202 se of an activated NK cell population during acute hepatitis C, that is largely restored upon viral c

203 Compared with patients with acute hepatitis C, those with non-ABCDE hepatitis had a

204 ther these observations indicate that during acute hepatitis C, virus evolution was driven primarily

205 egylated interferon alfa-2b for treatment of acute hepatitis C.

206 as playing a critical role in the outcome of acute hepatitis C.

207 longitudinally from the time of diagnosis of acute hepatitis C.

208 drome of chronic liver GVHD presenting as an acute hepatitis can be recognized in a patient at risk w

209 HCV infection can result in acute hepatitis, chronic hepatitis, and cirrhosis, which

210 3 had preexisting HCV and the cause of their acute hepatitis could not be determined; of the remainin

211 levels of arginase observed in patients with acute hepatitis could suppress the function of activated

212 on, during acute flares of disease, and with acute hepatitis D superinfection.

213 , the patient developed an unexpected severe acute hepatitis despite persistence of anti-HBs.

214 for many years after clinical recovery from acute hepatitis, despite the presence of serum antibodie

215 The delayed onset of acute hepatitis does not result from delayed recruitment

216 nfected children with or without evidence of acute hepatitis during the first year of life.

217 In total, 2713 acute hepatitis E cases were diagnosed, of which 1376 we

218 A case of acute hepatitis E in a researcher following a scalpel in

219 were assembled from blood donors (n = 372), acute hepatitis E patients (n = 94), five laboratory ani

220 Several cases of acute hepatitis E showed portal and periportal hepatitis

221 Acute hepatitis E virus (HEV) infection is a leading cau

222 eripheral blood and liver tissue revealed an acute hepatitis E virus infection (genotype 3).

223 the past decade, an increasing frequency of acute hepatitis E was noted in Germany and other Europea

224 9 patients with anti-HEV IgM indicated that acute hepatitis E was the most likely diagnosis for 7 an

225 les, typhoid and parathyroid, leishmaniasis, acute hepatitis E, and HIV/AIDS), we used natural histor

226 man sera obtained 2 months to 13 years after acute hepatitis E, and postinoculation chimpanzee sera),

227 type I interferon in preventing symptomatic acute hepatitis E.

228 ely) in normal rats and in rats with induced acute hepatitis, fatty liver, or cirrhosis.

229 during immunosuppression can lead to severe acute hepatitis, fulminant liver failure, and death.

230 Recurring outbreaks of acute hepatitis have been a significant cause of morbidi

231 oups with hepatitis C, such as patients with acute hepatitis, human immunodeficiency virus coinfectio

232 w for the first time in an animal model that acute hepatitis impairs the repair of oxidative DNA base

233 th chimpanzees and rhesus monkeys and caused acute hepatitis in both.

234 We induced acute hepatitis in C57BL/6 mice by intravenous injection

235 The recent epidemic of acute hepatitis in children across the world has highlig

236 Investigation into a recent cluster of acute hepatitis in children from the southeastern United

237 virus (HEV) infections are a major cause of acute hepatitis in developing and industrialized countri

238 (HEV) is an emerging virus causing epidemic acute hepatitis in developing countries as well as spora

239 Theiler's disease is an acute hepatitis in horses that is associated with the ad

240 Hepatitis E virus (HEV) induces acute hepatitis in humans with a high fatality rate in p

241 atitis A virus (HAV) is associated only with acute hepatitis in humans, HAV RNA persists within the l

242 A common cause of acute hepatitis in humans, hepatitis A virus (HAV) repli

243 , hepatitis A virus (HAV), a common cause of acute hepatitis in humans, is unique in that it is hepat

244 eutralizing antibody following resolution of acute hepatitis in Ifnar1(-/-) mice and that macrophages

245 navirus, mouse hepatitis virus (MHV), causes acute hepatitis in its natural host and provides a usefu

246 s been found to prevent injury in a model of acute hepatitis in mice through downregulation of tumor

247 y to wild-type virus but was unable to cause acute hepatitis in mice.

248 elated to hepatitis C virus (HCV) and causes acute hepatitis in tamarins (Saguinus species), making i

249 GB virus-B (GBV-B) causes an acute hepatitis in tamarins characterized by increased a

250 IL-33 in hepatocytes is blocked during ConA-acute hepatitis in TRAIL-deficient mice compared to WT m

251 Induction of acute hepatitis in wild-type C57BL/6 mice released large

252 was investigated after the induction of ConA-acute hepatitis in wildtype (WT), perforin(-/-) , tumor

253 ccine capable of protecting chimpanzees from acute hepatitis induced by challenge with heterologous v

254 In conclusion, PEG IFN-alpha therapy in acute hepatitis induces high rates of sustained virologi

255 We report an unusual acute hepatitis infection in a previously healthy man ca

256 d mortality using natural history models for acute hepatitis infections and GBD's cause-of-death ense

257 at eventually became chronic carriers had an acute hepatitis involving the same cell types, but at di

258 arance of the hepatitis B virus (HBV) during acute hepatitis is associated with a strong, polyclonal,

259 The expression of IL-33 during acute hepatitis is dependent on TRAIL, but not on FasL o

260 ther products, in contrast, tend to cause an acute hepatitis-like injury.

261 agulation system, which was concomitant with acute hepatitis, minor deficit of hepatic factor synthes

262 < .01) but were significantly reduced in the acute hepatitis model (82% and -36%, respectively).

263 ), new anti-HCV seropositivity with clinical acute hepatitis (n=21), or HCV strain sequencing after a

264 [n = 6]) and diffuse liver diseases (induced acute hepatitis [n = 6], fatty liver [n = 6], or cirrhos

265 this series involving 44 young children with acute hepatitis of uncertain cause, human adenovirus was

266 An outbreak of acute hepatitis of unknown aetiology in children was rep

267 was present in the majority of children with acute hepatitis of unknown cause admitted to Children's

268 has been an increase in reports of cases of acute hepatitis of unknown cause in children.

269 ermine the disease etiology in patients with acute hepatitis of unknown etiology (HUE), serum specime

270 Severe acute hepatitis of unknown etiology in children is under

271 antibody repertoires of nine cases of severe acute hepatitis of unknown etiology treated at Children'

272 AAV-2 is a likely etiologic agent of severe acute hepatitis of unknown etiology.

273 Every specificity shown during acute hepatitis persisted in normal liver tissue more th

274 rging zoonotic pathogen and a major cause of acute hepatitis, requires advanced diagnostics for multi

275 The events were acute hepatitis, respiratory failure, pneumonia, atrial

276 is of liver-infiltrating immune cells during acute hepatitis revealed that expression of P2Y(2)R in b

277 ella abortus 2308 at 5 x 10(5) CFU developed acute hepatitis similar to many natural hosts but, unlik

278 or not with hemophagocytic syndromes, and to acute hepatitis syndromes.

279 r, CH1581 and CH1579 developed a less severe acute hepatitis than CH1422.

280 subjects, viremia was higher at the peak of acute hepatitis than it was when the disease began, and

281 the virus experienced a prolonged episode of acute hepatitis that coincided with a CD38+ IFN-gamma- C

282 e to hepatitis B virus and in the subsequent acute hepatitis that ensues.

283 health care workers, four of whom developed acute hepatitis that progressed to chronicity while one

284 he U.K. Health Security Agency for confirmed acute hepatitis that was not hepatitis A through E and d

285 titers of >10(4.7) IU/mL, and development of acute hepatitis; the chronicity rate was 56%.

286 Acute hepatitis then occurred after the withdrawal, or d

287 t, like in humans, can advance stepwise from acute hepatitis to chronic hepatitis and hepatocellular

288 nd virus that underlies the progression from acute hepatitis to chronic liver disease, cirrhosis, and

289 binant virus to infect tamarins and to cause acute hepatitis was determined.

290 Acute hepatitis was induced in C56BL/6N mice by administ

291 Using an in vivo Con A challenge model of acute hepatitis, we observed reduced survival and increa

292 In this period, 21 cases of acute hepatitis were recorded with one among them diagno

293 d survived an average of 10 days, dying from acute hepatitis with an extensive hepatic infiltration o

294 morrhagic shock syndrome and less frequently acute hepatitis with liver failure and encephalopathy.

295 Hepatitis E virus infection causes an acute hepatitis with spontaneous resolution in the major

296 d animals by tail vein injection resulted in acute hepatitis, with a variety of pathological findings

297 E virus (HEV) infection is a major cause of acute hepatitis worldwide.

298 Hepatitis E virus (HEV) is a major cause of acute hepatitis worldwide.

299 us (HEV) is one of the most common causes of acute hepatitis worldwide.

300 y transmitted RNA virus, is a major cause of acute hepatitis worldwide.