Mode of HCV infection examined by polymorphism of hypervariable region-1 in cases of acute hepatitis C after accidental exposure to blood-borne pathogens

[Guest guest]

J Med Virol. 2005 Jan;75(1):35-41.

Mode of HCV infection examined by polymorphism of hypervariable region-1 in

cases of acute hepatitis C after accidental exposure to blood-borne

pathogens.

Takeda T, Tatsumi N, Nakayama Y, Yasuda T, Nishiguchi S, Seki S.

Department of Hepatology, Graduate School of Medicine, Osaka City

University, Osaka, Japan.

Acute hepatitis C is known to respond better to interferon therapy than

chronic hepatitis C. The reason for this difference remains unclear. The

present study was undertaken to examine HCV quasispecies in blood from

patients with acute hepatitis C caused by accidental exposure to blood-borne

pathogens and in blood from the source patients. Three patients who

developed hepatitis C (recipient patients; R-Pt.) and two patients who

served as a source of HCV infection (source patients; S-Pt.) were the

subjects of this study. The number of quasispecies and the genetic diversity

in hypervariable region-1 (HVR-1) were examined on the basis of fluorescence

single-strand conformation polymorphism and sequence analysis (FSSA). On the

day of the accident, the number of quasispecies and genetic diversity were

13 and 36 in S-Pt.1 and 6 and 20 in S-Pt.3, respectively. At the time of

diagnosis of acute hepatitis, the number of quasispecies and nucleotide

diversity were 2 and 2 in R-Pt.1, 2 and 0 in R-Pt.2, and 4 and 0 in R-Pt.3,

respectively. Immediately before the start of treatment, the number of

quasispecies and genetic diversity were 4 and 4 in R-Pt.1, 2 and 0 in

R-Pt.2, and 3 and 0 in R-Pt.3., respectively. In three R-Pts, interferon

therapy resulted in eradication of HCV. These findings indicate that in the

early stage of HCV infection, only a portion of HCV transmitted from S-Pts

to R-Pts can proliferate. The low number of quasispecies of HCV appears to

be one of the reasons why acute hepatitis responds well to interferon

therapy. J. Med. Virol. 75:35-41, 2005. © 2005 Wiley-Liss, Inc.

PMID: 15543585 [PubMed - in process]

[Guest guest]

J Med Virol. 2005 Jan;75(1):35-41.

Mode of HCV infection examined by polymorphism of hypervariable region-1 in

cases of acute hepatitis C after accidental exposure to blood-borne

pathogens.

Takeda T, Tatsumi N, Nakayama Y, Yasuda T, Nishiguchi S, Seki S.

Department of Hepatology, Graduate School of Medicine, Osaka City

University, Osaka, Japan.

Acute hepatitis C is known to respond better to interferon therapy than

chronic hepatitis C. The reason for this difference remains unclear. The

present study was undertaken to examine HCV quasispecies in blood from

patients with acute hepatitis C caused by accidental exposure to blood-borne

pathogens and in blood from the source patients. Three patients who

developed hepatitis C (recipient patients; R-Pt.) and two patients who

served as a source of HCV infection (source patients; S-Pt.) were the

subjects of this study. The number of quasispecies and the genetic diversity

in hypervariable region-1 (HVR-1) were examined on the basis of fluorescence

single-strand conformation polymorphism and sequence analysis (FSSA). On the

day of the accident, the number of quasispecies and genetic diversity were

13 and 36 in S-Pt.1 and 6 and 20 in S-Pt.3, respectively. At the time of

diagnosis of acute hepatitis, the number of quasispecies and nucleotide

diversity were 2 and 2 in R-Pt.1, 2 and 0 in R-Pt.2, and 4 and 0 in R-Pt.3,

respectively. Immediately before the start of treatment, the number of

quasispecies and genetic diversity were 4 and 4 in R-Pt.1, 2 and 0 in

R-Pt.2, and 3 and 0 in R-Pt.3., respectively. In three R-Pts, interferon

therapy resulted in eradication of HCV. These findings indicate that in the

early stage of HCV infection, only a portion of HCV transmitted from S-Pts

to R-Pts can proliferate. The low number of quasispecies of HCV appears to

be one of the reasons why acute hepatitis responds well to interferon

therapy. J. Med. Virol. 75:35-41, 2005. © 2005 Wiley-Liss, Inc.

PMID: 15543585 [PubMed - in process]

[Guest guest]

J Med Virol. 2005 Jan;75(1):35-41.

Mode of HCV infection examined by polymorphism of hypervariable region-1 in

cases of acute hepatitis C after accidental exposure to blood-borne

pathogens.

Takeda T, Tatsumi N, Nakayama Y, Yasuda T, Nishiguchi S, Seki S.

Department of Hepatology, Graduate School of Medicine, Osaka City

University, Osaka, Japan.

Acute hepatitis C is known to respond better to interferon therapy than

chronic hepatitis C. The reason for this difference remains unclear. The

present study was undertaken to examine HCV quasispecies in blood from

patients with acute hepatitis C caused by accidental exposure to blood-borne

pathogens and in blood from the source patients. Three patients who

developed hepatitis C (recipient patients; R-Pt.) and two patients who

served as a source of HCV infection (source patients; S-Pt.) were the

subjects of this study. The number of quasispecies and the genetic diversity

in hypervariable region-1 (HVR-1) were examined on the basis of fluorescence

single-strand conformation polymorphism and sequence analysis (FSSA). On the

day of the accident, the number of quasispecies and genetic diversity were

13 and 36 in S-Pt.1 and 6 and 20 in S-Pt.3, respectively. At the time of

diagnosis of acute hepatitis, the number of quasispecies and nucleotide

diversity were 2 and 2 in R-Pt.1, 2 and 0 in R-Pt.2, and 4 and 0 in R-Pt.3,

respectively. Immediately before the start of treatment, the number of

quasispecies and genetic diversity were 4 and 4 in R-Pt.1, 2 and 0 in

R-Pt.2, and 3 and 0 in R-Pt.3., respectively. In three R-Pts, interferon

therapy resulted in eradication of HCV. These findings indicate that in the

early stage of HCV infection, only a portion of HCV transmitted from S-Pts

to R-Pts can proliferate. The low number of quasispecies of HCV appears to

be one of the reasons why acute hepatitis responds well to interferon

therapy. J. Med. Virol. 75:35-41, 2005. © 2005 Wiley-Liss, Inc.

PMID: 15543585 [PubMed - in process]

[Guest guest]

J Med Virol. 2005 Jan;75(1):35-41.

Mode of HCV infection examined by polymorphism of hypervariable region-1 in

cases of acute hepatitis C after accidental exposure to blood-borne

pathogens.

Takeda T, Tatsumi N, Nakayama Y, Yasuda T, Nishiguchi S, Seki S.

Department of Hepatology, Graduate School of Medicine, Osaka City

University, Osaka, Japan.

Acute hepatitis C is known to respond better to interferon therapy than

chronic hepatitis C. The reason for this difference remains unclear. The

present study was undertaken to examine HCV quasispecies in blood from

patients with acute hepatitis C caused by accidental exposure to blood-borne

pathogens and in blood from the source patients. Three patients who

developed hepatitis C (recipient patients; R-Pt.) and two patients who

served as a source of HCV infection (source patients; S-Pt.) were the

subjects of this study. The number of quasispecies and the genetic diversity

in hypervariable region-1 (HVR-1) were examined on the basis of fluorescence

single-strand conformation polymorphism and sequence analysis (FSSA). On the

day of the accident, the number of quasispecies and genetic diversity were

13 and 36 in S-Pt.1 and 6 and 20 in S-Pt.3, respectively. At the time of

diagnosis of acute hepatitis, the number of quasispecies and nucleotide

diversity were 2 and 2 in R-Pt.1, 2 and 0 in R-Pt.2, and 4 and 0 in R-Pt.3,

respectively. Immediately before the start of treatment, the number of

quasispecies and genetic diversity were 4 and 4 in R-Pt.1, 2 and 0 in

R-Pt.2, and 3 and 0 in R-Pt.3., respectively. In three R-Pts, interferon

therapy resulted in eradication of HCV. These findings indicate that in the

early stage of HCV infection, only a portion of HCV transmitted from S-Pts

to R-Pts can proliferate. The low number of quasispecies of HCV appears to

be one of the reasons why acute hepatitis responds well to interferon

therapy. J. Med. Virol. 75:35-41, 2005. © 2005 Wiley-Liss, Inc.

PMID: 15543585 [PubMed - in process]