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Selective transmission of hepatitis C virus quasi species through a needlestick accident in acute resolving hepatitis.
Clinical Infectious Diseases 2006 May 2
BACKGROUND: Little is known about the transmission of variant hepatitis C virus (HCV) genome through needlestick injuries.
METHODS: To demonstrate how HCV quasi species are transmitted and adapt to the new host in acute resolving infection, we analyzed the nucleotide and deduced amino acid sequences of the hypervariable region 1 (HVR-1) in the E2 domain of HCV in both the source of the virus ("donor") and the person who received the virus through a needlestick accident ("recipient"). In addition, we also performed phylogenetic analysis of HCV quasi species in these patients to document the viral transmission.
RESULTS: We obtained a total of 33 clones at different time points by using polymerase chain reaction amplification and cloning and sequencing of HVR-1. A predominant HVR-1 variant (in 4 of 10 isolates) in the donor was not present in the recipient 6 and 14 weeks after the accident. In contrast, a minor variant (in 1 of 10 isolates) in the donor became the predominant strain in the recipient 6 weeks (in 10 of 12 isolates) and 14 weeks (in 6 of 11 isolates) after the accident. Additional phylogenetic analysis showed high homology of nucleotide sequences between isolates obtained from the donor and isolates obtained from the recipient. In addition, the variants in the recipient's virus showed substantial genetic preservation in the course of acute resolving hepatitis.
CONCLUSIONS: These data suggested that a minor HCV variant from a donor was transmitted to the recipient through a needlestick injury and that it prevailed as the dominant species. The preserved genetic homogeneity of the transmitted viral variants in patients with acute HCV infection may account for their clinical outcomes of resolving hepatitis.
METHODS: To demonstrate how HCV quasi species are transmitted and adapt to the new host in acute resolving infection, we analyzed the nucleotide and deduced amino acid sequences of the hypervariable region 1 (HVR-1) in the E2 domain of HCV in both the source of the virus ("donor") and the person who received the virus through a needlestick accident ("recipient"). In addition, we also performed phylogenetic analysis of HCV quasi species in these patients to document the viral transmission.
RESULTS: We obtained a total of 33 clones at different time points by using polymerase chain reaction amplification and cloning and sequencing of HVR-1. A predominant HVR-1 variant (in 4 of 10 isolates) in the donor was not present in the recipient 6 and 14 weeks after the accident. In contrast, a minor variant (in 1 of 10 isolates) in the donor became the predominant strain in the recipient 6 weeks (in 10 of 12 isolates) and 14 weeks (in 6 of 11 isolates) after the accident. Additional phylogenetic analysis showed high homology of nucleotide sequences between isolates obtained from the donor and isolates obtained from the recipient. In addition, the variants in the recipient's virus showed substantial genetic preservation in the course of acute resolving hepatitis.
CONCLUSIONS: These data suggested that a minor HCV variant from a donor was transmitted to the recipient through a needlestick injury and that it prevailed as the dominant species. The preserved genetic homogeneity of the transmitted viral variants in patients with acute HCV infection may account for their clinical outcomes of resolving hepatitis.
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