Selective transmission of hepatitis C virus genotypes and quasispecies in humans and experimentally infected chimpanzees.

This study determined whether selective transmission of hepatitis C virus (HCV) species occurred among human and chimpanzee recipients of contaminated blood products or plasma containing multiple genotypes, subgenotypes and quasispecies. Commercially prepared factor VIII concentrate (lot DO56), produced prior to HCV testing and inactivation, was subsequently found by direct cloning to contain the following subgenotypes: 1a and 1b (73 % of clones), 2a (13 % of clones), 2b (11 % of clones) and 3a (4 % of clones). A patient transfused with factor VIII concentrate DO56 was diagnosed with clinical non-A, non-B hepatitis and subsequently found to be infected with HCV subgenotype 1b. Among five chimpanzees inoculated experimentally with the same factor VIII concentrate, two were infected only with HCV subgenotype 1a and three were infected with approximately equivalent clonal proportions of subgenotypes 1a and 1b. HCV hypervariable region 1 (HVR1) quasispecies analysis of the DO56 factor VIII concentrate and a serum specimen from the single chimpanzee that developed a chronic HCV infection following inoculation with DO56 showed 0-56 % nucleotide variation. However, specimens from chimpanzees infected in the second to fourth passages of the DO56 inoculum had 0-8 % HVR1 quasispecies nucleotide variation. The high HVR1 quasispecies variation in the factor VIII concentrate and its first passage in chimpanzees indicates the presence of multiple HCV isolates, whereas the low variation in the second to fourth chimpanzee passages suggests transmission of a single HCV isolate. These findings strongly suggest selective transmission of HCV isolates during experimental chimpanzee infection and among humans exposed to multiple HCV species.

Hepatitis C virus transmission from an anesthesiologist to a patient.

BACKGROUND: An anesthesiologist was diagnosed as having acute hepatitis C 3 days after providing anesthesia during the thoracotomy of a 64-year-old man (patient A). Eight weeks later, patient A was diagnosed as having acute hepatitis C. METHODS: We performed tests for antibody to hepatitis C virus (HCV) on serum samples from the thoracotomy surgical team and from surgical patients at the 2 hospitals where the anesthesiologist worked before and after his illness. We determined the genetic relatedness of the HCV isolates by sequencing the quasispecies from hypervariable region 1. RESULTS: Of the surgical team members, only the anesthesiologist was positive for antibody to HCV. Of the 348 surgical patients treated by him and tested, 6 were positive for antibody to HCV. Of these 6 patients, isolates from 2 (patients A and B) were the same genotype (1a) as that of the anesthesiologist. The quasispecies sequences of these 3 isolates clustered with nucleotide identity of 97.8% to 100.0%. Patient B was positive for antibody to HCV before her surgery 9 weeks before the anesthesiologist's illness onset. The anesthesiologist did not perform any exposure-prone invasive procedures, and no breaks in technique or incidents were reported. He denied risk factors for HCV. CONCLUSIONS: Our investigation suggests that the anesthesiologist acquired HCV infection from patient B and transmitted HCV to patient A. No further transmission was identified. Although we did not establish how transmission occurred in this instance, the one previous report of bloodborne pathogen transmission to patients from an anesthesiologist involved reuse of needles for self-injection.