Journal of Virology, July 2007, p. 7328, Vol. 81, No. 13
0022-538X/07/$08.00+0 doi:10.1128/JVI.00880-07
| AUTHOR'S CORRECTION |
Department of Microbiology, School of Dental Medicine, and Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Volume 81, no. 10, p. 5102-5111, 2007. Just prior to publication, we discovered that the L72A mutant clone used in our study contained an additional mutation in gH2 (F163L). It is unclear at this time whether the structural and functional defect we see with our clone is due to the F163L mutation, the L72A mutation, or a combination of the two amino acid changes. This finding does not diminish the fact that the other mutations to the N-terminal region of gH2 described in this paper (
64,
72,
48-71,
48-63,
62-72, and L66A) affect gH/gL function. F163 lies in an unstudied region of gH2. We are addressing this issue.
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