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Volume 16, Number 9—September 2010

Dispatch

KI and WU Polyomaviruses and CD4+ Cell Counts in HIV-1–infected Patients, Italy

Muhammed Babakir-Mina, Massimo Ciccozzi, Francesca Farchi, Massimiliano Bergallo, Rossana Cavallo, Gaspare Adorno, Carlo Federico Perno, and Marco CiottiComments to Author 
Author affiliations: Author affiliations: Foundation University Hospital Tor Vergata, Rome, Italy (M. Babakir-Mina, G. Adorno, C.F. Perno, M. Ciotti); Istituto Superiore di Sanita’, Rome (M. Ciccozzi, F. Farchi); University of Turin, Turin, Italy (M. Bergallo, R. Cavallo)

Main Article

Figure

Maximum likelihood phylogenetic analysis of KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV) small T antigen sequences. Strains identified in this study are in boldface. The tree was rooted by using the midpoint rooting method. Branch lengths were estimated by using the best fitting nucleotide substitution (Hasegawa, Kishino, and Yano) model according to a hierarchical likelihood ratio test (6,7) and were drawn to scale. Scale bar indicates 0.8 nt substitutions per site. Asterisks along the b

Figure. Maximum likelihood phylogenetic analysis of KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV) small T antigen sequences. Strains identified in this study are in boldface. The tree was rooted by using the midpoint rooting method. Branch lengths were estimated by using the best fitting nucleotide substitution (Hasegawa, Kishino, and Yano) model according to a hierarchical likelihood ratio test (6,7) and were drawn to scale. Scale bar indicates 0.8 nt substitutions per site. Asterisks along the branches indicate significant statistical support for the clade subtending that branch (p<0.001 by the zero-branch-length test and bootstrap support >65%).

Main Article

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