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Selective Ablation of Human T-Cell Lymphotropic Virus Type 1 p12I Reduces Viral Infectivity In Vivo
Nathaniel D. Collins,
Garret C. Newbound,
Björn Albrecht,
Jennifer L. Beard,
Lee Ratner, and
Michael D. Lairmore
From the Center for Retrovirus Research and the Department of
Veterinary Biosciences, The Ohio State University, Columbus, OH; the
Departments of Medicine, Pathology, and Molecular Microbiology,
Washington University School of Medicine, St Louis, MO; and the
Comprehensive Cancer Center, The Arthur James Cancer Hospital and
Research Institute, The Ohio State University, Columbus, OH.
Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic
agent of adult T-cell leukemia and HTLV-1-associated myelopathy. Novel,
yet conserved RNA transcripts encoded from open reading frames (ORFs) I
and II of the viral pX region are expressed both in vitro and in
infected individuals. The ORF I mRNA encodes the protein
p12I, which has been shown to localize to cellular
endomembranes, cooperate with bovine papillomavirus E5 in
transformation, as well as bind to the IL-2 receptor  and  chains
and the H+ vacuolar ATPase. It is unknown what role
p12I plays in the viral life cycle. Using an infectious
molecular clone of HTLV-1 (ACH) and a derivative clone,
ACH.p12I, which fails to produce the p12I
message, we investigated the importance of p12I in infected
primary cells and in a rabbit model of the infection. ACH.p12I was infectious in vitro as shown by viral passage
in culture and no qualitative or quantitative differences were noted
between ACH and ACH.p12I in posttransfection viral antigen
production. However, in contrast to ACH, ACH.p12I failed to
establish persistent infection in vivo as indicated by reduced
anti-HTLV-1 antibody responses, failure to demonstrate viral p19
antigen production in peripheral blood mononuclear cell (PBMC)
cultures, and only transient detection of provirus by polymerase chain
reaction in PBMC from ACH.p12I-inoculated rabbits. These
results are the first to show the essential role of HTLV-1
p12I in the establishment of persistent viral infection in
vivo and suggest potential new targets in antiviral strategies to
prevent HTLV-1 infection.
Blood, Vol. 91 No. 12 (June 15), 1998:
pp. 4701-4707
© 1998 by The American Society of Hematology.
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