The
name of the
family Polyomaviridae, derives from the early
observation that
cells infected with
murine polyomavirus induced multiple (poly)
tumors (omas) in immunocompromised
mice. Subsequent studies showed that many members of this
family exhibit the capacity of
mediating cell transformation and
tumorigenesis in different
experimental models. The transformation process mediated by these
viruses is driven by viral pleiotropic regulatory
proteins called T (
tumor)
antigens.
Similar to other viral
oncoproteins T antigens target cellular regulatory factors to favor
cell proliferation,
immune evasion and
downregulation of
apoptosis. The first two
human polyomaviruses were isolated over 45 years ago. However, recent advances in the
DNA sequencing technologies led to the rapid identification of additional twelve new
polyomaviruses in different
human samples. Many of these
viruses establish
chronic infections and have been associated with conditions in immunosuppressed individuals, particularly in
organ transplant recipients. This has been associated to viral reactivation due to the
immunosuppressant therapy applied to these
patients. Four
polyomaviruses namely,
Merkel cell polyomavirus (MCPyV), Trichodysplasia spinulosa
polyomavirus (TSPyV), John Cunningham
Polyomavirus (JCPyV) and
BK polyomavirus (BKPyV) have been associated with the development of specific malignant
tumors. However, present evidence only supports the
role of MCPyV as a
carcinogen to
humans. In the present
review we present a summarized discussion on the current
knowledge concerning the
role of MCPyV, TSPyV, JCPyV and BKPyV in
human cancers.