Whereas oncogenic retroviruses are common in animals, human T-lymphotropic virus 
1 (HTLV-1) is the only transmissible retrovirus associated with cancer in humans 
and is etiologically linked to adult T-cell leukemia. The leukemogenesis process 
is still largely unknown, but relies on extended survival and clonal expansion 
of infected cells, which in turn accumulate genetic defects. A common feature of 
human tumor viruses is their ability to stimulate proliferation and survival of 
infected pretumoral cells and then hide by establishing latency in cells that 
have acquired a transformed phenotype. Whereas disruption of the DNA repair is 
one of the major processes responsible for the accumulation of genomic 
abnormalities and carcinogenesis, the absence of DNA repair also poses the 
threat of cell-cycle arrest or apoptosis of virus-infected cells. This study 
describes how the HTLV-1 p30 viral protein inhibits conservative homologous 
recombination (HR) DNA repair by targeting the MRE11/RAD50/NBS1 complex and 
favors the error-prone nonhomologous-end-joining (NHEJ) DNA-repair pathway 
instead. As a result, HTLV-1 p30 may facilitate the accumulation of mutations in 
the host genome and the cumulative risk of transformation. Our results provide 
new insights into how human tumor viruses may manipulate cellular DNA-damage 
responses to promote cancer.