New research shows that a protein made by a cancer-causing virus that was thought to be unimportant for its replication is in fact critically needed by the virus to initiate an infection and to reproduce.
The study examined the human T lymphotropic virus type 1 (HTLV-1) and a protein it makes called p13. The protein is one of the virus' so-called accessory proteins, proteins that earlier studies done in laboratory-grown cells suggested that the virus could live without.
But this new study – done using an animal model that the virus can infect – suggests that HTLV-1 needs the p13 protein to successfully infect the body and reproduce.
The research, published in the April 1 issue of the Journal of Virology, was led by scientists with The Ohio State University Cancer Program and OSU College of Veterinary Medicine.
“It is important to understand the function of these accessory molecules so we know if they should be incorporated into vaccines or targeted by new drugs as a way to prevent infection,” says principal investigator Michael Lairmore, professor and chair of veterinary biosciences and a member of the OSU Comprehensive Cancer Center.
“This viral protein is also important to study because it travels to the mitochondria of infected cells.” Mitochondria produce the cell's energy supply and store enzymes that carry out the process of natural cell death, or apoptosis.
“These findings should help us begin to learn whether this viral protein influences cell survival, perhaps by extending the life of the cell,” Lairmore says.
HTLV-1 infects an estimated 15 to 20 million people worldwide. About 5 percent of those infected develop adult T cell leukemia or lymphoma (ATLL), an aggressive disease characterized by a long latent period and the proliferation of T lymphocytes. The virus is spread by sexual activity, infected blood and breast milk.
For this study, Lairmore and a group of collaborators developed a mutant strain of HTLV-1 that lacked p13. The researchers then infected one batch of rabbit T cells with the mutant virus and a second batch of rabbit T cells with a strain of normal HTLV-1.
Last, they inoculated six rabbits with T cells infected with virus that lacked the p13 protein and six rabbits with T cells infected with the normal virus. (HTLV-1 spreads when an infected cell touches an uninfected cell.)
The rabbits inoculated with the virus lacking p13 remained uninfected, while all six rabbits receiving cells with normal HTLV-1 became infected.
“Our findings are the first to indicate that the HTLV-1 p13 protein plays an essential biological role during the early phase of virus infection in an animal model,” Lairmore says.
Next, the researchers will study the function of p13 in HTLV-1 infection, and how it affects mitochondria.
Funding from the National Cancer Institute and from the Fogarty Foundation, National Institutes of Health, supported this research.
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