Researchers continue to unfold the curious link between HIV and GB Virus C (GBV-C).
“Every study that shows persistent [GBV-C] infection over time has shown a survival benefit to HIV co-infected patients. How does this work? Why does this virus improve survival among people with HIV? Can we use it therapeutically?” Jack T Stapleton, MD, of the University of Iowa posed these questions at a press conference at the 49th Annual Meeting of the Infectious Diseases Society of America in Boston Friday.
Discovered in 1995, GBV-C was formerly known as hepatitis G until they discovered it does not cause hepatitis nor does it seem to be responsible for any disease.
Building on previous research that has shown this “good virus” inhibits HIV replication and over time provides a survival benefit for those co-infected, Stapleton and his team of researchers have now discovered how much of the protein is required to inhibit HIV. They found that by looking at the GBV-C viral proteins, the envelope or the surface protein of the virus actually inhibits HIV if you inject it into cells or if you produce it inside cells. Simply introducing GBV-C outside of the HIV cell had no effect.
This research expands potential use of the GBV-C protein as an effective treatment that could be taken orally and would not contribute to antibiotic resistance.
“If we put this peptide on top of cells it does not inhibit, but if we introduce it inside the cell it does inhibit HIV,” Stapleton said. “We looked at how much of the protein was required to inhibit HIV by making a series of deletions…” to the string of amino acids, he said.
The team found that a 17 amino acid peptide inhibits HIV – but does not inhibit mumps or yellow fever, indicating there is some specificity to how long of a string of amino acids is needed.
“If you make a whole protein, you have to have multiple copies for the viral protein to inhibit HIV… If you adjust the peptide – you make it a little longer and get it into cells – then you see inhibition,” Stapleton said.
The researchers also found that if you produce the peptide in the cell it’s much more potent – a phenomenon they cannot explain at this point.
Expression of GBV-C E2 protein motifs in a CD4+ T cell line (Jurkat) inhibits HIV-1 entry and replication. [Full Abstract]