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What has intrigued the scientific community is the more recently discovered relationship of GBV-C with HIV infection.
GBV-C replicates in CD[4.sup.+] T lymphocytes and other peripheral blood mononuclear cells, inhibiting HIV replication by inducing chemokines, downregulating HIV co-receptors and modulating cytokine profiles (30).
In summary, this commonly occuring flavivirus GBV-C has taken an unusual journey in recorded scientific literature from a candidate hepatitis virus to an innocent bystander to, possibly, a beneficial virus!
"GBV-C decreases the number of [available] receptors on the surface of a cell, and that limits the amount of HIV getting into cells" says Jack T.
The test-tube findings might explain why co infection with GBV-C inhibits HIV from disabling the immune system in HIV-positive people, Stapleton suggests.
After adjustment for treatment, baseline CD4 and T-cell counts, age, sex, race, and mode of transmission, the mortality difference was statistically significant; those without GBV-C infection were 3.7 times more likely to die as were those with the GBV-C, said Dr.
In a similar study, 197 HIV-positive patients were tested and 33 were found to be GBV-C RNA positive, 112 had detectable GBV-C antibodies, and 52 tested negative for GBV-C.
The authors have received requests for GBV-C that could be used therapeutically in HIV-infected patients, according to Dr.
Studies show distinct species of the GBV virus, named GBV-A, GBV-B, and GBV-C. Further studies show these species are not genotypes of HCV and that GBV-A and GBV-C are closely related.
A few studies had already indicated that GBV-C infection might slow HIV progression, says Jack T.
Among the 144 with GBV-C in their blood, 41 had died by the time the researchers analyzed the data.
The findings suggest that GBV-C hinders HIV replication, Stapleton says.