Almost one century ago, in 1917, the Austrian neurologist Julius Wagner von Jauregg was able to obtain improvement in patients with late stage symptomatic neurosyphilis, by infecting them with the malaria parasite. This approach might appear strange to physicians in the contemporary era of antimicrobial treatment. However, at that time it was by far the most effective option and it earned its discoverer the Nobel Prize for Medicine in 1927. Thus, even an infection with obligatory pathogens may result in harm reduction under certain conditions. GB virus C is a flavivirus that is closely related to hepatitis C virus. The name GB virus stems from early experiments on the transmission of acute hepatitis from humans to marmoset monkeys. One of the first source patients had the initials "G.B." and was a 34-year old colleague of the author of the experiment (Deinhardt 1967). Later on, two hepatotropic viruses, GB virus A (GBV-A) and GB virus B (GBV-B), were isolated from these monkeys. Two independent research groups simultaneously discovered the related GB virus C (GBV-C) in humans with hepatitis in the middle of the 1990s. Subsequently, the GB virus C has promoted the discussion as to whether the natural course of HIV infection might be modulated in a favorable way by this particular coinfection. In addition, because GBV-C was first found in humans with hepatitis, and due to its close relationship to the hepatitic GBV-A and GBV-B viruses, GBV-C was also called "hepatitis G virus (HGV)" by one research group. This name should no longer be used, because it has since been shown that GBV-C neither causes hepatitis nor worsens preexisting hepatitis (Berenguer 1996, Tillmann 1998, Rambusch 1998, Stark 1999). In fact, GBV-C is not a hepatotropic but a lymphotropic virus. Despite intensive research, GBV-C has not been shown to cause any other known disease.
The virus can be found in six different genotypes (Muerhoff 2006) and it is frequently and worldwide found in humans: approximately 10 to 40 % of blood donors have specific antibodies against GBV-C and up to 5 % of them show GBV-C virus replication. Assuming that the virus is apathogenic, affected individuals are not excluded from the donation of blood and consequently, serological diagnostics on GBV-C are not routinely performed. Two serological markers for GBV-C infection exist: GBV-C viremia is determined using a PCR method; and antibodies to the envelope region E2 (anti-E2) are detected by ELISA. As they are mutually exclusive, either GBV-C viremia or the presence of anti-E2 is detectable in GBV-C infected individuals. In most cases, GBV-C viremia is transient and ends with sero-conversion to anti-E2, resulting in immunity to new infections. However, this does not seem to be a lifelong immunity (Table 1). Transmission of GBV-C occurs par-enterally and mucosally, thus similar to HIV, HBV and HCV infections.
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