Infection with GB virus C and reduced mortality among HIV-infected patients.
BACKGROUND
The flavivirus GB virus C (GBV-C, also designated hepatitis G virus) was identified in a search for hepatitis viruses, but no disease is currently known to be associated with it. We investigated the relation between coinfection with GBV-C and the long-term outcome in patients infected with the human immunodeficiency virus (HIV).


METHODS
A total of 197 HIV-positive patients were followed prospectively beginning in 1993 or 1994. Of these patients, 33 (16.8 percent) tested positive for GBV-C RNA, 112 (56.9 percent) had detectable antibodies against the GBV-C envelope protein E2, and 52 (26.4 percent) had no marker of GBV-C infection and were considered unexposed. We assessed the relation between GBV-C infection and the progression of HIV disease. We also tested 169 GBV-C-positive plasma samples with a quantitative branched-chain DNA (bDNA) assay in order to investigate possible correlations between GBV-C viral load and both the CD4+ cell count and the HIV load.


RESULTS
Among the patients who tested positive for GBV-C RNA, survival was significantly longer, and there was a slower progression to the acquired immunodeficiency syndrome (AIDS) (P<0.001 for both comparisons). Survival after the development of AIDS was also better among the GBV-C-positive patients. The association of GBV-C viremia with reduced mortality remained significant in analyses stratified according to age and CD4+ cell count. In an analysis restricted to the years after highly active antiretroviral therapy became available, the presence of GBV-C RNA remained predictive of longer survival (P=0.02). The HIV load was lower in the GBV-C-positive patients than in the GBV-C-negative patients. The GBV-C load correlated inversely with the HIV load (r=-0.33, P<0.001) but did not correlate with the CD4+ cell count.


CONCLUSIONS
Coinfection with GBV-C is associated with a reduced mortality rate in HIV-infected patients. GBV-C is not known to cause any disease, but it is possible that its presence leads to an inhibition of HIV replication. However, GBV-C infection could also be a marker for the presence of other factors that lead to a favorable HIV response.
Tillmann
H L
HL
Department of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, Germany. tillmann@tx-amb.mh-hannover.de
Heiken
H
H
Knapik-Botor
A
A
Heringlake
S
S
Ockenga
J
J
Wilber
J C
JC
Goergen
B
B
Detmer
J
J
McMorrow
M
M
Stoll
M
M
Schmidt
R E
RE
Manns
M P
MP
D000328:Adult; D000914:Antibodies, Viral / Q000097:blood; D018791:CD4 Lymphocyte Count; D018450:Disease Progression; D005260:Female; D018067:Flaviviridae / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification; D006678:HIV / Q000302:isolation & purification; D015658:HIV Infections / Q000150:complications / Q000401:mortality* / Q000821:virology; D006525:Hepatitis, Viral, Human / Q000150:complications* / Q000821:virology; D006801:Humans; D008297:Male; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012367:RNA, Viral / Q000032:analysis; D016019:Survival Analysis; D019562:Viral Load; D014766:Viremia
D000914:Antibodies, Viral; D012367:RNA, Viral