Jedním z kandidátů na etiologické agens neobjasněných virových hepatitid (VHN) je od roku 1995 objevený virus GBV-C/HGV. U pacientů s VHN jsme zjistili v prvém odběru vysokou prevalenci virémie: 76,3 %, prokazovanou pozitivitou GBV-C/I3GV RNA. Porovnávali jsme ji se skupinami pacientů v hemodialyzačním programu (HD), kde byla 18,8 %, s hematoonkologickým onemocněním (BD): 25,6 % a s koinfekcí HBV a HCV (CI): 95,5 %. U opakovaně vyšetřovaných pacientů jsme také sledovali dynamiku virémie a protilátek s cflem objasnit průběh infekce. Závažným zjištěním bylo časté vymizení virémie, po 6,5 měsících, pozorované ve všech skupinách. Nejčastěji u VHN, v 55,9 % případů, u HD v 7,8 %, BD v 12,1 % a CI v 36,4 %. Vymizení virémie nemusí znamenat clearance viru, ale může signalizovat přechod GBV-C/I3GV do stavu perzistence bez diagnostikovatelných markerů infekce, s možností exacerbace virové replikace. Časté vymizení virémie, společně s jejím vysokým nálezem v prvém odběru u VHN, oproti ostatním skupinám, tak podporuje hypotézu úzké kauzální souvislosti virémie GBV-C/HGV s klinickými projevy infekce. U akutních průběhů, s obrazem VHN, GBV-C/I3GV RNA pozitivitou a elevací transamináz, je tak vysoká pravděpodobnost probíhající infekce GBV-C/HGV.

For etiologically obscure (some 4%) víral hepatitis agens are sought and tested to make elucidation of their cause possible. One of the candidates is since 1995 the netyly discovered virus GBV-C/HGV. Despite intense research its relationship to víral hepatitis of obscure origin (VHN) has not been elucidated so far. In the submitted paper the authors attempted to contribute to the elucidation of etiologickl associations of GBV-C/HGV infection and VHN by comparing the dynamics of markers of the infection in a group of 59 patients with VHN, two control groups exposed to a high risk of parenteral operations and a third comparative group. The hrst control group comprised 64 patients in a long-term haemodialyzation programme (HD), the second group was formed by 82 patients with haematooncological disease (BD). The third comparative group comprised 22 patients coinfected (CI) with virus of hepatitis C (VHC), or possibly hepatitis B (VHB). The patients with VHN were HBsAg, anti HCV and anti HEV negative. In the majority in the hrst blond sample transaminases were elevated which was one of the main reasons for examination of GBV-C/HGV RNA. Prevalence of GBV-C/HGV infection, proved by the presence of at least one of the two markers of current or past infection (GBV-C/HGV RNA, antiGBV-C/HGV) was in the comprred VHN, HD and BD groups as follows: SS.1%, 59.4% and 43.9%. The frequency of GBV-C/HGV positivity was highest in VHN - 76.3%. In control groups HD and BD GBV-C/HGV RNA positivity was substantially lower, 18.8% and 25.6% resp. Long-term continuous viraemia was recorded in patients with VHN in 18.6%. In groups HD and BD it was half that value: 9.3% and 9.18%. In patients with VHN surprisingly after 6.5 months a marked rise of negative findings occurred (5.6x) without the expected increase of antibodies. A similar finding was recorded also in the other groups (HD and BD), incl. CI patients. Disappearance of viraemia was observed most frequently in VHN (55.9%). In groups HD and BD GBV-C/HGV RNA disappeared only in 7.8% and 12.1% resp. In treated patients of the CI group víral RNA was present in 45.5% and fit disappeared in 36.4%. On the other hand, seroconversion to antibodies was comparable in VHN, HD and BD (11.9%, 9.4%, 8.5%), only in group CI fit was higher (18.2%), obviously in conjunction with treatment of concurrent HCV or HBV infection. Disappearance of viraemia without subsequent seroconversion occurs in GBV-C/I3GV infection frequently, the highest rate was observed by the authors in patients with VHN. Disappearance of viraemia does not necessarily imply clearance of GBV-C/HGV but may be due to a change of GBV-C(HGV finto a state of persistence without positive laboratory markers of the infection. Persistence of the virus could also be the reason of the assumed conditioned pathogenicity of the virus, and the effect of frequent disappearance of both markers could explain some controversial epidemiological observations when in studies only static data without dynamit associations esere used.

Státní zdravotní ústav Praha 10

New virus GBV-C/HGV, one of the possible causal agents of hepatitis with an obscure etiology

Nový virus GBV-C/HGV jako jeden z možných původců etiologicky nevyjasněných hepatitid = New virus GBV-C/HGV, one of the possible causal agents of hepatitis with an obscure etiology /

Lit: 49

Souhrn: eng