Imunobiologija virusne hepatitis C infekcije

Iako imunosni odgovor moţe očistiti HCV u potpunosti, izloţenost virusu često progredira u kroničnu infekciju.Kronične HCV infekcije povezane su sa deregulacijom uroĎene i stečene imunosti,antivirusne citotoksičnosti te apoptoze u jetrenom okolišu, štozajedno utječe na ishod infekcije, na odgovor na terapiju te doprinosi razvoju jetrene fibroze i ciroze. HCV ostvaruje tu imunosnu deregulaciju izbjegavanjem domaćinovoj uroĎenoj imunostiu više točaka čime sprječava učinkovitupočetnu koordinaciju imunosti koja stimulira cijeli imunosni odgovor, uključujući i stečenu imunost. Nedostatna funkcija imunosti dovodi do povećane replikacije virusa i doprinosi odrţanju infekcije. Unutar jetrenog mikrookoliša, više različitih tipova stanicadoprinosi imunosnom odgovoru prema HCV paoštećenje bilo kojeg aspekta uroĎenog odgovora od strane HCV-a moţe dovesti doneučinkovitog imunosnog odgovora, kako u mehanizmima prirodnog čišćenja tako i tijekom odstranjivanja virusa liječenjem, koji vodi u napredovanje jetrene bolesti. Potpuno razumijevanje mehanizama kojim virusnamodulacija imunosnog odgovora utječe na ishod infekcije zahtijeva definiranjespektra antivirusnih i imunomodulacijskih citokina koji reguliraju suradnju izmeĎurazličitihvrsta stanica unutar sloţenog jetrenog tkiva.Istraţivanja pokušavaju objasniti pojave i ključne čimbenike potrebne za uspješnu otpornost na HCV. Razvojem personalizirane medicine, ovaznanja mogu omogućiti individualno prilagoĎene terapije HCV-a na temeljupoznavanje reaktivnosti domaćina i virusnih genotipova. Razumijevanje ovihdetaljnih komponenti učinkovitog imunosnog odgovora na HCV na razini uroĎene i adaptivne imunosti biti će korisno za usmjeravanje razvojadugo ţeljenogcjepiva protiv HCV.Although the immune system can clear hepatitis C virus, infection oftencarries forward into a chronic phase. Chronic HCV is inducing dysregulation of adaptive and innate immune response, antiviral cytotoxicity and hepatocyte apoptosis in the liver, whichtogether reflects to a infection outcome and therapy efficassy and probablycontribute to hepatic fibrosis and cirrhosis. HCV achives thisimmune system dysregulation by escaping the host immune response at different points to inhibit the initial coordination of immunitythat induces the whole immune response, including adaptive, specific immunity,which anablesthe increase of the viral replication and contributes to establishment of chronic infection. Within the liver tissue environment, multiple immune cell typescontribute to the antiviral response toward HCV. A prevention of any part of the innate immune response by HCV could resultby an ineffective immunity, both in natural HCV clearance and virus clearance during the treatment, what could anable the infection to progress toa liverdisease. A full understanding of how viral modulationof immune system affects HCV infection outcome will require identification of the numerous antiviraland immunomodulatory cytokines that mediate the cross-talk betweenthe various immune and non-immune cell types within the complex hepatic tissue. Research to continue in these discoveries and developments are focused to reveal the key factors required for successful antiviral immunity to HCV. In the ongoing age of personalized medicine, this knowledge could lead to individually made HCV therapies based on knowledge of both viral strategiesand host characteristics. A detailed understanding of these components of an effective immunity to HCV at the non-specific and adaptive levels will be useful tool to guide the research development of the long-desired HCV vaccine