Uloga virusa u nastanku malignih tumora kod ljudi

Procjenjuje se da virusne infekcije pridonose nastanku 15 – 20 % svih malignih tumora ljudi. Kao obligatorni intracelularni paraziti, virusi kodiraju proteine koji reprogramiraju signalne puteve odgovorne za kontrolu proliferacije, diferencijacije, smrti stanice, genomskog integriteta, kao i prepoznavanja od strane imunološkog sustava. Virusni sustavi podržavaju koncept da je za razvoj tumora potrebna akumulacija međusobno povezanih događaja. Virusi koji su do sada prihvaćeni kao etiološki čimbenici ljudskih malignoma uključuju hepatitis B virus, Epstein-Barr virus, humani papiloma virus, virus leukemije ljudskih T-stanica, hepatitis C virus, te još nekoliko ljudskih onkogenih virusa. Obično protekne niz godina od infekcije do razvoja tumora i većina inficiranih osoba ne razvije rak, iako imunološki kompromitirane osobe pokazuju veći rizik za nastanak tumora povezanih s virusima. Malo je vjerojatno da je virus sam dovoljan da transformira normalnu stanicu u tumorsku. Vjerojatnija je mogućnost da kombinirano djelovanje virusnih proteina i mutacije staničnih gena zajedno vode tumorogenezi.
It is estimated that viral infections contribute to 15-20 % of all human cancers. As obligatory intracellular parasites, viruses encode proteins which reprogramme host cellular signalling pathways which in turn control proliferation, differentiation, cell death, genomic integrity, and recognition by the immune system. Viral systems support the concept that cancer development occurs by accumulation of multiple cooperating events. Viruses are now accepted as etiologic factors of human cancer, and include hepatitis B virus, Epstein-Barr virus, human papillomaviruses, human T-cell leukemia virus and hepatitis C virus, plus several candidate human cancer viruses. Many years may pass between initial infection and tumor appearance. Most infected individuals do not develop cancer, although immunocompromised individuals are at elevated risk of viral-associated cancers. It is unlikely that a tumor virus is sufficient to convert a normal cell to a tumor cell. Rather, a combination of the action of viral proteins and cellular gene mutation cooperate to drive tumorogenesis.