HepG2 cells (derived from HCC (hepatocellular carcinoma) tissue of 15 y American Caucasoid, who has died) contain Hemagglutinin-neuraminidase (Newcastle disease virus; NDV; -ssRNA) and HAdV (Human adenovirus; dsDNA virus; Packaging protein 3 (Late L1 52 kDa protein))/HIV (retrovirus of +ssRNA; Protein Rev and Gag-Pol polyprotein (with RT and IN) )/HCV (+ssRNA virus; Genome polyprotein with protease and RdRP) (see PDMD method, file HepG2 fucoidan).

Normal fetal hepatocyte Hc cells have no HAdV and NDV, but contain HIV-2 (Env polyprotein; no RT and IN) and HCV (Genome polyprotein with protease and RdRP).

Although this Hemagglutinin-neuraminidase is a sialidase protein of  -ssRNA virus of NDV, the proteins of NDV have disappeared by fucoidan treatment 0.102 mg/mL for three days (see file; HepG2 fucoidan).   Though, HIV-1 (Protein Nef)/HCV (Genome polyprotein without protease but with RdRP)/HAdV (DNA polymerase and Fiber protein) have been remained.

HCC tissue of the patient with PBC (Primary Biliary Cirrhosis) also contains Fusion glycoprotein (NDV) and Hemagglutinin-neuraminidase (NDV) with Nucleoprotein (FluB) and HAdV/HIV-1, HIV-2, SIV (Gag-Pol polyprotein with RT and IN)/HCV (Genome polyprotein with protease and RdRP), and this patient has died.

One LC (liver cirrhosis) tissue with leprosy contains Neuramindase (Influenza B virus; FluB; -ssRNA), and HAdV (Protein VI )/HCV (Genome polyprotein; with protease and RdRP), and this patient  has died.   There has been a retroviral protein of Serine/threonine-protein kinase-transforming protein Rmil (Avian rous-associated virus), but no HIV-1/HIV-2/SIV in this LC tissues, therefore the HIV-1/HIV-2/SIV is a marker of HCC tissue.    Neuramindase (FluB) is essential for this patient to die.

One HCC tissue (diagnosed as + HCV by clinical test) contains no protein of NDV, but contains SIV (Gag polyprotein; with RT and IN)/HCV (Genome polyprotein; with protease)/HAdV (Early E3B 14 KD protein and Fiber protein),  and this patient has survived.   He has Influenza A virus (FluA; Nucleoprotein and RNA-directed RNA polymerase subunit P2) and Influenza C virus (FluC; RNA-directed RNA polymerase subunit P3), but has no Neuramindase of Influenza B virus (FluB).   It is noteworthy that both NDV and FluB is not so independently  toxic to healthy persons. 

Therefore, co-expression of HIV-1 (Gag-Pol polyprotein; with RT and IN)/HCV (Genome polyprotein; with protease and RdRP)/HAdV/NDV (Hemagglutinin-neuraminidase) or  HIV-1 (Gag-Pol polyprotein; with RT and IN)/HCV (Genome polyprotein; with protease and RdRP)/HAdV/FluB (Neuramindase) seems to destine to die, but SIV/HIV-2/HCV/HAdV and no Neuramindase of NDV or FluB seems to destine to survive (see file; Feed by Measure,,).

By the way, I do not know how many passages of cell division has been occurred or has passed in the HepG2.

Furthermore, it is noteworthy that NDV and influenza B virus (FluB; -ssRNA) may induce the host metallo-aminopeptidase gene; i.e.,  Aminopeptidase PILS in HepG2 (-fucoidan; NDV) (when +fucoidan HepG2 does not produce aminopeptidase) and  Aminopeptidase N (GP150) in HCC tissue (with PBC; NDV) and in LC tissue (with Leprosy; FluB), respectively.

One survived patient (+HCV) has  Aminopeptidase N in HCC tissue (+Nucleoprotein of FluA, and +RdRP of FluA and FluC) may be induced by FluC, but has not in LC tissue (without FluC; +Neuraminidase of FluA).   This patient has no Neuraminidase in HCC tissue, but has Neuraminidase of FluA.

Therefore, this result indicates that the viral Neuraminidase of NDV or FluB and the Metallo-aminopeptidase of the host cell induced by NDV and FluB

co-operatively have induced the death of these three sadly deceased patients. 

 Thank you sir ,for your reply.