Influenza virus viral protein production

One experimental tool in this direction is provided by some enveloped animal viruses which mature at the cell surface of infected cells (K Sri inen and Renkonen, 1977 Lenard, 1978). Such viruses include influenza virus, Semliki Forest virus (SFV), Sindbis virus, and vesicular stomatitis virus (VSV). They are extremely simple in makeup and hence are very well characterized. They can be tagged with biochemical probes in many different ways. They infect many animal cells in culture, and after infection turn the cells into factories for the production of virus progeny. The protein-synthesizing machinery of the host cell is programmed by the viral RNA to make viral proteins exclusively and these include the viral surface glycoproteins. These are synthesized with signal peptides and inserted into the ER membrane (Katz et ai, 1977 Garoff et... 

The degree of infection specifies the intracellular amount of viral protein and corresponds to the equivalent number of virus particles inside the cell assuming that a complete virus particle comprises 4000 viral proteins Ml and NP (3000 Ml/virion +1000 NP/virion [6]). Schulze-Horsel et al. [3] show that the intracellular amount of viral Ml and NP proteins is coupled linearly with the cell s fluorescence caused by immunostaining against influenza A virus Ml and NP. The uptake or production of 4000 viral Ml and NP proteins or 1 virus particle respectively will lead to an increase of Jby 1 the eelTs fluoreseence will increase by 2.66 FU/virion (fluorescence units, data not shown). 

Once inside the cell, the viral genome can elicit the help of the host cell s replication and protein biosynthesis capabilities in order to produce new copies of viral DNA or RNA, together with new structural proteins and essential enzymes. For the rhinoviruses (common cold viruses), their RNA is already able to function as a blueprint (messenger RNA, m-RNA) for protein production - they are termed RNA-(+)-viruses. The other major RNA viruses (e.g., influenza) have to make a complementary copy of their RNA before this can function as m-RNA - these are termed RNA-(—)-viruses. Whether the virus is (+) or (—), its m-RNA codes for an RNA polymerase, which controls the production of new copies of viral RNA. To ensure that the correct (+) or (—) form is made, the RNA polymerase first catalyses the production of a complimentary RNA strand - (+) requires a (—) strand and (—) requires a (+) strand, and then uses this as a template for the production of the complimentary (native) RNA form. 

As indicated above, these data do not tell us whether a function" is lacking in MDBK which is essential for viral protein or RNA synthesis, or whether a macromolecule is synthesized which prevents the translation of viral proteins or viral RNA synthesis. Since MDBK can be infected productively by other viruses (Bovine enterovirus, influenza), it must be a molecule specific for the mengo-MDBK cell interaction. The greatest enigma in our data is the origin of the early ENA replicase, since very little (or no) protein synthesis occurs. 

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