Serum contains virus inhibitors.. But which inhibitors.. I too am curious to know.

Hii,

I think it should be related with the inactivation of the trypsin by the FBS. In my knowledge, Human H1N1 wsn strain is the only known strain, to replicate in absence of trypsin.  It depends on your protocol whether there is any trypsin present or not. 

Thankyou.

Attachment of Influenza A virus require lysis of HA (Which is made up of 2 subunit HA1 & HA2) After lysis it will attached to sialic acid receptor to cell. for this TPCK Trypsin is required for lysis of HA subunit. If Serum is present in media it cause inactivation of TPCK Trypsin. Except in case of H5N1 which not require lysis of HA SUBUNIT  it will directly attached.

Yes, thank you very much everybody.  However, I am still wondering that why during the viral infection process, serum was absent in the medium besids at the beginning of viral attachment to the cells?  During entire experiment, serum was not present in the medium.

There's a bunch of reasons.

Yes, most strains of flu (excepting HPAI H5 and H7s and a handful of plasminogen-dependent strains) are largely trypsin (or other exogenous protease) dependent for replication in cell culture. This is to cleave the HA so it becomes fusion competent (not receptor-binding competent - that activity is present in the uncleaved trimer). So if you're growing a stock or performing a low MOI multicycle replication experiment, serum is left out to avoid inactivating the trypsin. If you're doing a single cycle/high MOI infection and you don't care about titreing what comes out, then serum can be added back after the adsorption period.

Serum is left out at the point of infection because it contains inhibitors - decoy receptor molecules and other factors. There's a whole load of ancient literature on this (PMID 18904216 is one of the first) and if anyone's interested they can Pubmed "influenza", "serum" and "inhibitor" and read from the bottom up. The inhibition was virus strain and serum species specific, and although I don't recall the story in detail, I suspect the "francis inhibitor" and "beta inhibitors" etc were a mix of different flavours of sialic acid mucoids as well as other protein-based inhibitors that we might now call collectins/defensins etc.

I think that some serum samples include plasminogen which can activate influenza virus reproduction in cells.

Thank you very much Paul.  Good answer to the question. It's awesome to know. It's getting clearer. 

Blood serum contains non-specific inhibitors which interfere with virus binding to cultured cells. As for HA activation, one use TPCK-trypsin which also might be inactivated by protease inhibitors (abundant in any serum).