Abstract(s)
In the course of previous works, it was observed that the virus laboratory stock (T3DS) differs in
sequence from the virus encoded by the ten plasmids currently in use in many laboratories
(T3DK), and derived from a different original virus stock. Seven proteins are affected by these
sequence differences. In the present study, replication of T3DK was shown to be more sensitive to
the antiviral effect of interferon. Infection by the T3DK virus was also shown to induce the
production of higher amount of β and α-interferons compared to T3DS. Two proteins, the μ2 and
λ2 proteins, were found to be responsible for increased sensitivity to interferon while both μ2 and
λ1 are responsible for increased interferon secretion. Altogether this supports the idea that
multiple reovirus proteins are involved in the control of induction of interferon and virus
sensitivity to the interferon-induced response. While interrelated, interferon induction and
sensitivity can be separated by defined gene combinations. While both μ2 and λ2 were
previously suspected of a role in the control of the interferon response, other proteins are also
likely involved, as first shown here for λ1. This also further stresses that due caution should be
exerted when comparing different virus isolates with different genetic background.