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. 2008 Dec 24;83(5):2178–2187. doi: 10.1128/JVI.01787-08

TABLE 1.

Repression of IFN-induced IRF7 mRNA segregates with the T1L M1 and S2 gene segments and is associated with induction of myocarditis

Virusb Reovirus gene segments and proteinsa
Myocarditise
Outer capsid
Core
Nonstructural
S1 S4 M2 S2c M1d L1 L2 L3 S3 M3
E3 3 3 1 3 3 3 3 3 3 3
EW26 1 1 3 3 1 3 3 1 1 1
EW50 1 3 3 3 3 1 1 1 3 3
DB93A 1 1 3 3 3 1 3 3 1 3
EW29 3 1 1 3 3 3 3 1 1 1
T3D 3 3 3 3 3 3 3 3 3 3
DB95 3 3 3 3 3 1 3 3 1 3
EW43 3 1 1 1 3 3 3 1 3 1
3HA1 1 3 3 3 3 3 3 3 3 3 ND
DB181 1 3 3 1 1 1 1 1 1 1 +
EW89 3 1 3 3 1 1 3 1 1 3 +
EW60 1 1 3 1 1 1 1 1 1 1 +
EW100 3 1 3 1 1 3 3 1 3 3 +
T1L 1 1 1 1 1 1 1 1 1 1 +/−
8B 3 1 3 1 1 1 1 1 1 1 +
1HA3 3 1 1 1 1 1 1 1 1 1 ND
a

1, derivation from T1L; 3, derivation from T3D. Results from Fig. 2 were used for a nonparametric Kruskal-Wallis analysis to identify reovirus genes associated with inhibition of IFN signaling. P values for method A and method B (Fig. 2) at each of the two IFN doses were >0.05 (not significant) for all genes other than S2 and M1.

b

Viruses are listed in the same order as in Fig. 2.

c

T1L S2 is associated with inhibition of IFN signaling. Method A, P = 0.003 (1,000 U IFN) and P = 0.012 (100 U IFN). Method B, P = 0.007 (1,000 U IFN) and P = 0.039 (100 U IFN).

d

T1L M1 is associated with inhibition of IFN signaling. Method A, P = 0.006 (1,000 U IFN) and P = 0.006 (100 U IFN). Method B, P = 0.025 (1,000 U IFN) and P > 0.05 (100 U IFN).

e

Viruses are designated as myocarditic (+) or nonmyocarditic (−) based on references 60 and 61. ND, not determined. Induction of myocarditis is associated with inhibition of IFN signaling. Method A, P = 0.004 (1,000 U IFN) and P = 0.004 (100 U IFN). Method B, P = 0.004 (1,000 U IFN) and P = 0.004 (100 U IFN).