TABLE 1.

Paramyxovirus degradation of STAT1 and STAT2a

Cell lineSTATDegradation competence
HPIV2SV5
2fTGH (parent)1+
2+
U3A (STAT1 null)1NullNull
2
U3A + STAT1 (complemented)1+
2+
U3A + STAT1 Y701F1+
2+
U3A + STAT1 R602K1+
2+
U6A (STAT2 null)1
2NullNull
U6A + STAT2 (complemented)1++
2+
U6A + STAT2 Y690F1++
2+
U6A + STAT2 R601K1++
2+
U2A (IRF9 null)1+
2+
HEC-1B (IFNAR defect)1+
2+
U1A (Tyk2 null)1+
2+
U4A (Jak1 null)1+
2+
U6A + N1:C21
N1:C2
U6A + N2:C11++
N2:C1+
U3A + N1:C3N1:C3+
2+
U3A + N3:C1N3:C1
2
  • a 2fTGH cells are intact for all IFN signaling components, U1A, U2A, U3A, U4A, and U6A are IFN-unresponsive daughter lines. HEC-1B lacks high-affinity IFN-α/β receptors. STAT1 and STAT2 were detected by immunoblotting with specific antisera, and the chimeras were detected with anti-Flag antiserum. The ability of HPIV2 or SV5 infection to induce loss of STAT protein is indicated by + (degrades) or − (does not degrade). Cells infected at an MOI of ≥10 were assayed at 16 h postinfection.