Replication of merkel cell polyomavirus induces reorganization of promyelocytic leukemia nuclear bodies
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Replication of merkel cell polyomavirus induces reorganization of promyelocytic leukemia nuclear bodies. / Neumann, Friederike; Czech-Sioli, Manja; Dobner, Thomas; Grundhoff, Adam; Schreiner, Sabrina; Fischer, Nicole.
In: J GEN VIROL, Vol. 97, No. 11, 11.2016, p. 2926-2938.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Replication of merkel cell polyomavirus induces reorganization of promyelocytic leukemia nuclear bodies
AU - Neumann, Friederike
AU - Czech-Sioli, Manja
AU - Dobner, Thomas
AU - Grundhoff, Adam
AU - Schreiner, Sabrina
AU - Fischer, Nicole
PY - 2016/11
Y1 - 2016/11
N2 - Merkel cell polyomavirus (MCPyV) is associated with Merkel cell carcinoma (MCC), a rare but aggressive skin cancer. The virus is highly prevalent: 60-80% of adults are seropositive; however, cells permissive for MCPyV infection are unknown. Consequently, very little information about the MCPyV life cycle is available. Until recently, MCPyV replication could only be studied using a semi permissive in vitro replication system, which we and others previously published. MCPyV replication most likely depends on subnuclear structures such as PML nuclear bodies, which are known to play regulatory roles in the infection of many DNA viruses. Here, we investigate promyelocytic leukemia nuclear bodies (PML-NB) components as candidate host factors to control MCPyV DNA replication. We show that PML-NBs change in number and size in cells actively replicating MCPyV proviral DNA. We observe a significant increase in PML-NBs in cells positive for MCPyV viral DNA replication. Interestingly, a significant amount of cells actively replicating MCPyV does not show any Sp100 expression. While PML and Daxx have no effect on MCPyV DNA replication, MCPyV replication is increased in cells depleted for Sp100 highly suggesting that Sp100 is a negative regulator of MCPyV DNA replication.
AB - Merkel cell polyomavirus (MCPyV) is associated with Merkel cell carcinoma (MCC), a rare but aggressive skin cancer. The virus is highly prevalent: 60-80% of adults are seropositive; however, cells permissive for MCPyV infection are unknown. Consequently, very little information about the MCPyV life cycle is available. Until recently, MCPyV replication could only be studied using a semi permissive in vitro replication system, which we and others previously published. MCPyV replication most likely depends on subnuclear structures such as PML nuclear bodies, which are known to play regulatory roles in the infection of many DNA viruses. Here, we investigate promyelocytic leukemia nuclear bodies (PML-NB) components as candidate host factors to control MCPyV DNA replication. We show that PML-NBs change in number and size in cells actively replicating MCPyV proviral DNA. We observe a significant increase in PML-NBs in cells positive for MCPyV viral DNA replication. Interestingly, a significant amount of cells actively replicating MCPyV does not show any Sp100 expression. While PML and Daxx have no effect on MCPyV DNA replication, MCPyV replication is increased in cells depleted for Sp100 highly suggesting that Sp100 is a negative regulator of MCPyV DNA replication.
U2 - 10.1099/jgv.0.000593
DO - 10.1099/jgv.0.000593
M3 - SCORING: Journal article
C2 - 27580912
VL - 97
SP - 2926
EP - 2938
JO - J GEN VIROL
JF - J GEN VIROL
SN - 0022-1317
IS - 11
ER -
