Author: William Rodriguez; Aman Srivastav; Mandy Muller
Title: C19ORF66 broadly escapes viral-induced endonuclease cleavage and restricts Kaposi’s Sarcoma Associated Herpesvirus (KSHV) Document date: 2018_12_26
ID: 5a4i8v59_29
Snippet: Through knock down and overexpression assays, our data indicate that C19ORF66 is restricting 248 expression of KSHV early and delayed early genes, resulting in lower levels of viral reactivation 249 and reduced yield of infectious viral particles. C19ORF66 is known to be upregulated in 250 response to type I and type II IFNs (50,51) and to be upregulated in response to infection by a 251 number of unrelated viruses (35-42). Furthermore, C19ORF66 .....
Document: Through knock down and overexpression assays, our data indicate that C19ORF66 is restricting 248 expression of KSHV early and delayed early genes, resulting in lower levels of viral reactivation 249 and reduced yield of infectious viral particles. C19ORF66 is known to be upregulated in 250 response to type I and type II IFNs (50,51) and to be upregulated in response to infection by a 251 number of unrelated viruses (35-42). Furthermore, C19ORF66 was found to interact with the 252 NS3 protein of Hepatitis C Virus (52), localize to the replication complex of DENV [33], and 253 occasionally co-localize in the cytoplasmic compartment with HIV-1 Rev and Tat proteins (40), 254 pointing to a potential conserved role for C19ORF66 as a key player in the host-pathogen 255 response. While it is still unclear how C19ORF66 participates in the regulation of these viruses, 256
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