What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2013 April 26
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

View complete results in PubMed (results may change over time).

Edit saved search settings, or unsubscribe from these e-mail updates.

PubMed Results

Items 1 - 2 of 2

1.	Science. 2013 Apr 12;340(6129):207-11. doi: 10.1126/science.1235214. Persistent LCMV infection is controlled by blockade of type I interferon signaling. Teijaro JR, Ng C, Lee AM, Sullivan BM, Sheehan KC, Welch M, Schreiber RD, de la Torre JC, Oldstone MB. Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA. Comment in Immunology. An interferon paradox. [Science. 2013] Immunology. An interferon paradox.Odorizzi PM, Wherry EJ. Science. 2013 Apr 12; 340(6129):155-6. Abstract During persistent viral infections, chronic immune activation, negative immune regulator expression, an elevated interferon signature, and lymphoid tissue destruction correlate with disease progression. We demonstrated that blockade of type I interferon (IFN-I) signaling using an IFN-I receptor neutralizing antibody reduced immune system activation, decreased expression of negative immune regulatory molecules, and restored lymphoid architecture in mice persistently infected with lymphocytic choriomeningitis virus. IFN-I blockade before and after establishment of persistent virus infection resulted in enhanced virus clearance and was CD4 T cell-dependent. Hence, we demonstrate a direct causal link between IFN-I signaling, immune activation, negative immune regulator expression, lymphoid tissue disorganization, and virus persistence. Our results suggest that therapies targeting IFN-I may help control persistent virus infections.
	PMID: 23580529 [PubMed - indexed for MEDLINE]
	Related citations

2.	Science. 2013 Apr 12;340(6129):199-202. doi: 10.1126/science.1235047. Latency-associated degradation of the MRP1 drug transporter during latent human cytomegalovirus infection. Weekes MP, Tan SY, Poole E, Talbot S, Antrobus R, Smith DL, Montag C, Gygi SP, Sinclair JH, Lehner PJ. Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK. Abstract The reactivation of latent human cytomegalovirus (HCMV) infection after transplantation is associated with high morbidity and mortality. In vivo, myeloid cells and their progenitors are an important site of HCMV latency, whose establishment and/or maintenance require expression of the viral transcript UL138. Using stable isotope labeling by amino acids in cell culture-based mass spectrometry, we found a dramatic UL138-mediated loss of cell surface multidrug resistance-associated protein-1 (MRP1) and the reduction of substrate export by this transporter. Latency-associated loss of MRP1 and accumulation of the cytotoxic drug vincristine, an MRP1 substrate, depleted virus from naturally latent CD14(+) and CD34(+) progenitors, all of which are in vivo sites of latency. The UL138-mediated loss of MRP1 provides a marker for detecting latent HCMV infection and a therapeutic target for eliminating latently infected cells before transplantation.
	PMID: 23580527 [PubMed - indexed for MEDLINE]
	Related citations