Specialization to cell-free or cell-associated spread by BAC-cloned HCMV strains not determined by the UL128-131 and RL13 loci
Specialization to cell-free or cell-associated spread by BAC-cloned HCMV strains not determined by the UL128-131 and RL13 loci
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不由 UL128-131 和 RL13 位点决定的 BAC 克隆 HCMV 毒株的无细胞或细胞相关传播的专门化
DOI:
10.1101/760611
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发表时间:
2019
期刊:
影响因子:
--
通讯作者:
Brent J. Ryckman
中科院分区:
文献类型:
--
作者:
E. Schultz;J. Lanchy;L. Z. Day;Q. Yu;Christopher Peterson;Jessica Preece;Brent J. Ryckman
A widely held view is that clinical isolates of human cytomegalovirus (HCMV) are cell-associated and that mutations affecting the UL128-131 and RL13 loci arise during subsequent passage in culture and lead to the appearance of a cell-free spread phenotype. To distinguish the factors influencing cell-associated and cell-free spread, we analyzed the spread characteristics of three HCMV BAC-clones; Merlin (ME), which expresses high levels of UL128-131 and harbors a frameshift mutation within RL13, and TB40/e (TB) and TR, which are both low in UL128-131 and intact at RL13. Quantitation of the number of newly infected cells over 12 days by flow cytometry revealed remarkably similar spread efficiencies in fibroblasts among strains. However, comparing the inhibition of spread by neutralizing antibodies and the quantities and infectivity of progeny virus indicated that TB and TR spread was predominately cell-free, whereas spread of ME was predominantly cell-associated. While transcriptional repression of UL128-131 greatly enhanced cell-free spread by ME, the efficiency of the cell-associated mode was not affected. Spread in epithelial cultures was highly cell-associated for all strains, and ME was the most efficient. Repression of UL128-131 reduced the efficiency of ME spread in epithelial cells, but did not affect the predominate mode of spread. Spread in RL13-expressing cells was comparably reduced for all strains, and more pronounced in fibroblasts than in epithelial cells. RL13 effects could not be clearly explained by changes in production, release, or infectivity of progeny virus, and there were no changes to the proclivity of strains for cell-free or cell-associated spread. In sum, the specialization of HCMV strains to cell-free spread is linked to the quantity and infectivity of cell-free progeny, which can be influenced by UL128-131 levels, but the cell-associated specialist phenotype is likely determined by factors beyond the UL128-131 or RL13 loci. AUTHOR SUMMARY Experimental distinctions between cell-free and cell-associated modes of spread for HCMV have been largely relativistic. When cell-free spread is inhibited by neutralizing antibodies, or if particular strain of virus is poor at cell-free spread, then the observed spread may be simply defined as “cell-associated”. However, such a view does not easily lend towards analysis of the efficiency of cell-associated spread or the factors involved. In our study, we measured the kinetics of HCMV cell-free and cell-associated spread as independent processes and show evidence that HCMV strains can be highly specialized to one or the other mode of spread. The genetic factors that determine specialization for mode of spread are unclear, but given the genetic diversity of HCMV circulating in human populations, it seems likely that both modes of are represented. The efficacy of intervention approaches is likely affected by the mode of spread. For example, neutralizing antibodies are less effective to limit cell-associated spread. Our results provide a conceptual approach to evaluating intervention approaches such as neutralizing antibodies raised by vaccine candidates and drug compounds that target viral replication processes for their ability to limit cell-free or cell-associated modes of spread as independent processes.
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DOI:
10.1126/science.1227919
发表时间:
2012-11-23
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Stern-Ginossar N;Weisburd B;Michalski A;Le VT;Hein MY;Huang SX;Ma M;Shen B;Qian SB;Hengel H;Mann M;Ingolia NT;Weissman JS
通讯作者:
Weissman JS
影响因子:
6.7
作者:
Wagner FM;Brizic I;Prager A;Trsan T;Arapovic M;Lemmermann NA;Podlech J;Reddehase MJ;Lemnitzer F;Bosse JB;Gimpfl M;Marcinowski L;MacDonald M;Adler H;Koszinowski UH;Adler B
通讯作者:
Adler B
DOI:
10.1056/nejm198304213081603
发表时间:
1983
期刊:
The New England journal of medicine
影响因子:
--
作者:
Chou,S;Merigan,TC
通讯作者:
Merigan,TC
DOI:
10.1007/978-1-4939-1875-1_3
发表时间:
2015
期刊:
Methods in molecular biology (Clifton, N.J.)
影响因子:
--
作者:
Rooney, John P;Ryde, Ian T;Sanders, Laurie H;Howlett, Evan H;Colton, Meryl D;Germ, Kaylyn E;Mayer, Greg D;Greenamyre, J Timothy;Meyer, Joel N
通讯作者:
Meyer, Joel N
影响因子:
5.4
作者:
Yunis J;Farrell;Lawler;Davis-Poynter;Brizić;Jonjić;Stevenson
通讯作者:
Stevenson