English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Cytomegaloviruses (CMVs) are large, complex pathogens that persistently and systemically colonize most mammals. Human cytomegalovirus (HCMV) causes congenital harm, and has proved hard to control. One problem is that key vaccine targets - virus entry and spread in naive hosts - remain ill-defined. As CMVs predate human speciation, those of other mammals can provide new insight. Murine CMV (MCMV) enters new hosts via olfactory neurons. Like HCMV it binds to heparan, which is lacking from most differentiated apical epithelia but is displayed on olfactory neuronal cilia. It then spreads via infected dendritic cells (DCs), which migrate to draining lymph nodes (LNs), rejoin the circulation by entering high endothelial venules (HEVs), and extravasate into other tissues. This migration depends quantitatively on M33, a constitutively active viral G protein-coupled receptor (GPCR). The homologous US28 GPCR of HCMV can substitute for M33 in allowing MCMV-infected DCs to leave LNs via HEVs, so HCMV could potentially use the same route. The capacity of DCs to seed MCMV to tissues, and for other DCs to collect it for redistribution, suggest that DC recirculation chronically maintains and links diverse CMV reservoirs through lytic exchange.

Cytomegalovirus host entry and spread