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 Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The evolutionary survival of viruses relies on their ability to disseminate infectious progeny to sites of transmission. The capacity to subvert apoptosis is thought to be crucial for ensuring efficient viral replication in permissive cells, but its role in viral dissemination in vivo has not been considered. We show here that the murine cytomegalovirus (MCMV) m38.5 protein specifically counters the action of Bax. As predicted from our biochemical data, the capacity of m38.5 to inhibit apoptosis is only apparent in cells unable to activate Bak. Deletion of m38.5 resulted in an attenuated growth of MCMV in vitro. In vivo replication of the Deltam38.5 virus was not significantly impaired in visceral organs. However, m38.5 played a central role in protecting leukocytes from Bax-mediated apoptosis, thereby promoting viral dissemination to the salivary glands, the principal site of transmission. These results establish that in vivo MCMV replication induces the activation of Bax in leukocytes, but not other permissive cells, and that MCMV interferes with this process to attain maximum dissemination.

Virally mediated inhibition of Bax in leukocytes promotes dissemination of murine cytomegalovirus