Murine Cytomegalovirus exploits olfaction to enter new hosts

Farrell, Helen E., Lawler, Clara, Tan, Cindy S. E., MacDonald, Kate, Bruce, Kimberley, Mach, Michael, Davis-Poynter, Nick and Stevenson, Philip G. (2016) Murine Cytomegalovirus exploits olfaction to enter new hosts. mBio, 7 2: e00251-16.1-e00251-16.10. doi:10.1128/mBio.00251-16

Author Farrell, Helen E.
Lawler, Clara
Tan, Cindy S. E.
MacDonald, Kate
Bruce, Kimberley
Mach, Michael
Davis-Poynter, Nick
Stevenson, Philip G.
Title Murine Cytomegalovirus exploits olfaction to enter new hosts
Journal name mBio   Check publisher's open access policy
ISSN 2150-7511
Publication date 2016-04-26
Sub-type Article (original research)
DOI 10.1128/mBio.00251-16
Open Access Status DOI
Volume 7
Issue 2
Start page e00251-16.1
End page e00251-16.10
Total pages 10
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2017
Language eng
Formatted abstract
Viruses transmit via the environmental and social interactions of their hosts. Herpesviruses have colonized mammals since their earliest origins, suggesting that they exploit ancient, common pathways. Cytomegaloviruses (CMVs) are assumed to enter new hosts orally, but no site has been identified. We show by live imaging that murine CMV (MCMV) infects nasally rather than orally, both after experimental virus uptake and during natural transmission. Replication-deficient virions revealed the primary target as olfactory neurons. Local, nasal replication by wild-type MCMV was not extensive, but there was rapid systemic spread, associated with macrophage infection. A long-term, transmissible infection was then maintained in the salivary glands. The viral m131/m129 chemokine homolog, which influences tropism, promoted salivary gland colonization after nasal entry but was not required for entry per se. The capacity of MCMV to transmit via olfaction, together with previous demonstrations of experimental olfactory infection by murid herpesvirus 4 (MuHV-4) and herpes simplex virus 1 (HSV-1), suggest that this is a common, conserved route of mammalian herpesvirus entry. IMPORTANCE Cytomegaloviruses (CMVs) infect most mammals. Human CMV (HCMV) harms people with poor immune function and can damage the unborn fetus. It infects approximately 1% of live births. We lack a good vaccine. One problem is that how CMVs first enter new hosts remains unclear. Oral entry is often assumed, but the evidence is indirect, and no infection site is known. The difficulty of analyzing HCMV makes related animal viruses an important source of insights. Murine CMV (MCMV) infected not orally but nasally. Specifically, it targeted olfactory neurons. Viral transmission was also a nasal infection. Like HCMV, MCMV infected cells by binding to heparan, and olfactory surfaces display heparan to incoming viruses, whereas most other mucosal surfaces do not. These data establish a new understanding of CMV infections and a basis for infection control.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
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Created: Fri, 06 May 2016, 10:04:47 EST by Mrs Louise Nimwegen on behalf of School of Chemistry & Molecular Biosciences