# Mouse cytomegalovirus lacking sgg1 shows reduced import into the salivary glands

## TL;DR

This study shows that the sgg1 gene in mouse cytomegalovirus is important for the virus to enter salivary glands through infected myeloid cells.

## Contribution

The study reveals a specific role for the sgg1 gene in salivary gland colonization by MCMV, distinct from other tropism genes.

## Key findings

- A sgg1 null mutant is defective in infected myeloid cell entry into the salivary glands.
- The sgg1 gene plays a unique role in salivary gland colonization compared to MCK-2.
- Salivary gland colonization involves a complex, multi-step process.

## Abstract

Cytomegaloviruses (CMVs) transmit via chronic shedding from the salivary glands. How this relates to the broad cell tropism they exhibit in vitro is unclear. Human CMV (HCMV) infection presents only after salivary gland infection is established. Murine CMV (MCMV) is therefore useful to analyse early infection events. It reaches the salivary glands via infected myeloid cells. Three adjacent spliced genes designated as m131/129 (MCK-2), sgg1 and sgg1.1, positional homologues of the HCMV UL128/130/131 tropism determinants, are implicated. We show that a sgg1 null mutant is defective in infected myeloid cell entry into the salivary glands, a phenotype distinct from MCMV lacking MCK-2. These data point to a complex, multi-step process of salivary gland colonization.