ArticleJournal of virology2009
The M10 locus of murine gammaherpesvirus 68 contributes to both the lytic and the latent phases of infection.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Concerted action of gammaherpesvirus infection and moderate hyperoxia on lung structural development including effects on critical lung fibroblast functions in neonatal mice.Molecular and cellular pediatrics · 2026Article
- Targeting Host Metabolic and Epigenetic Rewiring Blocks Lytic Gammaherpesvirus Production.Viruses · 2026Article
- Kaposi's sarcoma-associated herpesvirus ORF61 protein sequesters APOBEC3B in filamentous aggregates.Journal of virology · 2025Article
- A Mouse Model to Study the Pathogenesis of γ-herpesviral Infections in Germinal Center B Cells.Cells · 2023Article
- ORF6 and ORF61 Expressing MVA Vaccines Impair Early but Not Late Latency in Murine Gammaherpesvirus MHV-68 Infection.Frontiers in immunology · 2019Article
- Nanoparticle exposure reactivates latent herpesvirus and restores a signature of acute infection.Particle and fibre toxicology · 2017Article
- The small noncoding RNAs (sncRNAs) of murine gammaherpesvirus 68 (MHV-68) are involved in regulating the latent-to-lytic switch in vivo.Scientific reports · 2016Article
- Multiple Lytic Origins of Replication Are Required for Optimal Gammaherpesvirus Fitness In Vitro and In Vivo.PLoS pathogens · 2016Article
- Systemic and local infection routes govern different cellular dissemination pathways during gammaherpesvirus infection in vivo.Journal of virology · 2013Article
- A structural basis for BRD2/4-mediated host chromatin interaction and oligomer assembly of Kaposi sarcoma-associated herpesvirus and murine gammaherpesvirus LANA proteins.PLoS pathogens · 2013Article
- Murine gammaherpesvirus 68 glycoprotein 150 does not contribute to latency amplification in vivo.Virology journal · 2012Article
- Molecular biology of Kaposi's sarcoma-associated herpesvirus and related oncogenesis.Advances in virus research · 2010Review
- Initiation of lytic DNA replication in Epstein-Barr virus: search for a common family mechanism.Future virology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Murine gammaherpesvirus 68 (MHV-68) is closely related to Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus (KSHV) and provides a small-animal model to study the pathogenesis of gammaherpesvirus (gammaHV) infections. According to the colinear organization of the gammaHV genomes, the M10 locus is situated at a position equivalent to the K12 locus of KSHV, which codes for proteins of the kaposin family. The M10 locus of MHV-68 has been predicted to code for three overlapping open reading frames (M10a, M10b, and M10c [M10a-c]) with unknown function. In addition, the M10 locus contains a lytic origin of replication (oriLyt). To elucidate the function of the M10 locus during lytic and latent infections, we investigated, both in vitro and in vivo, the following four recombinant viruses which were generated using MHV-68 cloned as a bacterial artificial chromosome: (i) a mutant virus with a deletion which affects both the coding region for M10a-c and the oriLyt; (ii) a revertant virus in which both the M10a-c coding region and the oriLyt were reverted to those of the wild type; (iii) a virus with an ectopic insertion of the oriLyt, which restores the function of the oriLyt but not the M10a-c coding region; and (iv) a mutant virus with a deletion in the oriLyt only. While the mutants were slightly attenuated with regard to lytic replication in cell culture, they showed severe growth defects in vivo. Both lytic replication and latency amplification were strongly reduced. In contrast, both the revertant virus and the virus with the ectopic oriLyt insertion grew very similarly to the parental wild-type virus both in vitro and in vivo. Thus, we provide genetic evidence that mutation of the oriLyt, and not of putative protein coding sequences within the M10a-c region, is responsible for the observed phenotype. We conclude that the oriLyt in the M10 locus plays an important role during infection of mice with MHV-68.
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