Next Article in Journal
Early Phase of the COVID-19 Outbreak in Hungary and Post-Lockdown Scenarios
Previous Article in Journal
Recombination Analysis of Non-Poliovirus Members of the Enterovirus C Species: Restriction of Recombination Events to Members of the Same 3DPol Cluster
Previous Article in Special Issue
In Vivo Characterization of a Bank Vole-Derived Cowpox Virus Isolate in Natural Hosts and the Rat Model
Open AccessArticle

Conserved Oligomeric Golgi (COG) Complex Proteins Facilitate Orthopoxvirus Entry, Fusion and Spread

1
Poxvirus and Rabies Branch, Centers for Disease Control and Prevention, Atlanta, GA 3033, USA
2
Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA 3033, USA
3
Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
4
Department of Microbiology and Immunology, Stanford University, Stanford, CA 94035, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Viruses 2020, 12(7), 707; https://doi.org/10.3390/v12070707
Received: 26 May 2020 / Accepted: 25 June 2020 / Published: 30 June 2020
Although orthopoxviruses (OPXV) are known to encode a majority of the genes required for replication in host cells, genome-wide genetic screens have revealed that several host pathways are indispensable for OPXV infection. Through a haploid genetic screen, we previously identified several host genes required for monkeypox virus (MPXV) infection, including the individual genes that form the conserved oligomeric Golgi (COG) complex. The COG complex is an eight-protein (COG1–COG8) vesicle tethering complex important for regulating membrane trafficking, glycosylation enzymes, and maintaining Golgi structure. In this study, we investigated the role of the COG complex in OPXV infection using cell lines with individual COG gene knockout (KO) mutations. COG KO cells infected with MPXV and vaccinia virus (VACV) produced small plaques and a lower virus yield compared to wild type (WT) cells. In cells where the KO phenotype was reversed using a rescue plasmid, the size of virus plaques increased demonstrating a direct link between the decrease in viral spread and the KO of COG genes. KO cells infected with VACV displayed lower levels of viral fusion and entry compared to WT suggesting that the COG complex is important for early events in OPXV infection. Additionally, fewer actin tails were observed in VACV-infected KO cells compared to WT. Since COG complex proteins are required for cellular trafficking of glycosylated membrane proteins, the disruption of this process due to lack of individual COG complex proteins may potentially impair the virus-cell interactions required for viral entry and egress. These data validate that the COG complex previously identified in our genetic screens plays a role in OPXV infection. View Full-Text
Keywords: COG complex; vaccinia; monkeypox; viral attachment; viral entry; glycosylation COG complex; vaccinia; monkeypox; viral attachment; viral entry; glycosylation
Show Figures

Figure 1

MDPI and ACS Style

Realegeno, S.; Priyamvada, L.; Kumar, A.; Blackburn, J.B.; Hartloge, C.; Puschnik, A.S.; Sambhara, S.; Olson, V.A.; Carette, J.E.; Lupashin, V.; Satheshkumar, P.S. Conserved Oligomeric Golgi (COG) Complex Proteins Facilitate Orthopoxvirus Entry, Fusion and Spread. Viruses 2020, 12, 707.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop