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UL34 Deletion Restricts Human Cytomegalovirus Capsid Formation and Maturation
Declan L Turner1, Rachel M Templin2, Adele A Barugahare1,3
1Infection and Immunity Program, Department of Microbiology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia.
Insights
Human Cytomegalovirus (HCMV) UL34 protein is essential for efficient virion production. Deleting UL34 reduces infectious virions by over 100-fold, impacting viral maturation.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Human Cytomegalovirus (HCMV) infects over 50% of the global population.
- HCMV causes severe issues in immunocompromised individuals and is a major cause of congenital defects.
- Understanding HCMV proteins, particularly those affecting virion maturation, is crucial.
Purpose of the Study:
- To investigate the function of the HCMV UL34 protein.
- To determine UL34's role in viral replication and virion production.
Main Methods:
- Generated a HCMV UL34 deletion mutant (ΔUL34).
- Analyzed viral DNA replication, protein expression (IE1, MCP, gB, UL26, UL83, UL99), and virion production.
- Examined viral assembly compartments and capsid maturation in the nucleus and cytoplasm.
Main Results:
- UL34 is expressed with leaky late kinetics and localizes to the nucleus.
- ΔUL34 mutant produced >100-fold fewer infectious virions but was dispensable for viral DNA replication.
- Virion maturation was abrogated in the cytoplasm, and nuclear replication compartments showed aberrant morphology with fewer capsids.
Conclusions:
- UL34 acts as an augmenting gene, critical for efficient HCMV virion production.
- UL34 plays a significant role in nuclear organization and capsid maturation during HCMV infection.
- Further research into UL34's function in these processes is warranted.
Abstract:
Over 50% of the world’s population is infected with Human Cytomegalovirus (HCMV). HCMV is responsible for serious complications in the immuno-compromised and is a leading cause of congenital birth defects. The molecular function of many HCMV proteins remains unknown, and a deeper understanding of the viral effectors that modulate virion maturation is required. In this study, we observed that UL34 is a viral protein expressed with leaky late kinetics that localises to the nucleus during infection. Deletion of UL34 from the HCMV genome (ΔUL34) did not abolish the spread of HCMV. Instead, over >100-fold fewer infectious virions were produced, so we report that UL34 is an augmenting gene. We found that ΔUL34 is dispensable for viral DNA replication, and its absence did not alter the expression of IE1, MCP, gB, UL26, UL83, or UL99 proteins. In addition, ΔUL34 infections were able to progress through the replication cycle to form a viral assembly compartment; however, virion maturation in the cytoplasm was abrogated. Further examination of the nucleus in ΔUL34 infections revealed replication compartments with aberrant morphology, containing significantly less assembled capsids, with almost none undergoing subsequent maturation. Therefore, this work lays the foundation for UL34 to be further investigated in the context of nuclear organization and capsid maturation during HCMV infection.
