Human Cytomegalovirus (HCMV) Tegument Protein pUL35 in the establishment of latency in models of quiescent infection

Abstract

Human Cytomegalovirus (HCMV) is a double stranded DNA, beta herpes virus that primarily infects those with transplants, advanced HIV/AIDS, cancer, newborns, and those with a compromised immune system. This virus is the leading cause of virus‐induced birth defects and can lead to death. HCMV is able to establish a latent phase of virus replication, in which the host is not producing infectious virus, but still retains the complete genome. It can remain in the host for its lifetime until replication is reactivated with the appropriate signal, where the virus can again cause disease. The HCMV tegument is composed of several cellular proteins and mRNAs, and it is unclear if these proteins play any role in the establishment of latency in the host. The tegument protein pUL35 has been shown to have an effect on viral transcription, but the role of this protein in latency is still unclear. The purpose of this study is to determine the role of tegument protein pUL35 in a model of latent infection. Recombinant HCMV was constructed in order to create a deletion of pUL35. Cell models of quiescent and lytic infection were then infected with recombinant virus and measured E, IE, and L gene expression along with genome copy number to determine latent or lytic replication. There are currently no vaccines for prevention and the antiviral therapy that is available has been effective where it can be used, but resistance can develop. The exploration of tegument proteins in latent models of infection could lead to the development of vaccines to target specific viral proteins.