Nontypeable Haemophilus influenzae challenge during gammaherpesvirus infection enhances viral reactivation and latency. Virology 2024 Sep;597:110153
Date
06/29/2024Pubmed ID
38941745Pubmed Central ID
PMC11257779DOI
10.1016/j.virol.2024.110153Scopus ID
2-s2.0-85196778582 (requires institutional sign-in at Scopus site)Abstract
Gammaherpesviruses are ubiquitous, lifelong pathogens associated with multiple cancers that infect over 95% of the adult population. Increases in viral reactivation, due to stress and other unknown factors impacting the immune response, frequently precedes lymphomagenesis. One potential stressor that could promote viral reactivation and increase viral latency would be the myriad of infections from bacterial and viral pathogens that we experience throughout our lives. Using murine gammaherpesvirus 68 (MHV68), a mouse model of gammaherpesvirus infection, we examined the impact of bacterial challenge on gammaherpesvirus infection. We challenged MHV68 infected mice during the establishment of latency with nontypeable Haemophilus influenzae (NTHi) to determine the impact of bacterial infection on viral reactivation and latency. Mice infected with MHV68 and then challenged with NTHi, saw increases in viral reactivation and viral latency. These data support the hypothesis that bacterial challenge can promote gammaherpesvirus reactivation and latency establishment, with possible consequences for viral lymphomagenesis.
Author List
Huss NP, Majeed ST, Wills BM, Tarakanova VL, Brockman KL, Jondle CNAuthors
Kenneth Brockman PhD Assistant Professor in the Microbiology and Immunology department at Medical College of WisconsinVera Tarakanova PhD Professor in the Microbiology and Immunology department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsDisease Models, Animal
Female
Gammaherpesvirinae
Haemophilus Infections
Haemophilus influenzae
Herpesviridae Infections
Mice
Mice, Inbred C57BL
Rhadinovirus
Virus Activation
Virus Latency