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Nontypeable Haemophilus influenzae challenge during gammaherpesvirus infection enhances viral reactivation and latency
被引:1
|作者:
Huss, Nicholas P.
[1
,2
]
Majeed, Sheikh Tahir
[1
,2
]
Wills, Brandon M.
[3
]
Tarakanova, Vera L.
[3
,4
]
Brockman, Kenneth L.
[3
]
Jondle, Christopher N.
[1
,2
,5
]
机构:
[1] Western Michigan Univ, Homer Stryker MD Sch Med, Dept Invest Med, Kalamazoo, MI 49007 USA
[2] Western Michigan Univ, Ctr Immunobiol, Homer Stryker MD Sch Med, Kalamazoo, MI 49007 USA
[3] Med Coll Wisconsin, Dept Microbiol & Immunol, Milwaukee, WI 53226 USA
[4] Med Coll Wisconsin, Canc Ctr, Milwaukee, WI 53226 USA
[5] 300 Portage St, Kalamazoo, MI 49007 USA
来源:
关键词:
Gammaherpesvirus;
EBV;
KSHV;
MHV68;
Germinal center response;
Latency;
Reactivation;
Bacterial challenge;
Acute bacterial infection;
NTHi;
EPSTEIN-BARR-VIRUS;
GAMMA-HERPESVIRUS LATENCY;
B-CELL RESPONSE;
PERIPHERAL-BLOOD;
GERMINAL CENTER;
IL-17;
LOAD;
PROTECTION;
CYTOKINE;
LYMPHOMA;
D O I:
10.1016/j.virol.2024.110153
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
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.
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